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I was reading about a viral list of dubious coronavirus tips on The Verge and reached this tip:
“Even if the virus gets into your mouth, drinking water or other liquids will wash them down through your throat and into the stomach. Once there, your stomach acid will kill all the virus,” one tip reads. Loren Rauch, an emergency room doctor in Los Angeles who has a master's degree in epidemiology, told Mother Jones this advice was “totally bogus.”
I asked a friend, who has a PhD. in cell biology, about this and she said that it's true that a virus would be killed by the stomach acid (i.e. due to high acidity, or low pH value, of stomach acid which could easily break the structure of the virus); however, she added that it's NOT true to think that drinking water would wash the virus from your respiratory system (i.e. trachea or lungs) into your stomach, so drinking water regularly does not necessarily help if it's in your respiratory system.
I was a bit confused since the doctor referenced in the article considered the whole advice as totally false; on the other hand, my friend thinks at least part of the advice, i.e. the virus being killed by stomach acid, is true.
Now, my question is not limited to coronavirus and I am not seeking medical advice or treatment here. I just want to know if my friend is scientifically correct, i.e. whether stomach acid is able to destroy the biological structure of a virus (any virus, and not necessarily coronavirus)? And if so, how does this work biologically?
Study on MERS coronavirus and HCoV-229E: "rapidly lost most of the infectivity in fasted-state simulated gastric fluid (FaSSGF; pH 2.0)" but "survived FeSSGF" (fed state, which is less acidic). See Figure 3. IOW, on empty stomach, the gastric acid rapidly deactivate the MERS coronavirus and the 229E coronavirus, but if there is food in the stomach then the virus survives. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5687858/
You know why rotovirus and polivirus vaccines are oral, not injected?
Becuase it's the immune system in your stomach that needs to be primed to kill those viruses, they are primarily GI infections (yes, polio is primarily a GI infection, it only sometimes infects nerve cells.)
The role of gastric acid in preventing foodborne disease and how bacteria overcome acid conditions
The secretion of hydrochloric acid by the stomach plays an important role in protecting the body against pathogens ingested with food or water. A gastric fluid pH of 1 to 2 is deleterious to many microbial pathogens however, the neutralization of gastric acid by antacids or the inhibition of acid secretion by various drugs may increase the risk of food- or waterborne illnesses. Peptic ulcer disease is often treated by decreasing or eliminating gastric acid secretion, and such treatment blocks the protective antibacterial action of gastric fluid. The majority of peptic ulcer disease cases originate from Helicobacter pylori infections. Treatment of H. pylori-induced peptic ulcers with antibiotics reduces the need for drugs that inhibit gastric acid secretion and thereby diminishes the risk of food- and waterborne illness for peptic ulcer disease patients. Many bacterial pathogens, such as Escherichia coli, Salmonella Typhimurium, and H. pylori, can circumvent the acid conditions of the stomach by developing adaptive mechanisms that allow these bacteria to survive in acid environments. As a consequence, these bacteria can survive acidic stomach conditions and pass into the intestinal tract, where they can induce gastroenteritis.
Gastrointestinal symptoms in COVID-19: What we know so far and why it is important
In this Special Feature, we round up the existing evidence on the gastrointestinal symptoms in COVID-19.
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All data and statistics are based on publicly available data at the time of publication. Some information may be out of date. Visit our coronavirus hub and follow our live updates page for the most recent information on the COVID-19 pandemic.
Respiratory symptoms are the most common symptom of COVID-19.
But according to a recent review, 53% of people hospitalized with COVID-19 experience at least one gastrointestinal (GI) symptom at any time during their illness.
And there’s increasing evidence that encountering GI symptoms with COVID-19, or developing COVID-19 alongside underlying GI conditions, may increase the risk of disease severity and negative complications.
In this Special Feature, Medical News Today review what we know so far about the relationship, prevalence, and impact of GI symptoms on COVID-19 infections.
Respiratory symptoms, such as coughing or trouble breathing, are the most common symptoms of COVID-19.
But early reports out of China made it clear that COVID-19 can also trigger GI system symptoms. The GI system includes:
- the mouth
- esophagus, the tube that connects to the stomach
- small and large intestines
- the anus
The first person with confirmed COVID-19 in the United States also experienced 2 days of nausea and vomiting before developing diarrhea. And one of the earliest American studies found that around 32% of patients with the disease experienced diarrhea, nausea, or loss of appetite.
The research is ever-evolving. But according to a review published this month analyzing 125 articles and a total of 25,252 patients, the most common GI symptoms associated with COVID-19 include:
- lack of appetite (19.9%)
- lack of smell or taste (15.4%)
- diarrhea (13.2%)
- nausea (10.3%)
- vomiting up blood or GI bleeding (9.1%)
Another review published in late January found much broader ranges of symptom prevalence rates, such as:
Less commonly, COVID-19 may also cause:
The disease may also destroy bowel tissues and reduce intestinal movement.
Right now, it seems most people who experience GI symptoms with COVID-19 develop them alongside respiratory symptoms.
However, a review from late 2020 found around 20% of people with COVID-19 infections only experience GI symptoms. And sometimes , these symptoms develop before respiratory symptoms or fever develop.
Early studies suggest GI symptoms tend to occur during the early stages of the infection. But more research is needed to confirm when GI symptoms develop in COVID-19 cases if there is a specific time frame.
Researchers are still learning more about how infection with SARS-CoV-2 affects different parts of the body.
There is evidence that SARS-CoV-2 can infect cells in the respiratory and GI tract, as well as cells in other locations in the body.
Most studies show the SARS-CoV-2 virus enters intestinal cells, or enterocytes, and respiratory cells using the angiotensin-converting enzyme 2 (ACE-2) protein as a receptor. The ACE-2 receptor is embedded in cellular membranes. It helps regulate blood pressure by controlling levels of the protein angiotensin, which encourages blood vessels to constrict and raise blood pressure.
The virus enters intestinal cells after its characteristic spike proteins bind to ACE-2. Once inside the cell, the virus uses the cells’ own machinery to produce copies of viral proteins and ribonucleic acid (RNA). RNA is the genetic material of retroviruses, such as SARS-CoV-2, much like human DNA.
When SARS-CoV-2 particles leave an infected cell, it triggers the release of cytokines, small proteins that play a role in inflammation. This process may cause GI symptoms.
GI symptoms can also occur as viruses destroy or damage GI tissues, especially pain, nausea, and diarrhea. Some research shows that COVID-19 may also change the gut microbiota, the community of microbes that normally inhabit the intestines or stomach.
Once in the GI tract, the virus can also travel through the portal vein, the vein that drains blood from the digestive tract. This can allow viruses to impact the vagus nerve, causing a nauseous sensation.
Nausea and diarrhea are also common symptoms of medications that healthcare professionals often use to manage COVID-19, such as antivirals and antibiotics.
There is increasing evidence that SARS-CoV-2 could pass on to others via fecal-oral transmission. This means people could acquire an infection by accidentally consuming or inhaling droplets of infected feces.
In fact, fecal samples from the first person with confirmed COVID-19 in the U.S. contained virus particles. Other coronaviruses can also cause viral shedding, referring to the release of viral particles in feces.
Some research even suggests people may shed viral particles in their feces after the virus is undetectable in the upper respiratory system, such as the lungs, nose, or throat.
If true, this could change how someone can spread the virus to others and for how long. But researchers have yet to determine whether the proteins and particles shed in feces are infectious, or capable of actually causing disease.
People who experience GI symptoms with COVID-may be more likely to develop negative health complications or risks.
A study from November 2020 found experiencing these symptoms heightened the risk of developing acute respiratory distress syndrome, as have several studies since then.
The study also found that experiencing GI symptoms increased the risk of undergoing procedures with major health risks, such as noninvasive mechanical ventilation and tracheal intubation.
And a report from October 2020 found children with COVID-19 who develop GI symptoms were more likely to experience severe, critical infections and cardiac impairments.
Another study from late January 2021 concluded that experiencing these symptoms also seems to increase the likelihood of developing severe disease and dying in adults. An even more current review found people with COVID-19 and GI symptoms on admission to the hospital were also more likely to develop acute heart and kidney damage or die from the disease.
Dozens of studies have also found that people with preexisting GI conditions are more likely to experience serious disease and negative complications.
Research published this month found people with GI conditions, such as Barrett’s esophagus, seem to be at an increased risk of developing severe COVID-19 symptoms and disease.
Some researchers speculate this connection probably exists because GI diseases can cause intestinal metaplasia, which replaces the stomach lining with cells similar to intestinal lining cells.
Many GI conditions may also make it easier to develop GI infections because they damage or weaken the intestinal or stomach lining. Some of these conditions, such as irritable bowel syndrome, also cause the over-expression of ACE-2, giving viruses more opportunities to enter cells.
Medications used to treat GI diseases or symptoms can also reduce stomach acid levels , making it easier to contract the virus from foods or other ingested substances. Normally, the stomach’s high acidity levels are strong enough to deactivate viral particles.
Less speculation exists as to why experiencing GI symptoms with COVID-19 seems to increase the risk of severe disease and poor outcomes in the absence of underlying conditions.
People with viral infections in their respiratory and GI tract are exposed to increased viral load when compared with people with infections in only the respiratory tract.
There are also around 100 times more ACE-2 receptors in the GI tract than respiratory organs, so it may be able to house more viruses when it acquires an infection.
People with symptoms impacting multiple organs also tend to experience more severe disease and poorer outcomes.
Early evidence seems consistent. But a wider scale, long-term studies need to determine the true relationship between GI symptoms, GI conditions, and COVID-19.
For example, some research indicates people who develop GI symptoms with COVID-19 may actually experience milder disease.
Knowing how often, when, and why COVID-19 causes GI symptoms could have significant benefits.
If these symptoms are as common as research shows, doctors and nurses could start testing people with these indicators, namely loss of smell and taste, fever, anorexia, and diarrhea, as highly specific for COVID-19 infection — even in people without respiratory symptoms. This could help identify potentially millions of COVID-19 cases earlier, including otherwise asymptomatic cases.
Tracking GI symptoms in a population may also help identify disease outbreaks before they occur.
A study comparing rates of internet searches for these symptoms commonly associated with COVID-19 in 15 states found that, in some states, surges in searches occurred 3–4 weeks before surges in case levels.
Researchers also need to know if preexisting GI diseases increase the risk of developing severe disease, negative complications, and dying. They will also have to figure out whether GI conditions make someone more susceptible, or prone, to developing COVID-19. This could teach healthcare professionals how to handle potential, active, or resolved cases of COVID-19 in people with GI diseases better.
It will also be important to learn whether COVID-19 can spread through feces and how long someone remains contagious.
In a review from early February , feces samples from 26.7% of individuals with confirmed COVID-19 contained viral RNA and shed infective particles for roughly 19 days.
If the disease can spread through feces, this could change current hygiene and self-isolation recommendations.
The Centers for Disease Control and Prevention (CDC) currently also only recommend people self-isolate for 10–20 days after symptom onset. If someone’s feces remain capable of spreading infection for longer, public health bodies may have to consider reviewing their guidelines.
If feces containing the new coronavirus can spread the infection, it will also be important to monitor and potentially treat wastewater to reduce transmission. The CDC already have the tools to help states create their own surveillance sampling strategies.
Researchers also need to learn more about the long-term GI impacts associated with COVID-19.
Some preliminary studies show certain symptoms may persist for weeks to months after recovering from the disease. A recent review found approximately 16% of people may still experience nausea and vomiting after recovering, while 12% may continue to experience digestive disorders.
It will take time to truly uncover when and why COVID-19 triggers GI symptoms, and how they impact disease severity and outcomes. And it will likely take much longer to figure out if, and how often, symptoms become long-term.
But as daunting as it sounds, this knowledge could bring about substantial improvements in how we diagnose, treat, monitor, and track COVID-19.
For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here.
Stomach acid and ACE2
Nakaya’s work offers a bit more insight into potential mechanisms. He and his team weren’t initially planning to look at the relationship between antacids and COVID-19 at all. Their project began as an offshoot of another one that Nakaya’s graduate student, Leandro Jimenez, had started. Jimenez had been analyzing the transcriptome data of patients with Barrett’s esophagus, a condition in which acid reflux causes damage to the lining of the esophagus.
The data from biopsies and a gene expression repository revealed increased expression of the gene ACE2, which encodes a cell surface protein that SARS-CoV-2 uses to enter human cells, in individuals with Barrett’s esophagus compared with individuals who did not have the condition. That increased gene activity was tied to regulation of intracellular pH pathways, specifically, their enrichment. That connection suggests increased ACE2 expression is linked with lower pH inside cells, possibly a result of exposure to stomach acid.
“And that raised a flag,” Nakaya says, which led his team to hypothesize that Barrett’s esophagus, as well as gastroesophageal reflux disease (GERD), may be a comorbidities of COVID-19 that hadn’t been identified before.
To test the link between stomach acid and SARS-CoV-2 infectivity, Nakaya’s team exposed human monocytes in cell culture to different pH conditions and then to SARS-CoV-2. The researchers used these immune cells because they are known to be susceptible to infection by the coronavirus, Nakaya says. Under normal oxygen levels, the cells in culture with a pH lower than 7.4 had a higher expression of ACE2 and also a higher viral load. The result indicates that intracellular pH may influence the ability of SARS-CoV-2 to infect cells and replicate within them.
But it wasn’t clear, says Nakaya, that the finding would have any clinical relevance, so the team dug into the medical records of patients in Manaus and São Paulo, Brazil, who had been hospitalized for COVID-19 and found that proton-pump inhibitors correlated with an increased risk of death. That association, Nakaya says, suggests that it might not be the drugs themselves that lead to worsening COVID-19 symptoms, but instead that the proton-pump inhibitors are, the team writes, “important markers of hidden comorbidities that involve the damage caused by the excess stomach acid in GI tissues.” In other words, the low pH that cells are dealing with—and that patients are trying to treat with a proton-pump inhibitor—might make the cells more vulnerable to SARS-CoV-2 infection.
The results, however, don’t explain why famotidine correlated with better outcomes in Conigliaro and Abrams’s study, supposing the drug is also used to suppress stomach acid. “We don’t think that stomach acid is the explanation for the findings,” says Abrams. “We really don’t know why we found what we did.”
The past work on HIV and the computational analysis suggest that famotidine works as an antiviral, and a study published today (October 7) also supports that idea. The research shows that ranitidine bismuth citrate, another histamine antagonist and antibiotic combo used to treat stomach acid, suppresses SARS-CoV-2 replication in infected golden Syrian hamsters and improves their virus-related pneumonia symptoms. But famotidine, Conigliaro says, may have benefits other than being antiviral it may actually prevent patients’ immune systems from overreacting to a SARS-CoV-2 infection and causing a life-threatening cytokine storm. There’s some evidence for this from an observational study in which patients severely ill with COVID-19 were given a cocktail of histamine blockers, one of which was famotidine, and had better outcomes than did patients receiving the standard of care whose cases were reported elsewhere. Those data and other research “seem to suggest that the anti-histamine effect is what prevents patients from getting the cytokine storm,” Conigliaro explains, noting that cells with the histamine-2 receptor are in the lungs as well as the stomach.
The results from those studies and his team’s work, he says, bolster the case for the clinical trial launched last spring to test famotidine as a treatment for COVID-19, results of which are still pending. The Department of Defense under the Discovery of Medical Countermeasures Against Novel Entities, or DOMANE, program is also studying famotidine as a COVID-19 treatment, according to Vanity Fair, and another famotidine trial in Bangladesh is also now recruiting patients.
“Most people’s attention is shifting towards vaccines rather than treatments,” Abrams says, but “with President Trump having COVID, that brings to light again the issue of treatments, especially since he was getting famotidine.”
For some, GI tract may be vulnerable to COVID-19 infection
Researchers at Washington University School of Medicine in St. Louis have found that patients with Barrett's esophagus may be vulnerable to coronavirus infection from what they swallow. Shown is an organoid built from tissue taken from patients with Barrett's esophagus. The cells resemble intestinal cells rather than normal esophagus cells. The red color notes the presence of a protein called actin that is found in intestinal cells, while the green marks the presence of the TMPRSS2 protein that binds to the SARS-CoV-2 virus.
No evidence so far indicates that food or drinks can transmit the virus that causes COVID-19, but new research at Washington University School of Medicine in St. Louis suggests that people with problems in the upper gastrointestinal (GI) tract may be vulnerable to infection after swallowing the virus.
Studying tissue from patients with a common disorder called Barrett’s esophagus, the researchers found that although cells in a healthy esophagus cannot bind to the SARS-CoV-2 virus, esophageal cells from patients with Barrett’s have receptors for the virus, and those cells can bind to and become infected by the virus that causes COVID-19.
The study is published online Jan. 20 in the journal Gastroenterology.
“There is no evidence yet that people with Barrett’s esophagus have higher rates of COVID-19 or are at any greater risk, but part of the reason is because that hasn’t been studied,” said senior investigator Jason C. Mills, MD, PhD. “Now that we’ve connected these dots, it may be worthwhile to look and see whether people with Barrett’s have higher rates of infection.”
Part of the reason it’s been considered safe to eat and drink most foods during the pandemic is that they are unlikely to carry viral particles. And even if some viral particles are attached to food, stomach acid neutralizes the SARS-CoV-2 virus.
But when stomach acid backs up, people develop a disorder called gastric reflux that can cause long-term damage to the esophagus. In those with reflux disease, which affects about one in five people in the U.S., acid from the stomach backs up into the esophagus, causing heartburn and damaging the lining of the esophagus. Over time, in some people with reflux, cells in the esophagus change and begin to resemble intestinal cells. Intestinal cells have receptors that can bind to the novel coronavirus, so Mills and his colleagues reasoned that in Barrett’s patients, the cells that line the esophagus also would develop receptors that can bind to the virus and become infected.
In addition, standard medical management for patients with Barrett’s esophagus is to suppress gastric acid secretions with drugs such as proton pump inhibitors. By reducing stomach acidity, those drugs may inadvertently make it possible for the virus to pass through the stomach and into the intestine, where even the normal, healthy cells carry receptors for SARS-CoV-2.
Many patients with COVID-19 — most of whom contract it by breathing in the viral particles — develop GI symptoms such as abdominal pain and diarrhea. The virus also has been found in the stool of COVID-19 patients. But this new study demonstrates that under the right circumstances, the virus also may have an impact in the upper part of the GI tract. As a result, Mills — a professor of medicine, of developmental biology, and of pathology and immunology — and his team believe esophageal cells in Barrett’s patients are potential gateways for infection.
“You can imagine that if someone already has low levels of the virus in their respiratory tract, that individual could swallow some respiratory secretions, and the virus could infect cells in the esophagus to make them sicker that way,” said Ramon U. Jin, MD, PhD, the paper’s co-first author and a clinical fellow in the Division of Medical Oncology who studies Barrett’s esophagus because it is a major risk factor for cancer of the esophagus. The other co-first author, Jeffrey W. Brown, MD, PhD, is an instructor in medicine in the Division of Gastroenterology.
In this study, the researchers analyzed tissue from 30 patients with Barrett’s esophagus and found that cells in the tissue samples all had receptors for the SARS-CoV-2 virus, which normal esophagus cells lack. They built and cultured mini organs from those and other esophagus tissue samples. Some of the sample organs were built with cells that came from healthy people while others came from patients with Barrett’s esophagus. The scientists built the mini esophaguses, called organoids, in a dish to learn how those model organs interacted with the SARS-CoV-2 virus.
The virus was able to bind to and infect mini organs built from tissue from people with Barrett’s esophagus. Moreover, the more the cells in a specific patient’s mini esophagus culture resembled intestine, the more the virus bound to and infected that culture.
“The worry would be that, particularly for Barrett’s patients, there even may be a susceptibility to infection from foods containing viral particles,” Mills said. “This study provides data to indicate that we need to take a closer look to investigate whether a substantial portion of the population may be susceptible to infection through what they swallow.”
Jin RU, Brown JW, Li QK, Bayguinov PO, Wang JS, Mills JC Tropism of SARS-CoV-2 for Barrett’s esophagus may increase susceptibility to developing COVID-19. Gastroenterology, Jan. 20, 2021.
This work was supported by the National Cancer Institute, the National Institute of Diabetes Digestive and Kidney Diseases and the National Heart, Lung, and Blood Institute of the National Institutes of Health (NIH). Grant number P30 CA091842, P30 DK052574, P30 CA006973, T32 HL007088, U54 CA163060, R21 DK111369, R01 DK105129, R01 DK110406. Additional support from an American Gastroenterological Association Foundation AGA-Takeda COVID-19 Rapid Response Research, the Department of Defense, the Children’s Discovery Institute of Washington University and St. Louis Children’s Hospital, the Foundation for Barnes-Jewish Hospital and the Alvin J. Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine in St. Louis.
Why doesn't your stomach acid destroy the nutrients in food?
I guess this stems from not knowing how your stomach digests food. Or maybe how nutrients work. I always heard that cooking food can remove some of the nutritional value, why doesn't your stomach do the same?
Your stomach's goal is to break down big foreign molecules, like proteins, into usable building blocks, like amino acids. It doesn't blast building blocks into their component atoms.
For the most part, cooking doesn't remove nutritional value either. Boiling or steaming food can lead to nutrients being leeched out by water, but unless you're burning the hell out of your food, nothing is being destroyed. In fact, cooking food increases the amount of calories you can get from it.
The majority of the nutrients we get from our food are absorbed in the small intestine which immediately follows the stomach. If the nutrients in our food were broken down by our stomach, then they wouldn't get to the small intestine and we wouldn't use them. Therefore, we evolved to make use of the nutrients that survived in sufficient quantities in our small intestines.
TLDR: We evolved to use the ones that make it to the small intestine.
Stomach acid does destroy some things, like organisms and certain compounds (Penicillin comes to mind.) Many things survive the acid, like vitamins, minerals, and some organisms (certain bacteria, spores, fungi, parasites.) The stomach functions to do the following:
break proteins into smaller polypeptides (amino acid chains). Acidic conditions are best for this. See pepsin
How E. coli passes safely through stomach acid
In some parts of the world, many small children become infected with severe diarrhea which often proves fatal. The condition is usually caused by strains of Escherichia coli (commonly known as E. coli) bacteria, and bacteria of the genus Yersinia. These bacteria attach themselves to the wall of the small intestine and use a needle-like apparatus to inject toxins into the tissue. Yet these bacteria usually enter the human body via the mouth -- and you would expect them to be killed off by the strong acid in the stomach, which provides a barrier against infection.
Members of the collaborative research center "The Bacterial Cell Envelope" at the University of Tübingen including researchers from the Tübingen University Hospitals as well as Jack C. Leo and Professor Dirk Linke of the Max Planck Institute for Developmental Biology investigated this phenomenon and discovered how these bacteria can protect themselves from acid and mechanical stress as they pass through the stomach. The results were published in the latest issue of Molecular Microbiology.
E. coli and Yersinia bacteria attack cells in the small intestine which absorb nutrients. They use adhesins such as intimin (a protein the name comes from "intimate adherence") to stick to intestinal epithelial cells and to subsequently form tiny channels between the bacteria and the intestinal cells. In this way they are able to introduce diarrhea-causing toxins into the intestine.
The intimin is inserted into the bacterial cell envelope, where it binds with the bacteria´s stabilizing structure, peptidoglycan, a mesh-like molecule consisting of sugars and amino acids. "But the binding of intimin with peptidoglycan only works under acid conditions," says Dirk Linke. "We assume that this mechanism protects against acidic and mechanical stress and that E. coli bacteria can pass through the stomach unharmed." Intimin therefore supports the infection process by bacteria which would otherwise have difficulty reaching the small intestine. The researchers suspect that intimin boosts the bacteria's virulence.
The collaborative research center SFB 766 "The Bacterial Cell Envelope: Structure, Function and Infection Interface" is funded by the German Research Foundation (DFG).
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How Viruses Work and How to Prevent and Eliminate Them Naturally
We have identified more than 2,000 viruses, though only 10% infect humans. Scientists used to think human viruses do not affect animals and animal viruses do not affect humans, but we now know that viruses not only jump species, sometimes they combine to create new strains. New strains can present a clear threat to human survival.
In 1918 the Spanish flu pandemic was a global killer. Estimates of the dead range from 20-100 million, up to 5% of the population–all within one year. Unlike previous flu pandemics and epidemics, this flu strain killed healthy adults, whereas most flu strains targeted children, the elderly, and the infirmed. More people died in this one-year pandemic than the four years of the bubonic plague.
We often hear that many dangerous strains of influenza begin in China. This belief is based on the dense population of humans living in close proximity to high populations of animals. Many dangerous viral strains have been found to originate in China jumping from birds or pigs to the human population. Birds alone have been found to carry as many as 15 viral strains.
A virus is a pathogenic, parasitic organism that isn’t classified as being alive, since a cell is an essential to our definition of life. A virus has no cell membrane, no metabolism, no respiration and cannot replicate outside of a living cell. A virus is a creepy half-live, single strand or double strand of DNA or RNA or both, looking for a cell to invade. Once inside, it reprograms the cell with its DNA or RNA and multiplies on mass, bursting through the cell with a thousand or more new virus strands seeking new cells to invade. RNA viruses mutate more easily than DNA viruses. (SARS, bird flu, West Nile virus, swine flu, hepatitis, measles, polio, yellow fever, and Ebola are among the many RNA viruses).
If two viruses invade the same cell (a bird virus and a human virus, for instance) their DNA can combine to form a new virus, a potentially virulent one. The same is true if two animal viruses combine and jump species to humans.
Viruses have two life cycles: the lytic cycle and the lysogenic cycle.
In the lytic cycle, the virus focuses on reproduction. It invades a cell, inserts its DNA and creates thousands of copies of itself, bursts through the cell membrane, killing the cell, and each new viral strand invades new cells replicating the process.
In the lysogenic cycle, viruses remain dormant within its host cells. The virus may remain dormant for years. Herpes and chickenpox are good examples. (Chicken pox can cause shingles in later life when the dormant virus reactivates.)
Our bodies fight off invading organisms, including viruses, all the time. Our first line of defense is the skin, mucous, and stomach acid. If we inhale a virus, mucous traps it and tries to expel it. If it is swallowed, stomach acid may kill it. If the virus gets past the first line of defense, the innate immune system comes into play. The phagocytes wage war and release interferon to protect surrounding cells. If they cannot destroy the invading force, the phagocytes call the lymphocytes into play.
Our lymphocytes, T cells and B cells, retain a memory of any previous infection that was serious enough to bring them into the battle. Antibodies were formed and the body knows how to fight any infection it recognizes. (This is how vaccinations work. The body has fought a similar infection). But viruses can mutate, sometimes so much that they body cannot recognize them as a similar infection they fought in the past. They can also be so fast acting, they can kill before the lymphocytes are brought into play.
Antiviral medications do not directly kill the virus they trap it within the cell, keeping it from reproducing. The only catch is that the anti-viral has to be taken with 48 hours of symptom onset or it doesn’t work.
Antibiotics don’t kill viruses. They kill bacteria, not viruses. And they kill good bacteria that we need to keep our gut in balance. Taking antibiotics when you have a viral infection can cause an immediate overgrowth of Candida, giving the immune system an additional system-wide infection to deal with when it needs all of its resources to fight a viral infection.
Conventional treatment is supportive treatment–fluids, medications for symptoms (such as asthma medication), but no medications have ever been developed to kill the virus itself.
Don’t panic. Most viruses don’t affect us. But still, it brings up a point. Viral infections are a symptom of a weak immune system. Your immune system is wholly dependant on your gut health. A sick gut has an abundance of fungi and other pathogens, and a healthy gut has a wide variety of beneficial bacteria. The supplements listed below are a half measure. A healthy nutrient dense diet, a healthy lifestyle, and a body void of as many toxins as possible is the first and foremost defense. If you want to skip the shortcuts and truly fortify your immune system, read the following articles:
A healthy immune system begins in the gut with a healthy balance of beneficial bacteria. For far too many Americans, Candida overgrowth compromises the immune system, as it is constantly fighting the battle to keep Candida in control.
If you do become ill, DO NOT feed the virus or the Candida with sugar. Yes, you need to drink a lot of fluids, but don’t drink sodas and sugary juices at this time. Cranberry lemonade sweetened with stevia is a good choice. Try it warm or cold.
Gargle. Gargle. Gargle. Gargling lowers the viral load, leaving your body with fewer invaders to replicate. Gargle with organic apple cider vinegar. Even better, sip on this Mother Earth Organic Root Cider. Cold’s and flu often start in the throat or the nasal cavities. At the first sign of a sore throat or sinus infection, sip on the root cider! If you don’t have it, use apple cider vinegar.
Also, remember that a fever is one of nature’s means to fight infection. Of course, you don’t want it to get too high (higher than 102) and drink plenty of fluids to prevent dehydration.
Vitamin A, vitamin D, vitamin E, and vitamin C are all vital nutrients for the immune system. If you take high doses of vitamin C to fight a virus, remember that you should not abruptly stop taking vitamin C. You should titrate down. Vitamin C is needed by the immune system to make interferon, which the immune system produces to protect healthy cells from viral invasion.
Zinc has been proven to be effective against the common cold and to be effective as a topical treatment for herpes sores. It is believed to be effective due to preventing replication of the virus. The immune system needs selenium to work properly and to build up the white blood cell count.
Berberine is an alkaloid compound found in several different plants, including European barberry, goldenseal, goldthread, Oregon grape, Phellodendron, and Coptis chinensis. It has antibacterial, anti-inflammatory, antiviral, anti-parasitic, and immune-enhancing properties. It’s been proven effective against a vast array of bacteria, protozoa, and fungi. It can be used topically on cuts and other wounds, and it’s perhaps most commonly used to treat gastrointestinal issues.
Probiotics are always helpful in maintaining gut health, especially when the body is under a viral attack that involves the digestive system. Probiotic foods and drinks without added sugar can help maintain a healthy balance of bacteria.
Garlic is anti-viral, anti-fungal, and antibacterial. You can take garlic in a tonic or if you can handle it, chew raw garlic. It not only will help fight the virus, it will help kill any secondary infections trying to take root.
Echinacea not only supports the immune system, it also has been proven to reduce the severity and duration of viral infections.
Colloidal silver is believed to interfere with the enzymes that allow viruses (bacteria and fungi as well) to utilize oxygen.
A double-blind trail showed elderberry extract’s ability to reduce symptoms of influenza and speed recovery. It also showed elderberry’s ability to enhance immune response with higher levels of antibodies in the blood. It is believed to inhibit a virus’s ability to penetrate healthy cells and protect cells with powerful antioxidant S. Elderberry has also been shown to inhibit replication in four strains of herpes viruses and reduce infectivity of HIV strains.
The flavonoids in green tea are believed to fight viral infections by preventing the virus from entering host cells and by inhibiting replication.
Though double-blind clinical trials are needed, olive leaf extract has been shown to inhibit replication of viruses. In one study, 115 of 119 patients had a full and rapid recovery from respiratory tract infections while 120 of 172 had a full and rapid recovery from viral skin infections such as herpes.
Pau d’arco has been used in indigenous medicine for generations. One of its compounds, lapachol, has proven effective against various viruses, including influenza, herpes simplex types I and II and poliovirus. It is believed to inhibit replication.
Studies have shown that glycyrrhizin, a compound found in licorice root was more effective in fighting samples of coronavirus from SARS patients than four antiviral drugs. It reduces viral replication, cell absorption, and the virus’s ability to penetrate cells. It is also being used to treat HIV.
St. John’s Wort has been proven effective against influenza, herpes simplex, and HIV.
If you’re prone to viral infections or are dealing with a chronic infection like HIV, as mentioned above, the first step is to get your gut in shape. This is absolutely imperative. The best article to do that with is Best Supplements To Kill Candida and Everything Else You Ever Wanted To Know About Fungal Infections & Gut Health. Everyone who is chronically ill has an abundance of Candida. Yes, everyone.
Provided your gut is healthy, or if you just feel the need to skip that part, here are the supplements to take in order to make sure your immune system is able to fight off viruses:
While there are most supplements listed above, the combination of these listed here is more than enough to balance out the body and ward off viral infection.
Norovirus tears across US stomach bug causing widespread misery
3. You can spread it after you get better
Just like influenza, norovirus is still being produced in your body after you get over symptoms from a bout. So people can spread it after they’ve returned to work.
Norovirus spreads via the fecal-oral route, so if people do not wash their hands very carefully after they have recovered from a bout of norovirus, they can spread it to others.
“Even once you feel better, you should still stay home at least one to two days,” Hall advises.
4. One person can infect hundreds
Because it spreads even after people feel better, patients can and do go back out into the world while they are still infectious.
Combine a sticky, hard-to-kill virus with invisible spread by people who don’t feel sick, and it makes a recipe for exponential spread.
Restaurant workers usually get little or no paid sick leave, so many workers come in sick, or too soon after they’ve recovered, and they can spread the virus to hundreds of customers. Food handlers, dishwashers, even staff who bus and clear tables, all can spread the germ.
“One ill food worker or even a worker who recovered has the potential to expose literally hundreds of people,” Hall said.
And vomiting once can create an aerosol of virus that settles on surfaces all around.
In 2010, nine soccer players all got sick from a plastic shopping bag that got norovirus splashed on it.
The makes norovirus the most common cause of acute gastroenteritis — stomach upset — in the United States. It makes 21 million people sick every year in the United States — 70,000 on average get sick enough to go to the hospital. As many as 800 people die, mostly elderly patients who become dehydrated.
5. Several vaccines are in the works
While norovirus is nowhere near the killer that influenza is, several teams of researchers are nonetheless working on vaccines to prevent it. Globally, norovirus kills 200,000 people a year.
It’s difficult in part because the virus mutates, and in part because the virus lives in the gut and it’s hard to make vaccines that work there.
Drugmaker Takeda has a vaccine that’s being tested in people now. At least one study has shown that about 20 percent of people of European origin have a genetic mutation that protects them from common norovirus strains, something that might help in development of better vaccines.
Maggie Fox is a senior writer for NBC News and TODAY, covering health policy, science, medical treatments and disease.