Havent there been worse viruses than this and nothing of this shutdown has occurred?? what am I missing; shit aint even fatal like that; shit is really getting out of hand and ridiculous....
"WW C"- COVID-19, GLOBAL CASES SURPASS 676 MILLION...CASES 676,609,955 DEATHS 6,881,955 US CASES 103,804,263 US DEATHS 1,123,836 8:30pm 1/28/24
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Yes and no. There have been viruses that had a higher death rate among those infected, but they were not as easily transmitted.
We haven't seen something like in long time fam...... Ebola was faster but contained. It never got here... but this thing is faster and can easily be confused .... especially with us in Allergy season.
Plus the worst part is that... It's not about us.. It's the older people like our parents and grandparents. We fuck up... and we can easily slip up and put our parents at risk. That's why we all have to be focused on this shit.
The virus isnt fatal!!! I dont understand why people dont get that; the overwhelming majority of people who get the virus dont even go into critical condition, let alone die; I just feel like this hysteria is ridiculous...
I understand that but its not a fatal virus; it operating like the cold or flu virus; so what is the hysteria for???
This thing has also spread worldwide faster.... Like we have known about this since Dec 1, 2019... It started in a small town in China.. Less then three months later we over 1000 cases in the US. I think the biggest problem is that China held on to this shit for a minute before it got out.
x
The ones recovering have reduced lung capacity and possibly irreparable lung damage. It aggressively attacks the lungs.
The ones recovering have reduced lung capacity and possibly irreparable lung damage. It aggressively attacks the lungs.
It's a respiratory virus fam..
How does that process cause respiratory problems?
As copies of the virus multiply, they burst out and infect neighboring cells. The symptoms often start in the back of the throat with a sore throat and a dry cough.
The virus then “crawls progressively down the bronchial tubes,” Dr. Schaffner said. When the virus reaches the lungs, their mucous membranes become inflamed. That can damage the alveoli or lung sacs and they have to work harder to carry out their function of supplying oxygen to the blood that circulates throughout our body and removing carbon dioxide from the blood so that it can be exhaled.
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“If you get swelling there, it makes it that much more difficult for oxygen to swim across the mucous membrane,” said Dr. Amy Compton-Phillips, the chief clinical officer for the Providence Health System, which included the hospital in Everett, Wash., that had the first reported case of coronavirus in the United States, in January.
The swelling and the impaired flow of oxygen can cause those areas in the lungs to fill with fluid, pus and dead cells. Pneumonia, an infection in the lung, can occur.
Some people have so much trouble breathing they need to be put on a ventilator. In the worst cases, known as Acute Respiratory Distress Syndrome, the lungs fill with so much fluid that no amount of breathing support can help, and the patient dies.
What Does the Coronavirus Do to the Body?
Here’s what scientists have learned about how the new virus infects and attacks cells and how it can affect organs beyond the lungs.
My girl works in the medical field... She describes it as the feeling that someone would get during an Asthma attack. It becomes harder to breathe. Those with healthy immune systems should pull through this with some pain and be fine... Basically fight through the illness ... but those with Weak immune systems, elder, or with developing immune systems are at risk.
When you think about weak immune systems... We are looking at folks in Jail or prison.. folks in nursing homes.. People with malnutrition.. People with Diabetes (like Tom Hanks) .... I could go on and on..
Plus this thing has already mutated twice and we don't have a cure.
So again.. It's not about the young kats... It's trying to prevent this thing from become completely uncontrollable. What if it develops into a more aggressive mutation or becomes no longer resistant to hot temperatures...
So somebody at my job got that shit
Lucky for me, not in the same building
Lucky for me, not in the same building
dude do yourself a favor.... don't give this fool any credence... only reason he's even showing a slight serious interest cause shit is getting real for the drag queen... they canceling all of his sports events that he'd usually be tricking at.... ne came in here callig the videos posted silly as videos to scare people with...I haven't panicked, just sharing today's news conference. It didn't even occur to me to go grocery shopping until reading various threads today and now it's hit closer to home. Muhfuckas around us need not go into panic mode but we can't control how others are gonna react.
Shit's gonna be like Black Friday shopping and I don't participate in that shit.
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only beef is the fatty beef tissue between that fool's ears...I'll just leave you two to settle your beefs.Y'all have at it.
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Keep an eye on this one fellas:
Coronavirus can remain in air for 3 hours, live on plastic for days, new study says
Published 10 hours ago
A new study suggests that the novel coronavirus COVID-19 can remain in the air for up to three hours, and live on surfaces such as plastic and stainless steel for up to three days.
The research, published in the medRxiv depository, also notes that the virus can remain on copper surfaces for four hours and cardboard for up to 24 hours. The research found it could stay on stainless steel and plastic for anywhere between two and three days.
"Our results indicate that aerosol and fomite transmission of HCoV-19 is plausible, as the virus can remain viable in aerosols for multiple hours and on surfaces up to days," the researchers wrote in the study, which has not yet been peer-reviewed.
Another study published in February concluded that if COVID-19 is similar to other coronaviruses, such as SARS or MERS, it could live on surfaces like metal, glass and plastic for up to nine days, Fox News previously reported. By comparison, the flu virus can only live on surfaces for approximately 48 hours.
That study, published in the Journal of Hospital Infection, suggested that coronaviruses could be "efficiently inactivated" with disinfectants that contain "62–71 percent ethanol, 0.5 percent hydrogen peroxide or 0.1 percent sodium hypochlorite within 1 minute," adding that other agents that contain "0.05–0.2% benzalkonium chloride or 0.02 percent chlorhexidine digluconate are less effective."
RELATED: Is it the flu, a cold or COVID-19? Different viruses present similar symptoms
Currently, there is no specific medicine to cure or treat COVID-19.
Coronavirus can remain in air for 3 hours, live on plastic for days, new study says
Published 10 hours ago
A new study suggests that the novel coronavirus COVID-19 can remain in the air for up to three hours, and live on surfaces such as plastic and stainless steel for up to three days.
The research, published in the medRxiv depository, also notes that the virus can remain on copper surfaces for four hours and cardboard for up to 24 hours. The research found it could stay on stainless steel and plastic for anywhere between two and three days.
"Our results indicate that aerosol and fomite transmission of HCoV-19 is plausible, as the virus can remain viable in aerosols for multiple hours and on surfaces up to days," the researchers wrote in the study, which has not yet been peer-reviewed.
Another study published in February concluded that if COVID-19 is similar to other coronaviruses, such as SARS or MERS, it could live on surfaces like metal, glass and plastic for up to nine days, Fox News previously reported. By comparison, the flu virus can only live on surfaces for approximately 48 hours.
That study, published in the Journal of Hospital Infection, suggested that coronaviruses could be "efficiently inactivated" with disinfectants that contain "62–71 percent ethanol, 0.5 percent hydrogen peroxide or 0.1 percent sodium hypochlorite within 1 minute," adding that other agents that contain "0.05–0.2% benzalkonium chloride or 0.02 percent chlorhexidine digluconate are less effective."
RELATED: Is it the flu, a cold or COVID-19? Different viruses present similar symptoms
Currently, there is no specific medicine to cure or treat COVID-19.
It's a respiratory virus fam..
How does that process cause respiratory problems?
As copies of the virus multiply, they burst out and infect neighboring cells. The symptoms often start in the back of the throat with a sore throat and a dry cough.
The virus then “crawls progressively down the bronchial tubes,” Dr. Schaffner said. When the virus reaches the lungs, their mucous membranes become inflamed. That can damage the alveoli or lung sacs and they have to work harder to carry out their function of supplying oxygen to the blood that circulates throughout our body and removing carbon dioxide from the blood so that it can be exhaled.
.
“If you get swelling there, it makes it that much more difficult for oxygen to swim across the mucous membrane,” said Dr. Amy Compton-Phillips, the chief clinical officer for the Providence Health System, which included the hospital in Everett, Wash., that had the first reported case of coronavirus in the United States, in January.
The swelling and the impaired flow of oxygen can cause those areas in the lungs to fill with fluid, pus and dead cells. Pneumonia, an infection in the lung, can occur.
Some people have so much trouble breathing they need to be put on a ventilator. In the worst cases, known as Acute Respiratory Distress Syndrome, the lungs fill with so much fluid that no amount of breathing support can help, and the patient dies.
What Does the Coronavirus Do to the Body?
Here’s what scientists have learned about how the new virus infects and attacks cells and how it can affect organs beyond the lungs.www.nytimes.com
My girl works in the medical field... She describes it as the feeling that someone would get during an Asthma attack. It becomes harder to breathe. Those with healthy immune systems should pull through this with some pain and be fine... Basically fight through the illness ... but those with Weak immune systems, elder, or with developing immune systems are at risk.
When you think about weak immune systems... We are looking at folks in Jail or prison.. folks in nursing homes.. People with malnutrition.. People with Diabetes (like Tom Hanks) .... I could go on and on..
Plus this thing has already mutated twice and we don't have a cure.
So again.. It's not about the young kats... It's trying to prevent this thing from become completely uncontrollable. What if it develops into a more aggressive mutation or becomes no longer resistant to hot temperatures...
I was debating whether or not to post this from a book I posted yesterday. It's not about the virus, but it explains the difference between RNA and DNA viruses. The corona virus is a RNA virus. It's a book on antiviral herbs. I'm posting this because it explains how the viruses act and your body responds, tho it does list a few herbs in this excerpt also. . WARNING: It's a long excerpt.
Viruses are typed in a number of ways: by size or shape, presence or absence of an enclosing capsule (not all have one), whether DNA or RNA based (and from that whether single or double stranded, positive or negative sense), their type of protein structure, and their manner of replication. DNA viruses are fairly reliable as viruses go because they have a kind of “copy-check” mechanism that RNA viruses lack. This means that when a DNA virus is making more of itself within a host cell, it uses a biofeedback loop to make sure the copies of itself are reasonably accurate. In contrast an RNA virus can’t.
It tends to make a whole lot of copies that vary, sometimes a great deal, from the original. Some of these copy differences are initiated intentionally by RNA viruses to increase their genetic varia-tion and, hence, survivability in the host. Because of this, while it is often possible to come up with a lasting vaccine for a DNA virus, it is very hard, if not impossible, to make one for an RNA virus. This also makes RNA viruses very hard to treat with pharmaceuticals; they, like bacteria, begin creating solutions to synthetic drugs the moment they encounter one. Evidence indicates that the mutation rate of the hepatitis C virus, for example, accelerates in response to interferon and ribavirin therapy in much the same way that bacterial alteration occurs in the presence of antibiotics. Infection with an RNA virus like West Nile or Japanese encephalitis is actually quite different than infection with a DNA virus.
While DNA viruses make billions more of themselves, RNA viruses make billions of similar but not identical viruses. It is something like a swarm of honeybees — all similar but all different. In fact it is much more accurate to think of an RNA infection as infection by a viral swarm. The ones most similar to each other are the ones that die off when the human immune system is first activated or a pharmaceutical drug that can recognize them is used. This leaves the others free to multiply unchecked and they multiply very fast indeed (some viruses producing a new generation every minute) while still making subtle changes in each new virus produced.
There is also evidence that both DNA and RNA viruses, like bacteria, share information among themselves in order to remain unaffected by medical treatments or immune systems. Similar viruses will actively share genetic structure to create very difficult-to-treat infections. Influenza viruses (for instance) specifically (and intentionally) both rearrange their genetic structures and insert entirely new genes within themselves on a regular basis in order to remain invisible to the human immune system. And they gather these new gene sequences from pigs and birds in Asia. This is why a new vaccine is needed every year for the flu.
Viruses, when not in a living cell, go into a state of hibernation much like plant seeds. In this state of dormancy they move with air currents, in water, or simply rest dormant on the ground until they come into contact with a life form that contains the cells they need to awaken from their long sleep. At that moment a virus’s first task is to get inside the new host organism, bypass its protective mechanisms, and find the proper host cell. Viruses use highly elegant analysis to address these challenges; they actually begin experimenting with new combinations of genes to adapt to the environment they face. Most of them have also generated a genetic structure that facilitates their entry into other host organisms after an initial infection begins. The rabies virus, for instance, affects a part of the brain that then causes uncontrolled biting. At the same time, the virus swarms in its billions into the saliva of infected animals. Then, every time the animal bites something the virus is transmitted to a new host. Influenza, and other respiratory viruses, enter respiratory droplets and then stimulate coughing or sneezing. Those droplets are then breathed in by new hosts. And still other viruses, spread by mosquitoes, flood into the blood and there stimulate the release of chemicals through the host skin surface that calls mosquitoes to the infected host so that the virus can be picked up and spread to others. Viruses are very good at getting from here to there.
Viruses spread by ticks or mosquitoes take advantage of the compounds in the arthropod saliva to facilitate their entry into the new host. The salival compounds reduce certain immune responses in the host to allow the arthropod to feed and often anesthetize the bite location as well. The lowered immune responses at that location allow the viruses to enter the new host in a place where there will be little resistance. Once inside the viruses will make their way to the draining lymph node nearest the bite location and be carried to the spleen via the lymph. There they will begin altering the host’s immune function, reducing the capacity of immune cells to recognize and kill invading microbes. Once that occurs, the viruses will catch a ride on immune cells, macrophages or monocytes usually, and begin spreading throughout the body. This is common for encephalitis viruses, for example. They will then travel in the lymph to the barrier between the brain and the rest of the body, release compounds that make the barrier more porous, enter the brain, and find the cells they really prefer: brain neurons.
Other viruses enter through being inhaled (influenza) or through sex (HIV) or through being eaten on food (enteroviruses). Once in the body, they hitch rides on whatever cells they have developed a taste for (usually immune cells, for those cells travel everywhere) and actively seek out their preferred location. Such is the case with HIV, which views T4 lymphocytes as the perfect host cells, or the Epstein-Barr virus, which has an affinity for human B cells, or the Japanese enceph-alitis virus, which loves monocytes.
To hitch rides, a virus uses chemo-tactic compounds that allow it to stick to its preferred “taxi” cell. The receptors on the surface of the virus fool the cell into thinking it is a compatible protein that has attached, and through a series of chemical communications, the virus gets the cell to let it inside. Basically, it gets the cell’s confidence, then abuses it. From there the virus is carried every-place it might need to go in the body. Once near its preferred location, it leaves its ride, attaches to the cell that is most specific for it, and once again fools the cell into taking it inside. Now it begins to replicate in its millions.
Once inside the primary habitat cell, the virus sheds its protein coat and begins taking over the cell. First it stops the cell from dying, which infected cells are programmed to do, and there it remains, protected from the rest of the immune system. It then breaks off pieces of itself and sends them into the nucleus of the cell, which is then tricked into making copies of the virus, using the viral proteins as a template. These new viral particles exit the nucleus, travel to the interior of the cell wall, and bubble out (viral budding, they call it). The cell dies during this process and bursts apart, and the viruses take up parts of the cell membrane and make themselves new viral protein coats with receptors for new host cells. And it all happens very quickly.
Thus the ancient struggle begins: finding out which is in better shape — the organism’s immune system or the replicating virus. If the virus is particularly strong or if the immune system is compromised in any way, the virus can really take hold and illness, sometimes severe illness, is inevitable.
the Influenza Virus
The influenza virus is a member of the Orthomyxoviridae family. It is an RNA virus and that means it alters its genetic structure very quickly. That is why a new flu shot is needed every year (for those in the Western world who have such things available). The old vaccine can only help prevent infection by the strain that has emerged in that particular year. The next year, it is not the same virus, merely a similar one. Influenza viruses spread around the world every year in seasonal epidemics; 250,000 to 500,000 people die from them each time.
About one-third of people who are infected remain asymptomatic; the rest get some degree of the “flu.” The first symptoms are usu-ally a feeling of being cold or achy and perhaps the beginnings of a fever. High fever alternating with severe chills sets in as the infection spreads. As the virus enters the lungs and sinus tissues mucous con-gestion begins. Coughing, body aches, fatigue, headache, and irritated eyes, nose, and throat are common. Some people will have diarrhea and abdominal pain. Vomiting. Sometimes. Yes.
The symptoms of the infection usually begin the third day after infection. But the virus is already well established by then. It starts replicating the second day, then begins “shedding ” viral particles that are released in increasing numbers for the next 5 to 7 days. The higher the fever, the more viral organisms that are being released. Children are extremely infectious compared to adults, with very high viral loads. They also tend to have very high fevers.
As the virus invades the lungs it stimulates inflammation in the tissues. The lung cells, filled with viruses, soon bulge outward and explode — the essence of viral shedding. Then the virus stimulates coughing, spreading the virus to new hosts via respiratory droplets. Pneumonia, a severe inflammation of the lungs accompanied by mas-sive fluid retention and an inability to breathe, is the main cause of death. People, in essence, drown.
There are three different groups of influenza viruses, denoted A, B, and C. Influenza A is the most virulent. Influenza B is a relatively stable virus and mutates much more slowly than A. Most people develop, in childhood, at least some immunity to it; it is much less dangerous. Influenza C is fairly rare. It does infect people, sometimes severely, but it usually causes only a mild illness, generally in children. When people talk about an influenza pandemic, what they are talking about is influenza A in one of its many genetically altered forms. The 1918 pandemic was caused by an influenza A strain.
There have been numerous pandemics of influenza over the years, each caused by a different strain of the virus. The one in 1918 was the beginning of the modern influenza pandemic era; such pandemics were much less common before then. There was a long rest after 1918. Since 1957, however, they have been occurring with greater frequency.
The most dangerous strains, currently, are H1N1, which caused the flu pandemic of 1918; H2N2, which caused the Asian flu pandemic in 1957; H3N2, which caused the Hong Kong flu pandemic in 1968; and a relatively new one, H5N1, known as avian or bird flu, which caused a pandemic in 2004. Then H1N1 came again. It was the source of the swine flu pandemic in 2009 and is a modified descendant of the 1918 H1N1 strain.
The influenza virus alters its genetic structure rather significantly every year by passing through both pigs and birds. And on that trip it exchanges genetic material with other viruses and reworks its own. Then it spreads around the world again by plane and boat, rail and car, infecting millions, causing what we call the yearly flu season. But every so often it develops a much more virulent strain, sometimes through unique genetic rearrangements, sometimes through species jumps, sometimes through both. The Asian flu pandemic in 2004 was a species jump. The swine flu epidemic of 2009 was a unique genetic rearrangement. It occurred when the virus took advantage of giant agribusiness animal crowding.
Viral geneticists have traced the lineage of the 2009 swine flu epidemic, a virulent H1N1 strain, to an H3N2 strain that emerged in 1998 in U.S. factory farms, specifically huge hog farms in which the animals are so tightly packed together that they literally cannot move. This H3N2 strain combined with another swine strain, a European H1N2 variant, rearranged genetic material into a new and very potent H1N1 form, and then emerged into the human population. The earliest infections occurred in La Gloria, Veracruz, Mexico, just adjacent to a huge hog farm. The workers became infected with the new strain, went home, infected others, many of whom traveled to other cities and towns, and the pandemic began. And it was particularly deadly for those who were infected. Among those hospitalized, depending on location, up to 31 percent were in intensive care units, and as many as 46 percent of those receiving intensive care died
One of the main fears that epidemiologists and viral geneticists have is the possibility of a combined swine and avian flu strain. The crowding of human food animals, similar to the crowding of soldiers in trenches in World War I, continually allows for the emergence of potently virulent strains. Chicken farms, in which unique avian flu strains can emerge, and hog farms, in which unique swine strains can emerge, are perfectly positioned to allow the combination of the two into one potent, and very deadly, influenza strain. This kind of combined strain can then pass easily into farm workers and thence into the population at large.
Researchers have found that, indeed, the H3N2 swine flu virus easily combines with H5N1 strains of avian flu. When that occurs, a tremendously pathogenic form of the virus emerges. It is, they insist, only a matter of time until it occurs on its own. In fact, studies of pigs on large farms adjacent to poultry farms have found such viral combinations already infecting pigs. That combined viral strain has not infected people . . . yet.
One of the main fears that epidemiologists and viral geneticists have is the possibility of a combined swine and avian flu strain. The crowding of human food animals, similar to the crowding of soldiers in trenches in World War I, continually allows for the emergence of potently virulent strains. Chicken farms, in which unique avian flu strains can emerge, and hog farms, in which unique swine strains can emerge, are perfectly positioned to allow the combination of the two into one potent, and very deadly, influenza strain. This kind of combined strain can then pass easily into farm workers and thence into the population at large.Researchers have found that, indeed, the H3N2 swine flu virus easily combines with H5N1 strains of avian flu. When that occurs, a tremendously pathogenic form of the virus emerges. It is, they insist, only a matter of time until it occurs on its own. In fact, studies of pigs on large farms adjacent to poultry farms have found such viral combinations already infecting pigs. That combined viral strain has not infected people . . . yet.
Infection dynamics and the Cytokine Cascade
Cytokines are physiological signaling molecules produced by the body for a variety of reasons. They are produced in the largest numbers during infections. Cytokines (and their cousins, chemokines) are generally part of the innate (rather than the adapted) immune system. They are intended to respond to incursions into our bodies by viruses and bacteria. Another way to think of them is as inflammatory molecules. They cause various sorts of inflammation in the body — they are why, when you cut yourself, the wound gets red and tender and swells. The cytokines rushing to the area create conditions in which many bacteria and viruses find it difficult to survive. Unfortunately for us, bacteria and viruses have also learned how to use our own immune responses for their purposes. They subvert them, quite often, to facilitate their infection of the body and their destruction of certain areas of the body. This facilitates their reproduction and allows them to gather nutrients. Influenza viruses love the lungs and it is where they cause the greatest damage.
Unlike encephalitis viruses, which love brain neurons but have to find their way to the brain after being injected into people by mos-quitoes, influenza viruses don’t have to work nearly so hard. They are taken to the location they like best simply because we need to breathe
Once inhaled, the viruses begin attaching to lung epithelial cells. They use a kind of agglutinin (a substance that glues things to itself — its name shares a root with the English word “glue”), a hemagglutinin, to bind to what are called sialic acid linkages on the surface of airway epithelial cells. (This is one mechanism by which plants such as Chinese skullcap and ginger stop influenza infections; they are hem-agglutinin inhibitors.) All viruses do this in their own way; they have an affinity for a unique receptor on the surface of specific cells and in one way or another they get to that location and those particular cells. Once there, they attach to that part of the cells. In a sense they use that part of the host cells’ membrane as a docking port.
As soon as it is attached to a cell, the virus begins to alter the per-meability of the cell wall, inducing alterations in the cell’s cytoskeleton and initiating endocytosis. In other words, it makes the cell surface more soft, causes the skeletal structure of the cell to bend apart, and tricks the cell into taking the virus inside it where it can’t be found by the immune system. It does this by using a particular kind of enzyme, neuraminidase — which is sometimes also called a sialidase because such enzymes catalyze, or break apart, the sialic acid linkages on the host cell surface. This is why neuraminidase inhibitors (such as Tamiflu, i.e., oseltamivir) are effective in the treatment of influenza; they inhibit the ability of the virus to enter host cells. This stops the infection. (Chinese skullcap, elder, licorice, rhodiola, ginger, isatis, Les-pedeza bicolor, Angelica keiskei, Amorpha fruticosa, quercetin, Alpinia zerumbet, Erythrina addisoniae,and Cleistocalyx operculatus are all neuraminidase inhibitors.) Neuraminidase inhibitors are effective against both influenza A and B strains.
During the process of endocytosis, the virus stimulates the cell to create what is called a vacuole, essentially a sealed bubble that will be held inside the cell. Cells do this to sequester substances that can damage them. Microbes have learned to use such vacuoles for their own purposes, usually to protect the virus or bacteria from intracel-lular antimicrobial actions
The virus uses its hemagglutinin to bind itself to the inside of the vacuole membrane, where it opens a pore to the cell’s cytoplasm, i.e., its interior spaces. To do this the virus uses what is called the M2 ion channel — ion channels are tiny pores in cells that allow charged molecules to enter and exit cells, bringing food in and allowing waste out. Using an M2 inhibitor blocks this process and literally stops the virus from replicating. (Lomatium is one of the most potent M2 inhibi-tors known, stronger than the pharmaceutical amantadine.) Use of the M2 channel is specific to the influenza A virus, which is why the development of blockers for it was considered crucial. Unfortunately, the extensive use of chemical M2 inhibitors such as amantadine in poultry farms has now created nearly complete resistance to them in all influenza A strains.
Once the pore is open, the virus disassembles itself and releases viral RNA and core proteins into the cytoplasm. (Chinese skullcap inhibits this kind of viral RNA release.) The core proteins and viral RNA form a complex that is taken into the nucleus of the cell, where the cell is stimulated to begin making copies of the viral RNA (each slightly different). The new viral RNA is combined with other newly manufactured virus components such as neuraminidase and hemagglutinin and assembled into new viruses. These attach to the inside of the host cell membrane, a bulge forms in the membrane, and the new viruses are expressed (viral budding or shedding) into the extracellular matrix surrounding the cell.
The cell is taken over by the virus in this process, its own components depleted during the creation of new viruses. Once its resources are gone, the cell dies and the newly created viruses move on to new host cells, beginning the process all over again.
The alveolar epithelial cells are specific sites for this process to occur. The alveoli are tiny sacs that are the terminal end of the respi-ratory tree. The air we breathe travels throughout the bronchial tree, eventually emerging into the alveoli, where the oxygen transfuses across very thin membranes into the blood. This is how our bodies remain oxygenated. In the cells lining those tiny sacs the viruses breed. They cause extreme inflammation, or swelling, of the cells in that location with resulting edema (fluid accumulation). All the infected cells burst open and die as new viruses are made. So, fewer alveoli are functional. Breathing is more difficult and the infected person has much less energy because oxygen is not making it into the blood in sufficient quantities. (This is why hospitals sometimes give the infected oxygen.) Pneumonia is when this process becomes severe, the sacs filling with increasing amounts of fluid while there are fewer and fewer functional alveoli.
Throughout the cellular infection and replication process, the virus is also stimulating the release of cytokines by the cell. These cytokines make the tight junctions between cells (and the cellular membranes) more porous and allow easier movement of viral particles through the extracellular matrix (and into the cells themselves). The cytokines are also stimulated in just such a way as to keep the parts of the immune system that can kill the viruses suppressed for as long as possible.
Toll-like receptors (TLRs) are pattern recognition receptors that can identify different types of microbes. The virus particles stimulate TLR3, which begins inducing the release of nuclear factor kappa-B (NF-κB) cytokines. NF-κB is an upstream cytokine, meaning that it is a powerful initiator of other inflammatory cytokines. NF-κB beginsvery specific types of cytokine cascades. Other types of initiators such as RIG-1, NOD2, and MDA5 are also released as part of the body’s reaction to a viral infection. Normally, these would strongly stimulate type 1 interferon (IFN) production (IFN-α and IFN-ß). And influenza viruses are generally very susceptible to these interferons. However, the influenza virus uses a protein, the NS1 protein, which blocks the induction of type 1 IFNs long enough to get established in the body.
(Upregulating the production of type I interferons with herbs such as licorice will help reduce the severity of the infection.) The virus also inhibits dendritic cell maturation and activation, lowering the response levels of T and B cells. (Increasing T cell counts is particu-larly effective in reducing influenza severity. Licorice, elder, red root, and zinc are specific for this.) These cells are part of the adaptive immune response; suppressing them protects the virus from attack. The body response also stimulates the release of type III interferons, to which the virus is less susceptible and which it does nothing to sup-press. These interferons have general, rather than specific, antiviral qualities and are upregulated within 3 to 6 hours of infection. This is what begins causing the general flu-like feelings that presage a full-blown flu episode. The virus itself does not make you feel “fluey.”
During this same time period, the infected airway cells (tracheo-bronchial and alveolar epithelial cells) begin generating specific cyto-kines and chemokines: interleukin-1 beta (IL-1ß), IL-6, IL-18 (which causes spikes in IFN-γ production), C-C chemokine ligand 5 (CCL5, also known as RANTES, “regulated and normal T cell expressed and secreted”), C-X-C chemokine ligand 10 (CXCL10). Then, some 12 to 16 hours later, other cytokines are produced: tumor necrosis factor alpha (TNF-α), IL-8, and CCL2 (also known as monocyte chemoattractant protein-1 or MCP-1). The expressed cytokines make the epithelial structures more porous. This assists faster viral penetration of the cells. It also stimulates the migration of immune cells to the sites of infection.
Interferon-gamma (IFN-γ) is a type 2 interferon, sometimes called macrophage-activating factor. It is this IFN that is crucial in the cyto-kine overinflammation that occurs during severe influenza. By stimu-lating it, the virus initiates a positive feedback loop in the cytokine process that leads, in severe infections, to cytokine storms.
CCL2 causes the migration of blood-derived monocytes into the alveolar airspaces. TNF-α and IL-1ß upregulate adhesion molecules (which include intercellular adhesion molecule 1, a.k.a. ICAM-1, and E-selectin) on the surface of the endothelial cells that line blood vessels. This helps the endothelial lining become more porous and stimulates the transendothelial migration of neutrophils to those locations. TNF-α induces monocyte and neutrophil movement across the epithelium through ICAM-1 and VCAM-1 (vascular cell adhe-sion molecule-1) upregulation. The consequence of this is increasing amounts of white-blood-cell-filled mucus in the lungs. (This is what we cough up during a flu infection.)
The size of the drainage lymph nodes in the lungs begins to increase. This helps, during a healthy resolution of infection, to drain more of the fluids from the lungs, preventing suffocation. Within those lymph nodes, areas called the geminal centers increase their size and development. The germinal centers are the sites where B lymphocytes are produced and are differentiated in order to attack the specific infection that is occurring. This is part of the adaptive humoral immune response. These lymph node locations (as well as those in peripheral tissues) can become overfull during severe infec-tions, slowing drainage and healthy adaptive immune responses. They can also, during severe influenza infections, be specifically attacked and damaged so that they do not function at all. This is a contributor to the mortality that sometimes occurs during cytokine storms. (This is why herbs such as red root, inmortal, and pleurisy root are useful; they all support the lymph structures in the lungs and periphery. Red root — Ceanothus spp. — is particular useful in the periphery for spleen and lymph enlargement and lymph drainage; inmortal — Asclepias asperula — is specific for optimizing lymph drainage from the lungs; pleurisy root — Asclepias tuberosa — is specific for reducing inflam-mation in the pleurae and lungs. They can be used interchangeably to some extent.) The lymph centers in the lungs are heavily affected during influenza, much more so than the periphery
Similarly to many viruses, while influenza viruses reproduce most efficiently in the alveolar epithelial cells, they can also infect other cells, specifically dendritic cells, monocytes, macrophages, neutro-phils, T cells, B cells, and natural killer (NK) cells. In response to being infected those cells also begin releasing cytokines and chemokines:
IFNs, IL-1α and IL-1ß, IL-6, TNF-α, CXCL8, CCL2 (MCP-1), CCL3 (a.k.a. macrophage inflammatory protein-1 alpha, or MIP-1α), CCL4, CXCL9, and CXCL10 through the ERK-1, ERK-2 (extracelluar-signal-regulated kinase 1 and 2), p38 MAPK (p38 mitogen-activated protein kinase), and JNK (c-Jun N-terminal kinase) pathways.
TNF-α, IL-1ß, IL-6, and IFN-γ are responsible for most of the nega-tive effects of the cytokine cascade. Mice that are unable to produce TNF-α consistently show decreased mortality, a reduced symptom picture, and less severe course of the disease. This holds true even if they are infected with the reconstituted, and very virulent, 1918 virus. Inhibition of TNF-α (especially) and IL-1ß has been found to signifi-cantly reduce the cytokine-based inflammation that occurs during influenza, alleviating symptoms and inhibiting viral spread. (Herbs specific for inhibiting TNF-α are kudzu, Chinese senega root, Chinese skullcap, elder, ginger, houttuynia, licorice, boneset, and cordyceps. Herbs specific for inhibiting IL-1ß are Japanese knotweed, Chinese senega root, Chinese skullcap, cordyceps, kudzu, and boneset.)
The virus can also inhibit the production of macrophages over time. This occurs because, over time, macrophages will begin pro-ducing anti-inflammatory cytokines such as IL-4 and IL-10. Once the bodily system is macrophage-depleted a prolonged inflammatory process occurs, keeping the infection going. Lung levels of IL-1ß, IL-6, and TNF-α all increase considerably at that point. Stimulating mono-cyte and dendritic cell maturation (cordyceps) and inducing IL-4 and IL-10 (Chinese skullcap, elder, houttuynia, licorice, cordyceps) will help counteract this
he virus is exceptionally sophisticated in its impacts. There are three stages of chemokine stimulation. The first, 2 to 4 hours postin-fection, is attended by the production of CXCL16, CXCL1, CXCL2, and CXCL3. These chemokines are specific for attracting neutro-phils, cytotoxic T cells, and NK cells. At 8 to 12 hours postinfection CXCL8, CCL3, CCL4, CCL5, CXCL9, CXCL10, and CXCL11 are being produced, which attract effector memory T cells. At 24 to 48 hours post infection, when dendritic cells are most present in the lymphoid tissues, the chemokine profile changes again in such a manner as to attract naive T and B cells. The effect of all this is the virus playing the immune system as a virtuoso plays a violin. Eventually the immune system catches up (usually) and the infection is stopped as influenza-specific antibodies are created.
Plants that reduce the other main cytokines that the virus stimu-lates will also help lessen disease severity and prevent lung damage. I think the most important are inhibitors of NF-κB (Chinese senega root, Chinese skullcap, ginger, houttuynia, kudzu, licorice, boneset, astragalus), IL-6 (kudzu, Chinese skullcap, isatis), IL-8 (cordyceps, isatis, Japanese knotweed), RANTES (licorice, isatis), MCP-1 (hout-tuynia), CXCL10 ( boneset), CCL2 ( boneset), the ERK pathway (kudzu, Chinese skullcap, cordyceps), the p38 pathway (Chinese skullcap, houttuynia, cordyceps ), and the JNK pathway (Chinese skullcap, cordyceps, lion’s mane). The reduction of these cytokines and pathways will reduce IFN-γ.
tissues, the chemokine profile changes again in such a manner as to attract naive T and B cells. The effect of all this is the virus playing the immune system as a virtuoso plays a violin. Eventually the immune system catches up (usually) and the infection is stopped as influenza-specific antibodies are created.Plants that reduce the other main cytokines that the virus stimu-lates will also help lessen disease severity and prevent lung damage. I think the most important are inhibitors of NF-κB (Chinese senega root, Chinese skullcap, ginger, houttuynia, kudzu, licorice, boneset, astragalus), IL-6 (kudzu, Chinese skullcap, isatis), IL-8 (cordyceps, isatis, Japanese knotweed), RANTES (licorice, isatis), MCP-1 (hout-tuynia), CXCL10 ( boneset), CCL2 ( boneset), the ERK pathway (kudzu, Chinese skullcap, cordyceps), the p38 pathway (Chinese skullcap, houttuynia, cordyceps ), and the JNK pathway (Chinese skullcap, cordyceps, lion’s mane). The reduction of these cytokines and pathways will reduce IFN-γ.Each type of influenza has a slightly different cytokine profile with slightly different cytokines more strongly represented. However, the protocols herein, directed to this form of cytokine profile, will be spe-cific enough for every strain, including the low pathogenic avian strain H9N2, which strongly upregulates transforming growth factor beta 2 (TGF-ß2), a different dynamic entirely. Medicinal plants already in use in the developed protocol are, however, specific for TGF-ß2, i.e., astragalus (the strongest) and Chinese skullcap. Magnolia officinalis, Ginkgo biloba, Folium syringae, Nigella sativa, Paeonia lactiflora, and Lonicera japonica are other plants specific for inhibiting TGF-ß2. (This is why lonicera, or Japanese honeysuckle, is commonly used in the treatment of respiratory infections in China — it alleviates wind heat and expels wind heat invasion. In other words, it reduces inflammation in the lungs and expels the virus or bacteria responsible.)
Normally, influenza viruses stay in the upper respiratory tract. However, during more severe infections they will infect the lower respiratory tract as well. Pneumonia is one serious complication from that. So are cytokine storms, should the disease really take hold.
Thus the ancient struggle begins: finding out which is in better shape — the organism’s immune system or the replicating virus. If the virus is particularly strong or if the immune system is compromised in any way, the virus can really take hold and illness, sometimes severe illness, is inevitable.
the Influenza Virus
The influenza virus is a member of the Orthomyxoviridae family. It is an RNA virus and that means it alters its genetic structure very quickly. That is why a new flu shot is needed every year (for those in the Western world who have such things available). The old vaccine can only help prevent infection by the strain that has emerged in that particular year. The next year, it is not the same virus, merely a similar one. Influenza viruses spread around the world every year in seasonal epidemics; 250,000 to 500,000 people die from them each time.
About one-third of people who are infected remain asymptomatic; the rest get some degree of the “flu.” The first symptoms are usu-ally a feeling of being cold or achy and perhaps the beginnings of a fever. High fever alternating with severe chills sets in as the infection spreads. As the virus enters the lungs and sinus tissues mucous con-gestion begins. Coughing, body aches, fatigue, headache, and irritated eyes, nose, and throat are common. Some people will have diarrhea and abdominal pain. Vomiting. Sometimes. Yes.
The symptoms of the infection usually begin the third day after infection. But the virus is already well established by then. It starts replicating the second day, then begins “shedding ” viral particles that are released in increasing numbers for the next 5 to 7 days. The higher the fever, the more viral organisms that are being released. Children are extremely infectious compared to adults, with very high viral loads. They also tend to have very high fevers.
As the virus invades the lungs it stimulates inflammation in the tissues. The lung cells, filled with viruses, soon bulge outward and explode — the essence of viral shedding. Then the virus stimulates coughing, spreading the virus to new hosts via respiratory droplets. Pneumonia, a severe inflammation of the lungs accompanied by mas-sive fluid retention and an inability to breathe, is the main cause of death. People, in essence, drown.
There are three different groups of influenza viruses, denoted A, B, and C. Influenza A is the most virulent. Influenza B is a relatively stable virus and mutates much more slowly than A. Most people develop, in childhood, at least some immunity to it; it is much less dangerous. Influenza C is fairly rare. It does infect people, sometimes severely, but it usually causes only a mild illness, generally in children. When people talk about an influenza pandemic, what they are talking about is influenza A in one of its many genetically altered forms. The 1918 pandemic was caused by an influenza A strain.
There have been numerous pandemics of influenza over the years, each caused by a different strain of the virus. The one in 1918 was the beginning of the modern influenza pandemic era; such pandemics were much less common before then. There was a long rest after 1918. Since 1957, however, they have been occurring with greater frequency.
The most dangerous strains, currently, are H1N1, which caused the flu pandemic of 1918; H2N2, which caused the Asian flu pandemic in 1957; H3N2, which caused the Hong Kong flu pandemic in 1968; and a relatively new one, H5N1, known as avian or bird flu, which caused a pandemic in 2004. Then H1N1 came again. It was the source of the swine flu pandemic in 2009 and is a modified descendant of the 1918 H1N1 strain.
The influenza virus alters its genetic structure rather significantly every year by passing through both pigs and birds. And on that trip it exchanges genetic material with other viruses and reworks its own. Then it spreads around the world again by plane and boat, rail and car, infecting millions, causing what we call the yearly flu season. But every so often it develops a much more virulent strain, sometimes through unique genetic rearrangements, sometimes through species jumps, sometimes through both. The Asian flu pandemic in 2004 was a species jump. The swine flu epidemic of 2009 was a unique genetic rearrangement. It occurred when the virus took advantage of giant agribusiness animal crowding.
Viral geneticists have traced the lineage of the 2009 swine flu epidemic, a virulent H1N1 strain, to an H3N2 strain that emerged in 1998 in U.S. factory farms, specifically huge hog farms in which the animals are so tightly packed together that they literally cannot move. This H3N2 strain combined with another swine strain, a European H1N2 variant, rearranged genetic material into a new and very potent H1N1 form, and then emerged into the human population. The earliest infections occurred in La Gloria, Veracruz, Mexico, just adjacent to a huge hog farm. The workers became infected with the new strain, went home, infected others, many of whom traveled to other cities and towns, and the pandemic began. And it was particularly deadly for those who were infected. Among those hospitalized, depending on location, up to 31 percent were in intensive care units, and as many as 46 percent of those receiving intensive care died
One of the main fears that epidemiologists and viral geneticists have is the possibility of a combined swine and avian flu strain. The crowding of human food animals, similar to the crowding of soldiers in trenches in World War I, continually allows for the emergence of potently virulent strains. Chicken farms, in which unique avian flu strains can emerge, and hog farms, in which unique swine strains can emerge, are perfectly positioned to allow the combination of the two into one potent, and very deadly, influenza strain. This kind of combined strain can then pass easily into farm workers and thence into the population at large.
Researchers have found that, indeed, the H3N2 swine flu virus easily combines with H5N1 strains of avian flu. When that occurs, a tremendously pathogenic form of the virus emerges. It is, they insist, only a matter of time until it occurs on its own. In fact, studies of pigs on large farms adjacent to poultry farms have found such viral combinations already infecting pigs. That combined viral strain has not infected people . . . yet.
One of the main fears that epidemiologists and viral geneticists have is the possibility of a combined swine and avian flu strain. The crowding of human food animals, similar to the crowding of soldiers in trenches in World War I, continually allows for the emergence of potently virulent strains. Chicken farms, in which unique avian flu strains can emerge, and hog farms, in which unique swine strains can emerge, are perfectly positioned to allow the combination of the two into one potent, and very deadly, influenza strain. This kind of combined strain can then pass easily into farm workers and thence into the population at large.Researchers have found that, indeed, the H3N2 swine flu virus easily combines with H5N1 strains of avian flu. When that occurs, a tremendously pathogenic form of the virus emerges. It is, they insist, only a matter of time until it occurs on its own. In fact, studies of pigs on large farms adjacent to poultry farms have found such viral combinations already infecting pigs. That combined viral strain has not infected people . . . yet.
Infection dynamics and the Cytokine Cascade
Cytokines are physiological signaling molecules produced by the body for a variety of reasons. They are produced in the largest numbers during infections. Cytokines (and their cousins, chemokines) are generally part of the innate (rather than the adapted) immune system. They are intended to respond to incursions into our bodies by viruses and bacteria. Another way to think of them is as inflammatory molecules. They cause various sorts of inflammation in the body — they are why, when you cut yourself, the wound gets red and tender and swells. The cytokines rushing to the area create conditions in which many bacteria and viruses find it difficult to survive. Unfortunately for us, bacteria and viruses have also learned how to use our own immune responses for their purposes. They subvert them, quite often, to facilitate their infection of the body and their destruction of certain areas of the body. This facilitates their reproduction and allows them to gather nutrients. Influenza viruses love the lungs and it is where they cause the greatest damage.
Unlike encephalitis viruses, which love brain neurons but have to find their way to the brain after being injected into people by mos-quitoes, influenza viruses don’t have to work nearly so hard. They are taken to the location they like best simply because we need to breathe
Once inhaled, the viruses begin attaching to lung epithelial cells. They use a kind of agglutinin (a substance that glues things to itself — its name shares a root with the English word “glue”), a hemagglutinin, to bind to what are called sialic acid linkages on the surface of airway epithelial cells. (This is one mechanism by which plants such as Chinese skullcap and ginger stop influenza infections; they are hem-agglutinin inhibitors.) All viruses do this in their own way; they have an affinity for a unique receptor on the surface of specific cells and in one way or another they get to that location and those particular cells. Once there, they attach to that part of the cells. In a sense they use that part of the host cells’ membrane as a docking port.
As soon as it is attached to a cell, the virus begins to alter the per-meability of the cell wall, inducing alterations in the cell’s cytoskeleton and initiating endocytosis. In other words, it makes the cell surface more soft, causes the skeletal structure of the cell to bend apart, and tricks the cell into taking the virus inside it where it can’t be found by the immune system. It does this by using a particular kind of enzyme, neuraminidase — which is sometimes also called a sialidase because such enzymes catalyze, or break apart, the sialic acid linkages on the host cell surface. This is why neuraminidase inhibitors (such as Tamiflu, i.e., oseltamivir) are effective in the treatment of influenza; they inhibit the ability of the virus to enter host cells. This stops the infection. (Chinese skullcap, elder, licorice, rhodiola, ginger, isatis, Les-pedeza bicolor, Angelica keiskei, Amorpha fruticosa, quercetin, Alpinia zerumbet, Erythrina addisoniae,and Cleistocalyx operculatus are all neuraminidase inhibitors.) Neuraminidase inhibitors are effective against both influenza A and B strains.
During the process of endocytosis, the virus stimulates the cell to create what is called a vacuole, essentially a sealed bubble that will be held inside the cell. Cells do this to sequester substances that can damage them. Microbes have learned to use such vacuoles for their own purposes, usually to protect the virus or bacteria from intracel-lular antimicrobial actions
The virus uses its hemagglutinin to bind itself to the inside of the vacuole membrane, where it opens a pore to the cell’s cytoplasm, i.e., its interior spaces. To do this the virus uses what is called the M2 ion channel — ion channels are tiny pores in cells that allow charged molecules to enter and exit cells, bringing food in and allowing waste out. Using an M2 inhibitor blocks this process and literally stops the virus from replicating. (Lomatium is one of the most potent M2 inhibi-tors known, stronger than the pharmaceutical amantadine.) Use of the M2 channel is specific to the influenza A virus, which is why the development of blockers for it was considered crucial. Unfortunately, the extensive use of chemical M2 inhibitors such as amantadine in poultry farms has now created nearly complete resistance to them in all influenza A strains.
Once the pore is open, the virus disassembles itself and releases viral RNA and core proteins into the cytoplasm. (Chinese skullcap inhibits this kind of viral RNA release.) The core proteins and viral RNA form a complex that is taken into the nucleus of the cell, where the cell is stimulated to begin making copies of the viral RNA (each slightly different). The new viral RNA is combined with other newly manufactured virus components such as neuraminidase and hemagglutinin and assembled into new viruses. These attach to the inside of the host cell membrane, a bulge forms in the membrane, and the new viruses are expressed (viral budding or shedding) into the extracellular matrix surrounding the cell.
The cell is taken over by the virus in this process, its own components depleted during the creation of new viruses. Once its resources are gone, the cell dies and the newly created viruses move on to new host cells, beginning the process all over again.
The alveolar epithelial cells are specific sites for this process to occur. The alveoli are tiny sacs that are the terminal end of the respi-ratory tree. The air we breathe travels throughout the bronchial tree, eventually emerging into the alveoli, where the oxygen transfuses across very thin membranes into the blood. This is how our bodies remain oxygenated. In the cells lining those tiny sacs the viruses breed. They cause extreme inflammation, or swelling, of the cells in that location with resulting edema (fluid accumulation). All the infected cells burst open and die as new viruses are made. So, fewer alveoli are functional. Breathing is more difficult and the infected person has much less energy because oxygen is not making it into the blood in sufficient quantities. (This is why hospitals sometimes give the infected oxygen.) Pneumonia is when this process becomes severe, the sacs filling with increasing amounts of fluid while there are fewer and fewer functional alveoli.
Throughout the cellular infection and replication process, the virus is also stimulating the release of cytokines by the cell. These cytokines make the tight junctions between cells (and the cellular membranes) more porous and allow easier movement of viral particles through the extracellular matrix (and into the cells themselves). The cytokines are also stimulated in just such a way as to keep the parts of the immune system that can kill the viruses suppressed for as long as possible.
Toll-like receptors (TLRs) are pattern recognition receptors that can identify different types of microbes. The virus particles stimulate TLR3, which begins inducing the release of nuclear factor kappa-B (NF-κB) cytokines. NF-κB is an upstream cytokine, meaning that it is a powerful initiator of other inflammatory cytokines. NF-κB beginsvery specific types of cytokine cascades. Other types of initiators such as RIG-1, NOD2, and MDA5 are also released as part of the body’s reaction to a viral infection. Normally, these would strongly stimulate type 1 interferon (IFN) production (IFN-α and IFN-ß). And influenza viruses are generally very susceptible to these interferons. However, the influenza virus uses a protein, the NS1 protein, which blocks the induction of type 1 IFNs long enough to get established in the body.
(Upregulating the production of type I interferons with herbs such as licorice will help reduce the severity of the infection.) The virus also inhibits dendritic cell maturation and activation, lowering the response levels of T and B cells. (Increasing T cell counts is particu-larly effective in reducing influenza severity. Licorice, elder, red root, and zinc are specific for this.) These cells are part of the adaptive immune response; suppressing them protects the virus from attack. The body response also stimulates the release of type III interferons, to which the virus is less susceptible and which it does nothing to sup-press. These interferons have general, rather than specific, antiviral qualities and are upregulated within 3 to 6 hours of infection. This is what begins causing the general flu-like feelings that presage a full-blown flu episode. The virus itself does not make you feel “fluey.”
During this same time period, the infected airway cells (tracheo-bronchial and alveolar epithelial cells) begin generating specific cyto-kines and chemokines: interleukin-1 beta (IL-1ß), IL-6, IL-18 (which causes spikes in IFN-γ production), C-C chemokine ligand 5 (CCL5, also known as RANTES, “regulated and normal T cell expressed and secreted”), C-X-C chemokine ligand 10 (CXCL10). Then, some 12 to 16 hours later, other cytokines are produced: tumor necrosis factor alpha (TNF-α), IL-8, and CCL2 (also known as monocyte chemoattractant protein-1 or MCP-1). The expressed cytokines make the epithelial structures more porous. This assists faster viral penetration of the cells. It also stimulates the migration of immune cells to the sites of infection.
Interferon-gamma (IFN-γ) is a type 2 interferon, sometimes called macrophage-activating factor. It is this IFN that is crucial in the cyto-kine overinflammation that occurs during severe influenza. By stimu-lating it, the virus initiates a positive feedback loop in the cytokine process that leads, in severe infections, to cytokine storms.
CCL2 causes the migration of blood-derived monocytes into the alveolar airspaces. TNF-α and IL-1ß upregulate adhesion molecules (which include intercellular adhesion molecule 1, a.k.a. ICAM-1, and E-selectin) on the surface of the endothelial cells that line blood vessels. This helps the endothelial lining become more porous and stimulates the transendothelial migration of neutrophils to those locations. TNF-α induces monocyte and neutrophil movement across the epithelium through ICAM-1 and VCAM-1 (vascular cell adhe-sion molecule-1) upregulation. The consequence of this is increasing amounts of white-blood-cell-filled mucus in the lungs. (This is what we cough up during a flu infection.)
The size of the drainage lymph nodes in the lungs begins to increase. This helps, during a healthy resolution of infection, to drain more of the fluids from the lungs, preventing suffocation. Within those lymph nodes, areas called the geminal centers increase their size and development. The germinal centers are the sites where B lymphocytes are produced and are differentiated in order to attack the specific infection that is occurring. This is part of the adaptive humoral immune response. These lymph node locations (as well as those in peripheral tissues) can become overfull during severe infec-tions, slowing drainage and healthy adaptive immune responses. They can also, during severe influenza infections, be specifically attacked and damaged so that they do not function at all. This is a contributor to the mortality that sometimes occurs during cytokine storms. (This is why herbs such as red root, inmortal, and pleurisy root are useful; they all support the lymph structures in the lungs and periphery. Red root — Ceanothus spp. — is particular useful in the periphery for spleen and lymph enlargement and lymph drainage; inmortal — Asclepias asperula — is specific for optimizing lymph drainage from the lungs; pleurisy root — Asclepias tuberosa — is specific for reducing inflam-mation in the pleurae and lungs. They can be used interchangeably to some extent.) The lymph centers in the lungs are heavily affected during influenza, much more so than the periphery
Similarly to many viruses, while influenza viruses reproduce most efficiently in the alveolar epithelial cells, they can also infect other cells, specifically dendritic cells, monocytes, macrophages, neutro-phils, T cells, B cells, and natural killer (NK) cells. In response to being infected those cells also begin releasing cytokines and chemokines:
IFNs, IL-1α and IL-1ß, IL-6, TNF-α, CXCL8, CCL2 (MCP-1), CCL3 (a.k.a. macrophage inflammatory protein-1 alpha, or MIP-1α), CCL4, CXCL9, and CXCL10 through the ERK-1, ERK-2 (extracelluar-signal-regulated kinase 1 and 2), p38 MAPK (p38 mitogen-activated protein kinase), and JNK (c-Jun N-terminal kinase) pathways.
TNF-α, IL-1ß, IL-6, and IFN-γ are responsible for most of the nega-tive effects of the cytokine cascade. Mice that are unable to produce TNF-α consistently show decreased mortality, a reduced symptom picture, and less severe course of the disease. This holds true even if they are infected with the reconstituted, and very virulent, 1918 virus. Inhibition of TNF-α (especially) and IL-1ß has been found to signifi-cantly reduce the cytokine-based inflammation that occurs during influenza, alleviating symptoms and inhibiting viral spread. (Herbs specific for inhibiting TNF-α are kudzu, Chinese senega root, Chinese skullcap, elder, ginger, houttuynia, licorice, boneset, and cordyceps. Herbs specific for inhibiting IL-1ß are Japanese knotweed, Chinese senega root, Chinese skullcap, cordyceps, kudzu, and boneset.)
The virus can also inhibit the production of macrophages over time. This occurs because, over time, macrophages will begin pro-ducing anti-inflammatory cytokines such as IL-4 and IL-10. Once the bodily system is macrophage-depleted a prolonged inflammatory process occurs, keeping the infection going. Lung levels of IL-1ß, IL-6, and TNF-α all increase considerably at that point. Stimulating mono-cyte and dendritic cell maturation (cordyceps) and inducing IL-4 and IL-10 (Chinese skullcap, elder, houttuynia, licorice, cordyceps) will help counteract this
he virus is exceptionally sophisticated in its impacts. There are three stages of chemokine stimulation. The first, 2 to 4 hours postin-fection, is attended by the production of CXCL16, CXCL1, CXCL2, and CXCL3. These chemokines are specific for attracting neutro-phils, cytotoxic T cells, and NK cells. At 8 to 12 hours postinfection CXCL8, CCL3, CCL4, CCL5, CXCL9, CXCL10, and CXCL11 are being produced, which attract effector memory T cells. At 24 to 48 hours post infection, when dendritic cells are most present in the lymphoid tissues, the chemokine profile changes again in such a manner as to attract naive T and B cells. The effect of all this is the virus playing the immune system as a virtuoso plays a violin. Eventually the immune system catches up (usually) and the infection is stopped as influenza-specific antibodies are created.
Plants that reduce the other main cytokines that the virus stimu-lates will also help lessen disease severity and prevent lung damage. I think the most important are inhibitors of NF-κB (Chinese senega root, Chinese skullcap, ginger, houttuynia, kudzu, licorice, boneset, astragalus), IL-6 (kudzu, Chinese skullcap, isatis), IL-8 (cordyceps, isatis, Japanese knotweed), RANTES (licorice, isatis), MCP-1 (hout-tuynia), CXCL10 ( boneset), CCL2 ( boneset), the ERK pathway (kudzu, Chinese skullcap, cordyceps), the p38 pathway (Chinese skullcap, houttuynia, cordyceps ), and the JNK pathway (Chinese skullcap, cordyceps, lion’s mane). The reduction of these cytokines and pathways will reduce IFN-γ.
tissues, the chemokine profile changes again in such a manner as to attract naive T and B cells. The effect of all this is the virus playing the immune system as a virtuoso plays a violin. Eventually the immune system catches up (usually) and the infection is stopped as influenza-specific antibodies are created.Plants that reduce the other main cytokines that the virus stimu-lates will also help lessen disease severity and prevent lung damage. I think the most important are inhibitors of NF-κB (Chinese senega root, Chinese skullcap, ginger, houttuynia, kudzu, licorice, boneset, astragalus), IL-6 (kudzu, Chinese skullcap, isatis), IL-8 (cordyceps, isatis, Japanese knotweed), RANTES (licorice, isatis), MCP-1 (hout-tuynia), CXCL10 ( boneset), CCL2 ( boneset), the ERK pathway (kudzu, Chinese skullcap, cordyceps), the p38 pathway (Chinese skullcap, houttuynia, cordyceps ), and the JNK pathway (Chinese skullcap, cordyceps, lion’s mane). The reduction of these cytokines and pathways will reduce IFN-γ.Each type of influenza has a slightly different cytokine profile with slightly different cytokines more strongly represented. However, the protocols herein, directed to this form of cytokine profile, will be spe-cific enough for every strain, including the low pathogenic avian strain H9N2, which strongly upregulates transforming growth factor beta 2 (TGF-ß2), a different dynamic entirely. Medicinal plants already in use in the developed protocol are, however, specific for TGF-ß2, i.e., astragalus (the strongest) and Chinese skullcap. Magnolia officinalis, Ginkgo biloba, Folium syringae, Nigella sativa, Paeonia lactiflora, and Lonicera japonica are other plants specific for inhibiting TGF-ß2. (This is why lonicera, or Japanese honeysuckle, is commonly used in the treatment of respiratory infections in China — it alleviates wind heat and expels wind heat invasion. In other words, it reduces inflammation in the lungs and expels the virus or bacteria responsible.)
Normally, influenza viruses stay in the upper respiratory tract. However, during more severe infections they will infect the lower respiratory tract as well. Pneumonia is one serious complication from that. So are cytokine storms, should the disease really take hold.
No. There have not.
It is miseducated statements like this as to why we are in the predicament we are now.
BREAKING:
After feeling ill when she returned from a trip to London…. Canadian prime minister Justin Trudeau's wife, Sophie tests positive for the coronavirus
nypost.com
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After feeling ill when she returned from a trip to London…. Canadian prime minister Justin Trudeau's wife, Sophie tests positive for the coronavirus
Canadian Prime Minister Justin Trudeau’s wife tests positive for coronavirus
Canadian Prime Minister Justin Trudeau’s wife has tested positive for the new coronavirus, his office confirmed Thursday night. Sophie Grégoire Trudeau, 44, started feeling sick late Wednesda…
nypost.com
Can you provide some pertinent bullet points that you intended for us to take away from this info? Were there things that you would have highlighted for us to draw from?I was debating whether or not to post this from a book I posted yesterday. It's not about the virus, but it explains the difference between RNA and DNA viruses. The corona virus is a RNA virus. It's a book on antiviral herbs. I'm posting this because it explains how the viruses act and your body responds, tho it does list a few herbs in this excerpt also. . WARNING: It's a long excerpt.
Viruses are typed in a number of ways: by size or shape, presence or absence of an enclosing capsule (not all have one), whether DNA or RNA based (and from that whether single or double stranded, positive or negative sense), their type of protein structure, and their manner of replication. DNA viruses are fairly reliable as viruses go because they have a kind of “copy-check” mechanism that RNA viruses lack. This means that when a DNA virus is making more of itself within a host cell, it uses a biofeedback loop to make sure the copies of itself are reasonably accurate. In contrast an RNA virus can’t.
It tends to make a whole lot of copies that vary, sometimes a great deal, from the original. Some of these copy differences are initiated intentionally by RNA viruses to increase their genetic varia-tion and, hence, survivability in the host. Because of this, while it is often possible to come up with a lasting vaccine for a DNA virus, it is very hard, if not impossible, to make one for an RNA virus. This also makes RNA viruses very hard to treat with pharmaceuticals; they, like bacteria, begin creating solutions to synthetic drugs the moment they encounter one. Evidence indicates that the mutation rate of the hepatitis C virus, for example, accelerates in response to interferon and ribavirin therapy in much the same way that bacterial alteration occurs in the presence of antibiotics. Infection with an RNA virus like West Nile or Japanese encephalitis is actually quite different than infection with a DNA virus.
While DNA viruses make billions more of themselves, RNA viruses make billions of similar but not identical viruses. It is something like a swarm of honeybees — all similar but all different. In fact it is much more accurate to think of an RNA infection as infection by a viral swarm. The ones most similar to each other are the ones that die off when the human immune system is first activated or a pharmaceutical drug that can recognize them is used. This leaves the others free to multiply unchecked and they multiply very fast indeed (some viruses producing a new generation every minute) while still making subtle changes in each new virus produced.
There is also evidence that both DNA and RNA viruses, like bacteria, share information among themselves in order to remain unaffected by medical treatments or immune systems. Similar viruses will actively share genetic structure to create very difficult-to-treat infections. Influenza viruses (for instance) specifically (and intentionally) both rearrange their genetic structures and insert entirely new genes within themselves on a regular basis in order to remain invisible to the human immune system. And they gather these new gene sequences from pigs and birds in Asia. This is why a new vaccine is needed every year for the flu.
Viruses, when not in a living cell, go into a state of hibernation much like plant seeds. In this state of dormancy they move with air currents, in water, or simply rest dormant on the ground until they come into contact with a life form that contains the cells they need to awaken from their long sleep. At that moment a virus’s first task is to get inside the new host organism, bypass its protective mechanisms, and find the proper host cell. Viruses use highly elegant analysis to address these challenges; they actually begin experimenting with new combinations of genes to adapt to the environment they face. Most of them have also generated a genetic structure that facilitates their entry into other host organisms after an initial infection begins. The rabies virus, for instance, affects a part of the brain that then causes uncontrolled biting. At the same time, the virus swarms in its billions into the saliva of infected animals. Then, every time the animal bites something the virus is transmitted to a new host. Influenza, and other respiratory viruses, enter respiratory droplets and then stimulate coughing or sneezing. Those droplets are then breathed in by new hosts. And still other viruses, spread by mosquitoes, flood into the blood and there stimulate the release of chemicals through the host skin surface that calls mosquitoes to the infected host so that the virus can be picked up and spread to others. Viruses are very good at getting from here to there.
Viruses spread by ticks or mosquitoes take advantage of the compounds in the arthropod saliva to facilitate their entry into the new host. The salival compounds reduce certain immune responses in the host to allow the arthropod to feed and often anesthetize the bite location as well. The lowered immune responses at that location allow the viruses to enter the new host in a place where there will be little resistance. Once inside the viruses will make their way to the draining lymph node nearest the bite location and be carried to the spleen via the lymph. There they will begin altering the host’s immune function, reducing the capacity of immune cells to recognize and kill invading microbes. Once that occurs, the viruses will catch a ride on immune cells, macrophages or monocytes usually, and begin spreading throughout the body. This is common for encephalitis viruses, for example. They will then travel in the lymph to the barrier between the brain and the rest of the body, release compounds that make the barrier more porous, enter the brain, and find the cells they really prefer: brain neurons.
Other viruses enter through being inhaled (influenza) or through sex (HIV) or through being eaten on food (enteroviruses). Once in the body, they hitch rides on whatever cells they have developed a taste for (usually immune cells, for those cells travel everywhere) and actively seek out their preferred location. Such is the case with HIV, which views T4 lymphocytes as the perfect host cells, or the Epstein-Barr virus, which has an affinity for human B cells, or the Japanese enceph-alitis virus, which loves monocytes.
To hitch rides, a virus uses chemo-tactic compounds that allow it to stick to its preferred “taxi” cell. The receptors on the surface of the virus fool the cell into thinking it is a compatible protein that has attached, and through a series of chemical communications, the virus gets the cell to let it inside. Basically, it gets the cell’s confidence, then abuses it. From there the virus is carried every-place it might need to go in the body. Once near its preferred location, it leaves its ride, attaches to the cell that is most specific for it, and once again fools the cell into taking it inside. Now it begins to replicate in its millions.
Once inside the primary habitat cell, the virus sheds its protein coat and begins taking over the cell. First it stops the cell from dying, which infected cells are programmed to do, and there it remains, protected from the rest of the immune system. It then breaks off pieces of itself and sends them into the nucleus of the cell, which is then tricked into making copies of the virus, using the viral proteins as a template. These new viral particles exit the nucleus, travel to the interior of the cell wall, and bubble out (viral budding, they call it). The cell dies during this process and bursts apart, and the viruses take up parts of the cell membrane and make themselves new viral protein coats with receptors for new host cells. And it all happens very quickly.
Thus the ancient struggle begins: finding out which is in better shape — the organism’s immune system or the replicating virus. If the virus is particularly strong or if the immune system is compromised in any way, the virus can really take hold and illness, sometimes severe illness, is inevitable.
the Influenza Virus
The influenza virus is a member of the Orthomyxoviridae family. It is an RNA virus and that means it alters its genetic structure very quickly. That is why a new flu shot is needed every year (for those in the Western world who have such things available). The old vaccine can only help prevent infection by the strain that has emerged in that particular year. The next year, it is not the same virus, merely a similar one. Influenza viruses spread around the world every year in seasonal epidemics; 250,000 to 500,000 people die from them each time.
About one-third of people who are infected remain asymptomatic; the rest get some degree of the “flu.” The first symptoms are usu-ally a feeling of being cold or achy and perhaps the beginnings of a fever. High fever alternating with severe chills sets in as the infection spreads. As the virus enters the lungs and sinus tissues mucous con-gestion begins. Coughing, body aches, fatigue, headache, and irritated eyes, nose, and throat are common. Some people will have diarrhea and abdominal pain. Vomiting. Sometimes. Yes.
The symptoms of the infection usually begin the third day after infection. But the virus is already well established by then. It starts replicating the second day, then begins “shedding ” viral particles that are released in increasing numbers for the next 5 to 7 days. The higher the fever, the more viral organisms that are being released. Children are extremely infectious compared to adults, with very high viral loads. They also tend to have very high fevers.
As the virus invades the lungs it stimulates inflammation in the tissues. The lung cells, filled with viruses, soon bulge outward and explode — the essence of viral shedding. Then the virus stimulates coughing, spreading the virus to new hosts via respiratory droplets. Pneumonia, a severe inflammation of the lungs accompanied by mas-sive fluid retention and an inability to breathe, is the main cause of death. People, in essence, drown.
There are three different groups of influenza viruses, denoted A, B, and C. Influenza A is the most virulent. Influenza B is a relatively stable virus and mutates much more slowly than A. Most people develop, in childhood, at least some immunity to it; it is much less dangerous. Influenza C is fairly rare. It does infect people, sometimes severely, but it usually causes only a mild illness, generally in children. When people talk about an influenza pandemic, what they are talking about is influenza A in one of its many genetically altered forms. The 1918 pandemic was caused by an influenza A strain.
There have been numerous pandemics of influenza over the years, each caused by a different strain of the virus. The one in 1918 was the beginning of the modern influenza pandemic era; such pandemics were much less common before then. There was a long rest after 1918. Since 1957, however, they have been occurring with greater frequency.
The most dangerous strains, currently, are H1N1, which caused the flu pandemic of 1918; H2N2, which caused the Asian flu pandemic in 1957; H3N2, which caused the Hong Kong flu pandemic in 1968; and a relatively new one, H5N1, known as avian or bird flu, which caused a pandemic in 2004. Then H1N1 came again. It was the source of the swine flu pandemic in 2009 and is a modified descendant of the 1918 H1N1 strain.
The influenza virus alters its genetic structure rather significantly every year by passing through both pigs and birds. And on that trip it exchanges genetic material with other viruses and reworks its own. Then it spreads around the world again by plane and boat, rail and car, infecting millions, causing what we call the yearly flu season. But every so often it develops a much more virulent strain, sometimes through unique genetic rearrangements, sometimes through species jumps, sometimes through both. The Asian flu pandemic in 2004 was a species jump. The swine flu epidemic of 2009 was a unique genetic rearrangement. It occurred when the virus took advantage of giant agribusiness animal crowding.
Viral geneticists have traced the lineage of the 2009 swine flu epidemic, a virulent H1N1 strain, to an H3N2 strain that emerged in 1998 in U.S. factory farms, specifically huge hog farms in which the animals are so tightly packed together that they literally cannot move. This H3N2 strain combined with another swine strain, a European H1N2 variant, rearranged genetic material into a new and very potent H1N1 form, and then emerged into the human population. The earliest infections occurred in La Gloria, Veracruz, Mexico, just adjacent to a huge hog farm. The workers became infected with the new strain, went home, infected others, many of whom traveled to other cities and towns, and the pandemic began. And it was particularly deadly for those who were infected. Among those hospitalized, depending on location, up to 31 percent were in intensive care units, and as many as 46 percent of those receiving intensive care died
One of the main fears that epidemiologists and viral geneticists have is the possibility of a combined swine and avian flu strain. The crowding of human food animals, similar to the crowding of soldiers in trenches in World War I, continually allows for the emergence of potently virulent strains. Chicken farms, in which unique avian flu strains can emerge, and hog farms, in which unique swine strains can emerge, are perfectly positioned to allow the combination of the two into one potent, and very deadly, influenza strain. This kind of combined strain can then pass easily into farm workers and thence into the population at large.
Researchers have found that, indeed, the H3N2 swine flu virus easily combines with H5N1 strains of avian flu. When that occurs, a tremendously pathogenic form of the virus emerges. It is, they insist, only a matter of time until it occurs on its own. In fact, studies of pigs on large farms adjacent to poultry farms have found such viral combinations already infecting pigs. That combined viral strain has not infected people . . . yet.
One of the main fears that epidemiologists and viral geneticists have is the possibility of a combined swine and avian flu strain. The crowding of human food animals, similar to the crowding of soldiers in trenches in World War I, continually allows for the emergence of potently virulent strains. Chicken farms, in which unique avian flu strains can emerge, and hog farms, in which unique swine strains can emerge, are perfectly positioned to allow the combination of the two into one potent, and very deadly, influenza strain. This kind of combined strain can then pass easily into farm workers and thence into the population at large.Researchers have found that, indeed, the H3N2 swine flu virus easily combines with H5N1 strains of avian flu. When that occurs, a tremendously pathogenic form of the virus emerges. It is, they insist, only a matter of time until it occurs on its own. In fact, studies of pigs on large farms adjacent to poultry farms have found such viral combinations already infecting pigs. That combined viral strain has not infected people . . . yet.
Infection dynamics and the Cytokine Cascade
Cytokines are physiological signaling molecules produced by the body for a variety of reasons. They are produced in the largest numbers during infections. Cytokines (and their cousins, chemokines) are generally part of the innate (rather than the adapted) immune system. They are intended to respond to incursions into our bodies by viruses and bacteria. Another way to think of them is as inflammatory molecules. They cause various sorts of inflammation in the body — they are why, when you cut yourself, the wound gets red and tender and swells. The cytokines rushing to the area create conditions in which many bacteria and viruses find it difficult to survive. Unfortunately for us, bacteria and viruses have also learned how to use our own immune responses for their purposes. They subvert them, quite often, to facilitate their infection of the body and their destruction of certain areas of the body. This facilitates their reproduction and allows them to gather nutrients. Influenza viruses love the lungs and it is where they cause the greatest damage.
Unlike encephalitis viruses, which love brain neurons but have to find their way to the brain after being injected into people by mos-quitoes, influenza viruses don’t have to work nearly so hard. They are taken to the location they like best simply because we need to breathe
Once inhaled, the viruses begin attaching to lung epithelial cells. They use a kind of agglutinin (a substance that glues things to itself — its name shares a root with the English word “glue”), a hemagglutinin, to bind to what are called sialic acid linkages on the surface of airway epithelial cells. (This is one mechanism by which plants such as Chinese skullcap and ginger stop influenza infections; they are hem-agglutinin inhibitors.) All viruses do this in their own way; they have an affinity for a unique receptor on the surface of specific cells and in one way or another they get to that location and those particular cells. Once there, they attach to that part of the cells. In a sense they use that part of the host cells’ membrane as a docking port.
As soon as it is attached to a cell, the virus begins to alter the per-meability of the cell wall, inducing alterations in the cell’s cytoskeleton and initiating endocytosis. In other words, it makes the cell surface more soft, causes the skeletal structure of the cell to bend apart, and tricks the cell into taking the virus inside it where it can’t be found by the immune system. It does this by using a particular kind of enzyme, neuraminidase — which is sometimes also called a sialidase because such enzymes catalyze, or break apart, the sialic acid linkages on the host cell surface. This is why neuraminidase inhibitors (such as Tamiflu, i.e., oseltamivir) are effective in the treatment of influenza; they inhibit the ability of the virus to enter host cells. This stops the infection. (Chinese skullcap, elder, licorice, rhodiola, ginger, isatis, Les-pedeza bicolor, Angelica keiskei, Amorpha fruticosa, quercetin, Alpinia zerumbet, Erythrina addisoniae,and Cleistocalyx operculatus are all neuraminidase inhibitors.) Neuraminidase inhibitors are effective against both influenza A and B strains.
During the process of endocytosis, the virus stimulates the cell to create what is called a vacuole, essentially a sealed bubble that will be held inside the cell. Cells do this to sequester substances that can damage them. Microbes have learned to use such vacuoles for their own purposes, usually to protect the virus or bacteria from intracel-lular antimicrobial actions
The virus uses its hemagglutinin to bind itself to the inside of the vacuole membrane, where it opens a pore to the cell’s cytoplasm, i.e., its interior spaces. To do this the virus uses what is called the M2 ion channel — ion channels are tiny pores in cells that allow charged molecules to enter and exit cells, bringing food in and allowing waste out. Using an M2 inhibitor blocks this process and literally stops the virus from replicating. (Lomatium is one of the most potent M2 inhibi-tors known, stronger than the pharmaceutical amantadine.) Use of the M2 channel is specific to the influenza A virus, which is why the development of blockers for it was considered crucial. Unfortunately, the extensive use of chemical M2 inhibitors such as amantadine in poultry farms has now created nearly complete resistance to them in all influenza A strains.
Once the pore is open, the virus disassembles itself and releases viral RNA and core proteins into the cytoplasm. (Chinese skullcap inhibits this kind of viral RNA release.) The core proteins and viral RNA form a complex that is taken into the nucleus of the cell, where the cell is stimulated to begin making copies of the viral RNA (each slightly different). The new viral RNA is combined with other newly manufactured virus components such as neuraminidase and hemagglutinin and assembled into new viruses. These attach to the inside of the host cell membrane, a bulge forms in the membrane, and the new viruses are expressed (viral budding or shedding) into the extracellular matrix surrounding the cell.
The cell is taken over by the virus in this process, its own components depleted during the creation of new viruses. Once its resources are gone, the cell dies and the newly created viruses move on to new host cells, beginning the process all over again.
The alveolar epithelial cells are specific sites for this process to occur. The alveoli are tiny sacs that are the terminal end of the respi-ratory tree. The air we breathe travels throughout the bronchial tree, eventually emerging into the alveoli, where the oxygen transfuses across very thin membranes into the blood. This is how our bodies remain oxygenated. In the cells lining those tiny sacs the viruses breed. They cause extreme inflammation, or swelling, of the cells in that location with resulting edema (fluid accumulation). All the infected cells burst open and die as new viruses are made. So, fewer alveoli are functional. Breathing is more difficult and the infected person has much less energy because oxygen is not making it into the blood in sufficient quantities. (This is why hospitals sometimes give the infected oxygen.) Pneumonia is when this process becomes severe, the sacs filling with increasing amounts of fluid while there are fewer and fewer functional alveoli.
Throughout the cellular infection and replication process, the virus is also stimulating the release of cytokines by the cell. These cytokines make the tight junctions between cells (and the cellular membranes) more porous and allow easier movement of viral particles through the extracellular matrix (and into the cells themselves). The cytokines are also stimulated in just such a way as to keep the parts of the immune system that can kill the viruses suppressed for as long as possible.
Toll-like receptors (TLRs) are pattern recognition receptors that can identify different types of microbes. The virus particles stimulate TLR3, which begins inducing the release of nuclear factor kappa-B (NF-κB) cytokines. NF-κB is an upstream cytokine, meaning that it is a powerful initiator of other inflammatory cytokines. NF-κB beginsvery specific types of cytokine cascades. Other types of initiators such as RIG-1, NOD2, and MDA5 are also released as part of the body’s reaction to a viral infection. Normally, these would strongly stimulate type 1 interferon (IFN) production (IFN-α and IFN-ß). And influenza viruses are generally very susceptible to these interferons. However, the influenza virus uses a protein, the NS1 protein, which blocks the induction of type 1 IFNs long enough to get established in the body.
(Upregulating the production of type I interferons with herbs such as licorice will help reduce the severity of the infection.) The virus also inhibits dendritic cell maturation and activation, lowering the response levels of T and B cells. (Increasing T cell counts is particu-larly effective in reducing influenza severity. Licorice, elder, red root, and zinc are specific for this.) These cells are part of the adaptive immune response; suppressing them protects the virus from attack. The body response also stimulates the release of type III interferons, to which the virus is less susceptible and which it does nothing to sup-press. These interferons have general, rather than specific, antiviral qualities and are upregulated within 3 to 6 hours of infection. This is what begins causing the general flu-like feelings that presage a full-blown flu episode. The virus itself does not make you feel “fluey.”
During this same time period, the infected airway cells (tracheo-bronchial and alveolar epithelial cells) begin generating specific cyto-kines and chemokines: interleukin-1 beta (IL-1ß), IL-6, IL-18 (which causes spikes in IFN-γ production), C-C chemokine ligand 5 (CCL5, also known as RANTES, “regulated and normal T cell expressed and secreted”), C-X-C chemokine ligand 10 (CXCL10). Then, some 12 to 16 hours later, other cytokines are produced: tumor necrosis factor alpha (TNF-α), IL-8, and CCL2 (also known as monocyte chemoattractant protein-1 or MCP-1). The expressed cytokines make the epithelial structures more porous. This assists faster viral penetration of the cells. It also stimulates the migration of immune cells to the sites of infection.
Interferon-gamma (IFN-γ) is a type 2 interferon, sometimes called macrophage-activating factor. It is this IFN that is crucial in the cyto-kine overinflammation that occurs during severe influenza. By stimu-lating it, the virus initiates a positive feedback loop in the cytokine process that leads, in severe infections, to cytokine storms.
CCL2 causes the migration of blood-derived monocytes into the alveolar airspaces. TNF-α and IL-1ß upregulate adhesion molecules (which include intercellular adhesion molecule 1, a.k.a. ICAM-1, and E-selectin) on the surface of the endothelial cells that line blood vessels. This helps the endothelial lining become more porous and stimulates the transendothelial migration of neutrophils to those locations. TNF-α induces monocyte and neutrophil movement across the epithelium through ICAM-1 and VCAM-1 (vascular cell adhe-sion molecule-1) upregulation. The consequence of this is increasing amounts of white-blood-cell-filled mucus in the lungs. (This is what we cough up during a flu infection.)
The size of the drainage lymph nodes in the lungs begins to increase. This helps, during a healthy resolution of infection, to drain more of the fluids from the lungs, preventing suffocation. Within those lymph nodes, areas called the geminal centers increase their size and development. The germinal centers are the sites where B lymphocytes are produced and are differentiated in order to attack the specific infection that is occurring. This is part of the adaptive humoral immune response. These lymph node locations (as well as those in peripheral tissues) can become overfull during severe infec-tions, slowing drainage and healthy adaptive immune responses. They can also, during severe influenza infections, be specifically attacked and damaged so that they do not function at all. This is a contributor to the mortality that sometimes occurs during cytokine storms. (This is why herbs such as red root, inmortal, and pleurisy root are useful; they all support the lymph structures in the lungs and periphery. Red root — Ceanothus spp. — is particular useful in the periphery for spleen and lymph enlargement and lymph drainage; inmortal — Asclepias asperula — is specific for optimizing lymph drainage from the lungs; pleurisy root — Asclepias tuberosa — is specific for reducing inflam-mation in the pleurae and lungs. They can be used interchangeably to some extent.) The lymph centers in the lungs are heavily affected during influenza, much more so than the periphery
Similarly to many viruses, while influenza viruses reproduce most efficiently in the alveolar epithelial cells, they can also infect other cells, specifically dendritic cells, monocytes, macrophages, neutro-phils, T cells, B cells, and natural killer (NK) cells. In response to being infected those cells also begin releasing cytokines and chemokines:
IFNs, IL-1α and IL-1ß, IL-6, TNF-α, CXCL8, CCL2 (MCP-1), CCL3 (a.k.a. macrophage inflammatory protein-1 alpha, or MIP-1α), CCL4, CXCL9, and CXCL10 through the ERK-1, ERK-2 (extracelluar-signal-regulated kinase 1 and 2), p38 MAPK (p38 mitogen-activated protein kinase), and JNK (c-Jun N-terminal kinase) pathways.
TNF-α, IL-1ß, IL-6, and IFN-γ are responsible for most of the nega-tive effects of the cytokine cascade. Mice that are unable to produce TNF-α consistently show decreased mortality, a reduced symptom picture, and less severe course of the disease. This holds true even if they are infected with the reconstituted, and very virulent, 1918 virus. Inhibition of TNF-α (especially) and IL-1ß has been found to signifi-cantly reduce the cytokine-based inflammation that occurs during influenza, alleviating symptoms and inhibiting viral spread. (Herbs specific for inhibiting TNF-α are kudzu, Chinese senega root, Chinese skullcap, elder, ginger, houttuynia, licorice, boneset, and cordyceps. Herbs specific for inhibiting IL-1ß are Japanese knotweed, Chinese senega root, Chinese skullcap, cordyceps, kudzu, and boneset.)
The virus can also inhibit the production of macrophages over time. This occurs because, over time, macrophages will begin pro-ducing anti-inflammatory cytokines such as IL-4 and IL-10. Once the bodily system is macrophage-depleted a prolonged inflammatory process occurs, keeping the infection going. Lung levels of IL-1ß, IL-6, and TNF-α all increase considerably at that point. Stimulating mono-cyte and dendritic cell maturation (cordyceps) and inducing IL-4 and IL-10 (Chinese skullcap, elder, houttuynia, licorice, cordyceps) will help counteract this
he virus is exceptionally sophisticated in its impacts. There are three stages of chemokine stimulation. The first, 2 to 4 hours postin-fection, is attended by the production of CXCL16, CXCL1, CXCL2, and CXCL3. These chemokines are specific for attracting neutro-phils, cytotoxic T cells, and NK cells. At 8 to 12 hours postinfection CXCL8, CCL3, CCL4, CCL5, CXCL9, CXCL10, and CXCL11 are being produced, which attract effector memory T cells. At 24 to 48 hours post infection, when dendritic cells are most present in the lymphoid tissues, the chemokine profile changes again in such a manner as to attract naive T and B cells. The effect of all this is the virus playing the immune system as a virtuoso plays a violin. Eventually the immune system catches up (usually) and the infection is stopped as influenza-specific antibodies are created.
Plants that reduce the other main cytokines that the virus stimu-lates will also help lessen disease severity and prevent lung damage. I think the most important are inhibitors of NF-κB (Chinese senega root, Chinese skullcap, ginger, houttuynia, kudzu, licorice, boneset, astragalus), IL-6 (kudzu, Chinese skullcap, isatis), IL-8 (cordyceps, isatis, Japanese knotweed), RANTES (licorice, isatis), MCP-1 (hout-tuynia), CXCL10 ( boneset), CCL2 ( boneset), the ERK pathway (kudzu, Chinese skullcap, cordyceps), the p38 pathway (Chinese skullcap, houttuynia, cordyceps ), and the JNK pathway (Chinese skullcap, cordyceps, lion’s mane). The reduction of these cytokines and pathways will reduce IFN-γ.
tissues, the chemokine profile changes again in such a manner as to attract naive T and B cells. The effect of all this is the virus playing the immune system as a virtuoso plays a violin. Eventually the immune system catches up (usually) and the infection is stopped as influenza-specific antibodies are created.Plants that reduce the other main cytokines that the virus stimu-lates will also help lessen disease severity and prevent lung damage. I think the most important are inhibitors of NF-κB (Chinese senega root, Chinese skullcap, ginger, houttuynia, kudzu, licorice, boneset, astragalus), IL-6 (kudzu, Chinese skullcap, isatis), IL-8 (cordyceps, isatis, Japanese knotweed), RANTES (licorice, isatis), MCP-1 (hout-tuynia), CXCL10 ( boneset), CCL2 ( boneset), the ERK pathway (kudzu, Chinese skullcap, cordyceps), the p38 pathway (Chinese skullcap, houttuynia, cordyceps ), and the JNK pathway (Chinese skullcap, cordyceps, lion’s mane). The reduction of these cytokines and pathways will reduce IFN-γ.Each type of influenza has a slightly different cytokine profile with slightly different cytokines more strongly represented. However, the protocols herein, directed to this form of cytokine profile, will be spe-cific enough for every strain, including the low pathogenic avian strain H9N2, which strongly upregulates transforming growth factor beta 2 (TGF-ß2), a different dynamic entirely. Medicinal plants already in use in the developed protocol are, however, specific for TGF-ß2, i.e., astragalus (the strongest) and Chinese skullcap. Magnolia officinalis, Ginkgo biloba, Folium syringae, Nigella sativa, Paeonia lactiflora, and Lonicera japonica are other plants specific for inhibiting TGF-ß2. (This is why lonicera, or Japanese honeysuckle, is commonly used in the treatment of respiratory infections in China — it alleviates wind heat and expels wind heat invasion. In other words, it reduces inflammation in the lungs and expels the virus or bacteria responsible.)
Normally, influenza viruses stay in the upper respiratory tract. However, during more severe infections they will infect the lower respiratory tract as well. Pneumonia is one serious complication from that. So are cytokine storms, should the disease really take hold.
The last paragraph lists a number of herbs that seem to be effective...from perusing the article.
what predicament would that be?
because all Im seeing is a bunch of folks responding to all the media fear mongering..
and now muthafuckas cant even get a toilet paper delivery from amazon or walmart...
the symptoms for this shit is a fuckin runny nose..
bruh
a fuckin runny nose....
U have not been paying attention. Don't let your ignorance get you and your family killed.
Lots of people die every year from the flu and we vaccinate the most vulnerable and have antiviral therapies (tamiflu). With this, we have no vaccine and no therapy and it also happens to be 8-10x more lethal than the flu. Our hospitals are about to be overrun and physicians will be forced to decide who lives and dies like in Italy.
YOU WERE WARNED!
I mainly wanted to get across HOW viruses work and how you get infected. How your body responds etc. How some are different. If the coronavirus is an RNA virus and it comes back every year, we will need a new vaccine every year. As bad as the flu is, this is worse.
Edit: I don't know how effective the herbs will be, this book was written before the outbreak and isn't specific to it, but the advantage of herbs vs some man made medicines, is that the viruses and bacteria don't normally become resistant to herbs. How the body reacts and responds emphasizes to me the importance of having a good nutritional base, adrenal support, etc to fight off the infection to begin with. Herbs aren't necessarily cures, but they support your body and it's functions. With anything, research and use at your own risk.
My sister just wanted me to tell her what to buy, but it's not that simple. You need to understand what is going on with your body to respond properly to your symptoms. So I recommend reading the book. I've uploaded this one and a few others.
I know (hope) we aren't going zombie apocalypse, but I have some homesteading books I'll post this weekend also.
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Actually if you have a runny nose you probably dont have it
Either LEAD with that succinct statement or summarize with it. You know most muhfuckas will respond with TL;DR and I READ.YOU WERE WARNED!
I mainly wanted to get across HOW viruses work and how you get infected. How your body responds etc. How some are different. If the coronavirus is an RNA virus and it comes back every year, we will need a new vaccine every year. As bad as the flu is, this is worse.