If you do get infected: what you need to know and to do

Surviving Deadly
Viral Epidemics

Humans have lived with viruses through their entire history
because viruses were already here when humans arrived.

By Durk Pearson & Sandy Shaw

The practice of medicine today is so specialized that each doctor is a healer of one disease and no more.

— Herodotus (circa 430 BC)

The atheists have produced a Christmas play. It’s called “Coincidence on Thirty-Fourth Street.”

— Jay Leno

Generally speaking, people are plagued with problems that they are unable to solve. To escape them they pick up a detective story, become completely absorbed, help bring the investigation to a successful conclusion, switch off the light and go to sleep.

— Erle Stanley Gardner


H umans have lived with viruses through their entire history because viruses were already here when humans arrived. Humans and viruses continue to coevolve, leading to the complexities of the human immune response to viruses and viral adaptations to every new attempt by human immune systems to foil viral infections. Viruses have killed hundreds of millions of people in modern times and there is no reason to think this threat will disappear in the foreseeable future.

The subject of this paper is how to be prepared for potentially large numbers of viral epidemics in the near future and beyond. Empires will rise and fall and pathogens will be right there to play a role. The Roman Empire in its declining years had similar problems to what we see in the developed world today, with populations that can vote for government redistribution of income to benefit themselves at the expense of a dwindling work force. The collapse of public services was a result in Rome. In the end, there simply wasn’t enough money to maintain the Roman sewage system, once one of the engineering wonders of the world. This was followed by epidemics, one after another until, within its final 15 or so years, Rome went from being the largest city in the world to being virtually abandoned.

Our purpose here is not how do we save the Roman Empire or a modern version of it or even to predict whether the U.S. may be approaching such a severe decline and fall, but how we live through a time when large epidemics exist while public services, such as the Centers for Disease Control (CDC) are telling people that, for example, one such viral threat, Ebola, is difficult to contract. Sadly, this is untrue and it is a frightening sign of the times that this is what we are getting in the way of advice from the leading agency that is supposed to be protecting the public health. Public confidence in the CDC is declining, as indeed it should be.

Meanwhile, we see people with deadly diseases traveling between areas rife with epidemic disease and the United States with little in the way of government restrictions. And now the President is preparing to send large numbers of uninfected military reserve into an area where a deadly viral epidemic is taking place, individuals that may return carrying the infection. And we see the President name an “Ebola czar” who is a lawyer with no medical education or background whatsoever. Why? Yes, good questions, but we leave the subject of why the government strategy to deal with the epidemic seems all too likely to worsen it to return to the focus of this article: what an individual can do to protect himself and his family from before to during a deadly epidemic.


  1. PREVENT BACTERIAL GROWTH IN REFRIGERATED FOOD BY SETTING THE TEMPERATURE LOWER THAN 54 degrees F. The government-recommended temperature of 54 degrees F for your refrigerator is based on the politics of energy usage NOT on the basis of what temperature is adequate to prevent the growth of bacteria in your food that could result in food poisoning. We set our own refrigerator at 33 degrees F so as to avoid this problem. We think that 54 degrees F is too high and, if used, is likely to be resulting in thousands of additional cases of food poisoning; there are currently over 100,000,000 cases of food poisoning a year in America and most of these result from improper food handling in the home.

  2. Be sure you have a good fever thermometer. This is something you should have on hand as a general tool for evaluating health status.

  3. Try to avoid crowds where you come repeatedly close to others. Even seemingly friendly parties with friends but also lots of strangers present ample opportunity to contract a contagious disease when you are trying to avoid one. Don’t forget that in an epidemic every human represents a potential source of disease.

  4. Wash your hands as often as you can when coming into contact with surfaces in public areas. Pathogens are heavily concentrated on familiar surfaces that you touch such as public building door handles or the push bar on supermarket carts. An important precaution is to always use an alcohol-based germicidal cleanser on the shopping cart push bar. Have a small container of such a cleaner with you when you leave home.

  5. Wash your hands after handling mail, which has passed through many human hands on its way to you.

  6. When exposed to possibly contaminated surfaces in public areas, try not to touch your face, eyes, and mouth, which can easily pick up pathogens from your hands.

  7. It is always advisable whether there is a threatening epidemic or not to have a 2- or 3-month supply of food that doesn’t require refrigeration on hand. The best supplies for this purpose are foods you normally eat and enjoy in canned and dried varieties, not emergency food of the sort that is only a last resort and that you wouldn’t eat under ordinary circumstances. A good source of protein, tasty yet inexpensive, is canned tuna, which has a good shelf life in the canned form (years).

  8. Take VITAMIN D as a prophylactic. As a nutrient, 4000 IU/day may be an appropriate dose for most adults for health maintenance. If a deadly viral infection arrives in your town, then you can increase your intake of vitamin D to 8000 IU/day. See the section on vitamin D below for more on this powerful immune-modulating nutrient and new evidence of its beneficial effects in retarding age-associated cognitive decline.

  9. Take VITAMIN C (1000 mg. three times a day) as a nutrient with important anti-infective properties.A1,A2


LAUNDRY SURFACTANT INACTIVATES ENVELOPED VIRUSES — The common surfactant sodium dodecyl sulfate (aka sodium lauryl sulfate) found in many shampoos and toothpastes as well as in clothing and dishwashing detergents was reported to be a topical antimicrobicidal agent in a study where it inactivated enveloped viruses including HIV, herpes simplex virus type 2 (genital herpes) and human papillomaviruses (genital warts).12 Hence, we recommend the use of this agent to wash clothing and dishes to protect against Ebola and other enveloped viruses. This study also found the surfactant to inactivate papillomavirus; papillomavirus is not enveloped.

BLEACH — Another useful way to disinfect clothing and household surfaces is by using chlorine bleach (Clorox is a stable commercially available brand), which has been shown to damage the viral envelope in enveloped viruses. Use the amount recommended on the label when washing clothing.

ALCOHOL-BASED GERMICIDAL HAND WIPES AND CLEANERS — These are effective in disrupting the envelopes of Ebola and other enveloped viruses.


  • Cover any open wounds or sores before going out in public. Remember, these viruses may be contracted by inadvertent contact with an infected person or even from the air they breathe out.

  • Do not use public transportation. It is already clear that you cannot be sure you are not travelling with infected individuals and you are VERY unlikely to get any warning if you are. It could be said that you should avoid public transport like the plague because a plague could be exactly what you would be avoiding.

  • Wear an antiviral facemask and nitrile or latex gloves when in public. Though you may feel silly doing this, especially if most people are not also doing so, feeling silly is a small price to pay when the price you may pay for NOT doing so is to get infected.

  • Wash any clothing immediately after returning home if you have to appear in public. Some shoes can also be washed. Change shoes at your door.

Sure, all these precautions are extremely inconvenient, but you can’t avoid it if you want to minimize your risk under risky conditions.


If you cannot avoid becoming infected by all the various techniques that you have read about — either here or elsewhere — one thing that you can still do that may help reduce your chances of dying from an infection is to take readily available substances that may avert the excessive inflammatory response that kills most people who die of the infections.1

An early genomic study (and possibly the first to identify unique molecular signatures associated with Ebola mortality) was published in 2011.1 As the authors of the study note, knowledge of these signatures tell you where you can begin in the development of treatments. In other words, your goal has to be not dying if you get infected. Ideally, you would find out how to prevent infection in the first place, but that may take a little longer (and, then, you might get infected anyway, despite efforts to prevent infection, so you had better know what to do if you do get infected).

The authors sum up their findings1 this way: “In human cases of fatal Ebola virus infection, the dysregulated expression of inflammatory mediators, including interferon, interleukins, monocyte chemoattractant protein 1, tumor necrosis factor alpha (TNF-alpha), and reactive oxygen species, are thought to contribute to disease progression. However, an early and controlled inflammatory response has been associated with recovery, suggesting that a well-regulated innate immune response is critical for control of Ebola virus infection.”


“A feature of the [1918] Spanish flu that made it so deadly was a dramatic inflammatory response to the virus culminating in a rapid ‘cytokine storm’ that resulted in severe lung tissue damage and death.” (Cell 137:593 (May 15, 2009))

A Description of the “CYTOKINE STORM” in a Recent Paper

“… there is evidence in both human sepsis and experimental sepsis (such as endotoxemia, infusion of live Escherichia coli, or CLP) that complement activation is occurring, followed by the cytokine storm, which is defined by the presence of numerous proinflammatory cytokines and chemokines in plasma. This even often evolves into multiorgan failure, although the extent to which the presence of numerous proinflammatory mediators in plasma can be directly linked to organ injury and failure is not clear. In the case of IL-1beta, TNF-alpha, and IL-6 (as well as IL-8 in humans), these cytokines have been described as having cardiosuppressive effects. The term cardiosuppressive refers to the fact that these cytokines, when added in vitro to CMs [cardiomyocytes, heart muscle cells], cause reversible contractile and relaxation defects.”G “… there is evidence that heart tissue obtained from autopsy specimens from humans with sepsis shows the presence of activated PARP ….”G PARP is a DNA damage response molecule that utilizes NAD+ to perform its function and, under sufficiently severe conditions, can deplete NAD+, resulting in mitochondrial dysfunction. This could be happening in the heart during sepsis.G

Even malaria, caused by a parasite Plasmodium fulciparum, has been described as being “primarily an inflammatory cytokine-driven disease.”H Cytokine storms have been associated with the 1918 Spanish flu pandemic, the 2003 severe acute respiratory syndrome (SARS) outbreak, and the H5N1 avian influenza infections first recognized in 1987.J

Overreaction of the inflammatory immune responses are associated with fatal outcomes in many diseases and there is growing knowledge on how to moderate these responses to help prevent the excessive release of inflammatory mediators and subsequent death.


A 2007 paperK provides a brief history of the term “cytokine storm.” The author notes that as of 2007, there were 55,000 Google hits for “cytokine storm,” having increased from 21,000 Google hits a year prior to that. (Today, Oct. 21, 2014, there were 336,000 Google hits for “cytokine storm.”) The expression was coined in 1993 by a group in Boston to describe their observation of massive releases of proinflammatory cytokines in graft-versus-host disease (GVHD). Scientists were already investigating this and a 1987 study was reportedK to have shown that a polyclonal anti-tumor necrosis factor alpha (anti-TNF-alpha) antibody reduced mortality in a mouse model of GVHD.

We mention here a few potentially protective agents working by suppressing release of excessively high levels of inflammatory cytokines without preventing the adequate releases needed for protective immune function, and natural products that may also provide protection against lethal viral infections but possibly by other mechanisms (such as interfering with viral entry into cells).


Because an agent has antiviral effects in in vitro (cell) studies, even if a physiologically relevant dose is used, does not mean that it will have the same effects in a human. Because an agent has antiviral effects in animal models, similarly, does not ensure that the substance will also have antiviral effects in a human. Indeed, when you get right down to it, because an agent has antiviral effects in a human study, even one of reasonable size and with adequate statistical power, does not mean that any particular person will get the same results due to variation between individuals in many factors that cannot be controlled (such as one’s genetic makeup).

Nevertheless, lack of CONCLUSIVE PROOF of an agent’s antiviral effects when projecting from in vitro, animal, and clinical studies to human use in a medical sense, does not mean that you can’t consider the possibility of such an effect in a particular individual. The interpretation of the totality of a body of scientific evidence, which usually has inconsistent evidence even when the overall body of evidence points to a certain interpretation, is therefore as much art as it is science. The studies that follow, therefore, are suggestive of protective effects against infectious diseases, not as purported silver bullets.

MELATONIN — A very recent paperA reports that melatonin may be useful as a treatment for Ebola because of certain of its effects that have been reported in published peer-reviewed scientific papers that includes suppression of the release of inflammatory cytokines (TNF-alpha, IFN-alpha, IL-6, IL-8, TF (tissue factor) MCP-1 (monocyte chemoattractant protein-1), etc. and the downstream events triggered by the release of these molecules such as the initiation of blood coagulation by TF. Melatonin acts as an anti-coagulation agent. In the paper,A Ebola infection is considered to be similar to septic shock, a condition that results from a runaway immune inflammatory response to infection. The authors predict in this 2014 paper that death from Ebola virus disease “may be significantly reduced as a result of melatonin administration.” They discuss the uncertainty of the proper dose because of limited dose response studies with melatonin, suggesting that early intervention with a large dose (20 mg or more for a single dose) might be necessary. In fact, if necessary and under severe conditions of an infection, melatonin could be taken in doses of 20 mg three or four times a day.

TAURINE — Although we have no data on taurine in the actual treatment of Ebola or, indeed, any of the hemorrhagic fever viruses, taurine is importantly involved in platelet aggregation and has been shown to prevent excessive sensitivity of platelets to aggregatory stimuli.B1 Increased tendency to coagulation is a part of the severe infections associated with epidemic viruses and bacteria. Moreover, as discussed in the next two paragraphs, taurine is a powerful antiinflammatory agent.

As one paper has explained, “… taurine reaches particularly high concentrations in tissues exposed to elevated levels of oxidants (e.g., inflammatory cells).”B2 “Indeed, at the site of inflammation, taurine is known to react with and detoxify hypochlorous acid [an extremely toxic oxidant] generated by the neutrophil myeloperoxidase (MPO)-halide system. This reaction results in the formation of less toxic taurine chloramine (TauCl). Both haloamines, TauCl and taurine bromamine (TauBr), the product of taurine reaction with hypobromous acid (HOBr), exert antimicrobial and anti-inflammatory properties.”B2 “TauCl and TauBr … show bactericidal, fungicidal, antiviral, and anti­parasitic properties, as demonstrated in vitro in a number of papers.”B2 A recent paperB3 reporting on the use of taurine bromamine as a topical bactericidal on skin, showed that “TauBr [taurine bromamine] in vitro has much stronger bactericidal activity than TauCl, with a potency that approaches that of HOCl, the most potent bactericidal agent of MPO-halide system.” “Importantly, TauBr killed all tested bacteria at non-cytotoxic anti-inflammatory concentrations.”

The authorsB2 have studied in their own lab the effects of taurine and its haloamines in the regulation of inflammation in rheumatoid arthritis. “Taurine haloamines inhibit the production of proinflammatory cytokines (TNF-alpha, IL-1beta, and IL-6).”B2 TNF-alpha is importantly involved in the pathogenesis of rheumatoid arthritis(RA) and agents that suppress TNF-alpha levels have been and are continuing to be studied in the search for therapy of RA. For example, they observed significant inhibition of production of IL-6, TNF-alpha, and IL-8 in joint adipose tissue explants obtained during surgery from RA patients and treated with LPS to induce inflammation.

Protective Action by Taurine Against Lung Damage During Infection

The authors of a recent paperB4 conducted experiments with hamsters treated with bacterial LPS to induce inflammatory responses as occurs in bacterial infection and found that, in comparison with control animals, the hamsters that received TAURINE treatment either before or after intrathacheal instillation with LPS had significantly reduced levels of lung cell apoptosis (programmed cell death), lipid peroxidation, and attenuation of the decrease in glutathione levels. The protective effects were greater when given before LPS treatment as compared to giving it afterward.

RESVERATROL — This molecule, on which a large amount of research has been done, is synthesized by at least 72 plant species including grapes and other fruits and is also famously found in red wine.C Resveratrol was reported in a 2005 paperC to inhibit influenza A viral replication in in vitro (cell) studies, but also reported in the same paperC to significantly improve the survival and decrease lung viral titers in mice infected with the virus. The mice were treated with either resveratrol by intraperitoneal injections of 1 mg/kg/day or placebo administered the same way for 7 days following inoculation of the virus. The placebo treated mice suffered 80% mortality by 10 days after inoculation whereas an average of 40% of the resveratrol treated mice survived to day 10, with the mean lung viral titers being 98% lower in the resveratrol treated mice compared to those that received placebo. None of the mice that survived to day 10 were observed to have signs of disease for the next three months and so were pronounced, “cured.”

The authors proposed a possible chemical pathway by which resveratrol interfered with viral replication.

FEVERFEW — The natural product feverfew, Tanacetum parthenium, an herb, is known to be a potent inhibitor of inflammatory cytokines, such as tumor necrosis factor alpha, that is released in potentially lethal amounts in inflammatory processes such as fatal viral infections. A recent paper1B reported experiments showing that feverfew extracts used to pretreat THP-1 cells then exposed to LPS had “dramatically” reduced LPS-mediated tumor necrosis factor-alpha release in a dose dependent manner. Cells treated in this way with the 1x concentration (equivalent to 0.01% dry weight) of feverfew was 46% of control cells that did not receive feverfew treatment. The LPS-mediated release of CCL2 (also called monocyte chemoattractant protein 1) in their cell model was also strongly reduced in a dose dependent manner. LPS-mediated CCL2 production by the THP-1 cells was 27% of control cells treated with the 1x concentration of feverfew extract. At the 5x concentration of feverfew, the authors reported that NO CCL2 production was detected. Parthenolide, an abundant sesquiterpene lactone found in feverfew, is a potent inhibitor of NFkappaB, a gene that is a master regulator of inflammatory mediators such as tumor necrosis factor alpha.1B2

Another paper1B3 reported significant protection by parthenolide against cardiovascular complications in endotoxic shock in rodents. The authors posit that this effect was mediated by the inhibition of NFkappaB.

BERBERINE — BERBERINE, an isoquinoline alkaloid found in the herb goldenseal was reported to inhibit in vitro growth of the potentially lethal infection by H1N1 influenza A virus in humans and, importantly, to inhibit the acute and possibly deadly host inflammatory response sometimes called a “cytokine storm.” Berberine has also been shown to inhibit the growth of several other viruses, including cytomegalovirus and herpes simplex virus. Berberine is so effective as an inhibitor of cytokine production in response to LPS (lipopolysaccharide, a bacterial cell constituent that is highly stimulative to the immune system) that it has been suggested as a potential treatment for endotoxemia (sepsis).2

FATTY ACID SYNTHASE INHIBITORS — FAS inhibitors have been identified as a target for antiviral therapy.3 Inhibition of FAS in cells suppressed the replication of both cytomegalovirus and influenza A, two enveloped viruses. The paper3 showed that fatty acid synthesis is essential for the replication of these two divergent enveloped viruses. Interestingly, fatty acid synthase (FAS) has been found to be necessary for the replication of bacteria and of many cancers as well. Natural fatty acid synthase inhibitors include quercetin,3A luteolin,3A kaempherol,3A EGCG (found in green tea).3B The diabetes drug metformin also reduces the expression of fatty acid synthase.4

FISH OILS — Study5 reported protection against influenza virus replication via RNA export machinery by Protectin D1, a lipid mediator made in the body from docosahexaenoic acid, an n-3 fatty acid. Treatment by PD-1 itself improved the survival and pathology of severe influenza, an RNA virus, even under conditions where known antivirals failed to prevent death.

QUERCETIN — A flavonoid found in many fruits and vegetables, as well as in black tea, red wine, onions, and other plant foods, has been reported to attenuate the effects of the proinflammatory cytokine TNF-alpha in human adipocytes (fat cells).D In addition, quercetin has been shown in several in vitro studies to have anti-viral effects against herpes simplex virus-1, adenovirus-3, polio virus type-1, parainfluenza virus type 3, and respiratory syncytial virus.E,F


VITAMIN D — The biologically active form of vitamin D has been shown to inhibit HIV-1 viral replication.6 It has also been shown to have immunomodulating effects on many inflammatory conditions, including infections.6B Importantly, Vitamin D has been reported in a recent paper6B2 to reduce the production of proinflammatory cytokines, which (the authors suggest) “may reduce the risk of cytokine storm in H1N1 [viral] infection.” (Emphasis added). The authors6B2 also describe a study (pg. 221) that demonstrated that “maintenance of a vitamin D serum concentration of 38 ng/ml or higher should significantly reduce the incidence of acute viral respiratory tract infections, including influenza, at least during the fall and winter in temperate zones.”

As Hippocrates said, “Whoever wishes to investigate medicine properly should proceed thus: in the first place to consider the seasons of the year.” The association of sunlight or the lack thereof with certain diseases had long been noticed, though the reason for the association wasn’t understood until recently. In 1981, Edgar Hope-Simpson reportedly proposed that “a ‘seasonal stimulus’ intimately associated with solar radiation explained the remarkable seasonality of epidemic influenza.” A review article reporting Hope-Simpson’s suggestion6C concluded that “vitamin D or lack of it may be Hope-Simpson’s ‘seasonal stimulus.’” They review data in their article that found evidence that vitamin D reduces the incidence of respiratory infections including an interventional study in children.

A recent review paper6D examined the relationship between vitamin D and inflammation, noting at the start that, “in vitro studies and some clinical studies suggest that vitamin D plays an important role in reducing inflammation.” Looking at the results of five large cross-sectional studies and two randomized controlled studies comparing vitamin D status with markers of inflammation in adults without acute illness or injury, the authors report that the association between 25-hydroxyvitamin D and inflammation markers are significant and inverse in study populations with low 25-hydroxyvitamin D levels (the higher the vitamin D level, the lower the markers of inflammation) and also inverse in adults with relatively high levels of inflammation (the higher the level of inflammation, the lower the level of vitamin D). They note that in the available randomized controlled vitamin D intervention studies, these relationships have not been observed, possibly (the authors suggest) because there have been so few of them and they may not have had participants with sufficiently low levels of vitamin D or high enough levels of inflammatory markers to detect the association.

It remains a truism that if you are going to test a hypothesis that a substance will produce a certain effect under particular conditions (e.g., reduce inflammation if inflammation is elevated), you need to establish that those conditions exist in your study subjects or you are not testing the hypothesis. There can be no doubt that many of the extremely expensive large intervention trials of nutrients (largely conducted under the auspices of giant taxpayer funded government bureaucracies) are not being performed with the appropriate conditions in the study population. (We note, however, that this review was funded under the auspices of one of the said giant taxpayer funded government bureaucracies, in this case U.S. Department of Agriculture, but is clearly said to reflect the opinions of the authors and not necessarily that of the USDA.)

It has been reported that three independent research groups6C have shown that 1,25(OH)2D, the biologically active form of vitamin D, “dramatically” stimulates genetic expression of antimicrobial peptides (AMP) by human monocytes, neutrophils, and other immune cells. These AMPs include defensins and cathelicidins that have broad-spectrum antimicrobial activity, including antiviral activity. For example, they have been reported to inactivate the influenza virus.6G

Finally, we note a recent paper showing that vitamin D mitigates cognitive decline by modulating the age-related increase in pro-inflammatory state and amyloid burden.6E

PENTOXIFYLLINE — Pentoxifylline (POF) is a xanthine (chemically related to caffeine, a methylxanthine) used in the treatment of vascular diseases such as intermittent claudication since 1984. The drug is cheap and has few side effects.6F There is considerable evidence that POF has antiinflammatory effects. For example, it has been shown to increase resistance to sepsis or endotoxin challenge in rats, mice, and humans, which has been attributed to decreased levels of circulating tumor necrosis factor alpha (TNF-alpha).6F In humans, POF has also been reported to decrease the release of TNF-alpha by peripheral blood monocytes. In a 1999 paper,6F pentoxifylline (POF) was found to inhibit in vitro the production of TNF-alpha by human alveolar macrophages from patients with active pulmonary sarcoidosis. Hence, POF may be helpful in preventing the excessive release of TNF-alpha as part of a viral “cytokine storm.”

SELENIUM — Selenium deficiency has been shown to increase the pathology of influenza virus infection by inducing increased lung damage in influenza-infected mice.7 One paper7B describes selenium’s role in fighting viral infections: “Dietary Se is [ ] known to have immunopotentiating effects … Thus, in addition to any direct effects exerted via (hypothetical) viral selenoproteins, Se deficiency can also weaken the immune system’s ability to fight viral infections, permitting increased replication, rapid mutation, and facilitating the emergence of more virulent strains …” as suggested in the case of cocksackievirus.7C

N-ACETYLCYSTEINE — Cysteine and its acetylated form NAC are precursors to glutathione, an immensely important cellular antioxidant. The cellular concentration of glutathione is depleted by viral infection, reducing the immune system’s ability to resist the virus. A human study of 262 subjects treated with 600 mg twice daily of NAC during the winter (flu season) had reduced incidence of clinically apparent disease.8 Another paper8B reported that cysteine in a cell study inhibited HIV-1 replication and NFkappaB activity. Depletion of reduced glutathione occurs early in HIV infection and many other diseases.

OREGANO AND CLOVE ESSENTIAL OILS — Electron micrography was used to detect the deterioration of viral envelopes in herpes simplex virus type 1 and Newcastle disease virus by treatment with oregano oil or clove oil, while non-enveloped viruses were not affected by either oil (the viral numbers did not differ from controls).9

LYCOPENE — A study reported that lycopene, a carotenoid found famously in tomatoes, could reduce liver damage resulting from hepatitis C virus, a highly persistent viral infection, in in vitro, animal, and clinical studies and described lycopene’s potential as a treatment for hepatitis C.10

IRON — AVOID IT IF YOU HAVE AN INFECTION. Iron is a required growth factor by bacteria. (Makes you wonder whether bleeding in the Middle Ages and later might have actually been beneficial in some patients with acute infection because of decreasing iron supplies available to pathogens.)

EGCG — Has been shown11 to inhibit a molecule that may be essential for Ebola viral infection. A 2014 paper reports that in vitro EGCG bound to a site on the molecule preventing it from promoting viral cellular entry.

CHOLINESTERASE INHIBITORS — ”[s]uppression of inflammation in the brain and in the periphery can be achieved by enhancing cholinergic signaling by administration of acetylcholinesterase inhibitors. The acetylcholinesterase inhibitor galantamine, acting through a central mechanism, has been shown to attenuate serum TNF and IL-6 to improve survival in a murine [mouse] model of endotoxaemia.” “This mechanism could explain the association between high choline dietary intake with reduced proinflammatory markers in serum.”13 Choline, as the precursor to acetylcholine, is also able to enhance cholinergic signaling.

A recent paper reported that alpha7 nicotinic cholinergic receptors may be a novel therapeutic target for inflammation-based disease. The paper notes studies suggesting that the inflammatory response in sepsis can be controlled by activating the CNS (central nervous system) cholinergic system. Further, they point out that cholinesterase inhibitors can control the inflammatory response in experimental sepsis, significantly improving survival if administered immediately after induction of sepsis, but not if treatment is delayed. “A number of preclinical studies have confirmed the therapeutic potential of targeting alpha7 nicotinic acetylcholine receptor-mediated anti-inflammatory effects through modulation of proinflammatory cytokines.” The cholinesterase inhibitor drug GALANTAMINE is an alpha7 nicotinic cholinergic agonist (activating the cholinergic anti-inflammatory pathway via the alpha7 nicotinic cholinergic receptor).14

These are just a few examples from a large and rapidly growing literature on ways to reduce the damage caused by dangerous viral infections and, hence, decrease the risk of mortality. Make yourself a hardened target to nasty viruses that we are sure to be seeing again and again. Though they will reappear in different forms, they will all be a threat by driving your immune system into a potentially deadly “cytokine storm.” If you’re hoping to live a long time, it would be a very sad story to be prevented from reaching that goal by a virus aided and abetted by poor public health practices (such as importing patients from areas of lethal viral epidemics and releasing them before they can show symptoms and other poor practices that are causing nurses to contract the disease themselves; perhaps we ought to add here that you should take any advice from the CDC or other government public health agencies with a very large grain of salt!). When bureaucrats give bad advice that causes severe harm, the all too common response when this becomes known is to cover up, dissemble, and double down, causing further harm. They frequently behave as if their biggest concern is maintaining their budget.


Adults who do not have contraindications to receiving flu shots (such as allergies to them) should get the flu shots issued each year. However, importantly, the CDC (Centers for Disease Control, a U.S. federal government agency) has announced that the flu shots made publicly available are only effective against about 50% of the circulating types of influenza to which the American public is exposed. Therefore, it is important to also employ techniques to avoid getting flu in the first place, many of which are discussed in our article.


A1. Bissell et al. Ascorbic acid inhibits replication and infectivity of avian RNA tumor viruses. Proc Natl Acad Sci U S A. 77(5):2711 – 5 (1980).
A2. Kim, Kim, Bae, et al. Vitamin C is an essential factor on the anti-viral immune responses through the production of interferon-alpha/beta at the initial stage of influenza A virus (H3N2) infection. Immune Netw. 13(2):70 – 4 (2013).
A. Tan, Korkmaz, Reiter, Manchester. Ebola virus disease: potential use of melatonin as a treatment. J Pineal Res. 57(4):381 – 4 (2014).
B1. Hayes, Pronczuk, et al. Taurine modulates platelet aggregation in cats and humans. Am J Clin Nutr. 49:1211 – 6 (1989).
B2. Marcinkiewicz and Kontny. Taurine and inflammatory disease. Amino Acids. 46:7 – 20 (2014).
B3. Mancinkiewicz. Taurine bromamine (TauBr) — its role in immunity and new perspectives for clinical use. J Biomed Sci. 17(Suppl 1):53 (2010).
B4. Bhavsar, Patel, Lau-Cam. Protective action of taurine, given as a pretreatment or as a posttreatment, against endotoxin-induced acute lung inflammation in hamsters. J Biomed Sci. 17(Suppl. 1):519 (2010).
C. Palamara, Nencioni, Aquilano, et al. Inhibition of influenza A virus replication by resveratrol. J Infect Dis. 191:1719 – 29 (2005).
D. Chuang et al. Quercetin is equally or more effective than resveratrol in attenuating tumor necrosis factor-alpha-mediated inflammation and insulin resistance in primary human adipocytes. Am J Clin Nutr. 92:1511 – 21 (2010).
E. Kaul et al. Antiviral effect of flavonoids on human viruses. J Med Virol. 15:71 – 9 (1985).
F. Chiang et al. In vitro antiviral activities of Caesalpinia pulcherrima and its related flavonoids. J Antimicrob Chemother. 52:194 – 8 (2003).
G. Atefi, Zetoune, Herron, et al. Complement dependency of cardiomyocyte release of mediators during sepsis. FASEB J. 25:2500 – 8 (2011).
H. Clark, Budd, et al. Human malarial disease: a consequence of inflammatory cytokine release. Malar J. 5:85 (2006).
J. Yiu, Graham, Stengel. Dynamics of a cytokine storm. PLoS One. 7(10):e45027 (2012).
K. Clark. The advent of the cytokine storm. Immunol Cell Biol. 85:271 – 3 (2007).
1. Cilloniz, Ebihara, Ni, et al. Functional genomics reveals the induction of inflammatory response and metalloproteinase gene expression during lethal Ebola virus infection. J Virol. 85(17):9060 – 8 (Sept. 2011).
1B. Chen and Cheng. Regulation of cellular metabolism and cytokines by the medicinal herb feverfew in the human monocytic THP-1 cells. Evid Based Complement Alternat Med. 6(1):91 – 8 (2009).
1B2. Kwok, Koh, Ndubuisi, et al. The anti-inflammatory natural product parthenolide from the medicinal herb Feverfew directly binds to and inhibits IkB kinase. Chem Biol. 8:759 – 66 (2001).
1B3. Sheehan, Wong, Hake, et al. Parthenolide, an inhibitor of the nuclear factor kappaB pathway, ameliorates cardiovascular derangement and outcome in endotoxic shock in rodents. Mol Pharmacol. 61(5):953 – 63 (2002).
2. Cecil, Davis, et al. Inhibition of H1N1 influenza A virus growth and induction of inflammatory mediators by the isoq uinoline alkaloid berberine and extracts of goldenseal (Hydrastis canadensis). Int Immunopharmacol. 11(11):1706 – 14 (2011).
3. Munger, Bennett, Parikh, et al. Systems-level metabolic flux profiling identifies fatty acid synthesis as a target for antiviral therapy. Nat Biotechnol. 26(10):1179 – 86 (2008).
3A. Brusselmans, Vrolix, et al. Induction of cancer cell apoptosis by flavonoids is associated with their ability to inhibit fatty acid synthase activity. J Biol Chem. 280(7):5636 – 45 (2005).
4. Algire, Amrein, et al. Metformin blocks the stimulative effect of a high-energy diet on colon carcinoma growth in vivo and is associated with reduced expression of fatty acid synthase. Endocr Relat Cancer. 17:351 – 60 (2010).
5. Morita, Kuba, Ichikawa, et al. The lipid mediator Protectin D1 inhibits influenza virus replication and improves severe influenza. Cell. 153:112 – 25 (2013).
6. Campbell and Spector. Hormonally active vitamin D3(1alpha,25-dihydroxycholecalciferol) triggers autophagy in human macrophages that inhibits HIV-1 infection. J Bio Chem. 286:18890 – 902 (2011).
6B. Guillot, Semerano, et al. Vitamin D and inflammation. Joint Bone Spine. 77:552 – 7 (2010).
6B2. Youssef, Miller, El-Abbassi, et al. Antimicrobial implications of vitamin D. Dermatoendocrinol. 3:4:220 – 229 (Oct. 2011).
6C. Cannell, Vieth, Umhau, et al. Epidemic influenza and vitamin D. Epidemiol Infect. 134:1129 – 40 (2006).
6D. Zanetti, Harris, Dawson-Hughes. Ability of vitamin D to reduce inflammation in adults without acute illness. Nutr Rev. 72(2):95 – 8 (2013).
6E. Briones and Darwish. Vitamin D mitigates age-related cognitive decline through the modulation of pro-inflammatory state and decrease in amyloid burden. J Neuroinflammation. 9:244 (2012).
6F. Marques, Zheng, Poulakis, et al. Pentoxifylline inhibits TNF-alpha production from human alveolar macrophages. Am J Respir Crit Care Med. 159:508 – 511 (1999).
6G. Daher et al. Direct inactivation of viruses by human granulocyte defensins. J Virol. 60:1068 – 74 (1986).
7. Beck, Nelson, Shi, et al. Selenium deficiency increases the pathology of an influenza virus infection. FASEB J. 15(8):1481 – 3. (April 27, 2001).
7B. Taylor and Ramanathan. Theoretical evidence that the Ebola virus Zaire strain may be selenium dependent: a factor in pathogenesis and viral outbreaks? J Orthomol Med. 10(3 & 4):131 – 8 (1995).
7C. Beck, Shi, et al. Rapid genomic evolu tion of a non-virulent Coxsackievirus B3 in selenium-deficient mice results in selection of identical virulent isolates. Nat Med. 1:433 – 6 (1995).
8. Flora et al. Attenuation of influenza-like symptomatology and improvement of cell-mediated immunity with long-term N-acetylcysteine treatment. Eur Respir J. 10:1535 – 41 (1997); also see Cai, Chen, et al. Inhibition of influenza infection by glutathione. Free Rad Biol Med. 34(7):928 – 36 (2003).
8B. Mihm, Ennen, et al. Inhibition of HIV-1 replication and NF-kappaB activity by cysteine and cysteine derivatives. Aids. 5:497 – 503 (1991).
9. Siddiqui et al. Effect of essential oils on the enveloped viruses: antiviral activity of oregano and clove oils on herpes simplex virus type 1 and Newcastle disease virus. Med Sci Res. 24:185 – 6 (1996).
10. Yadav D, Hertan HI, Schweitzer P, Norkus EP, Pitchumoni CS. Serum and liver micronutrient antioxidants and serum oxidative stress in patients with chronic hepatitis C. Am J Gastroenterol. 97(10):2634 – 9 (2002 Oct).
11. Reid, Shurtleff, Costantino, et al. HSPA5 is an essential host factor for Ebola virus infection. Antiviral Res. 109:171 – 4 (2014).
12. Howett, Neely, Christensen, et al. A broad-spectrum microbicide with virucidal activity against sexually transmitted viruses. Antimicrob Agents Chemother. 43(2):314 – 21 (1999).
13. Rosas-Balina and Tracey. Cholinergic control of inflammation. J Intern Med. 265:663 – 79 (2009).
14. Bencherif, Lippiello, Lucas, Marrero. Alpha7 nicotinic receptors as novel therapeutic targets for inflammation-based diseases. Cell Mol Life Sci. 68(6):931 – 949 (2011).

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