For those of you who don’t care about details and don’t want to ever read anything longer than a Tweet, let me summarize:
The coronavirus that currently has everyone freaked out is:
- Easily spread through person to person contact
- Has slightly better than a 2% mortality rate
- Kills primarily by initiating a cytokine storm or as a result of secondary pneumonia
- Is rapidly breaking containment
- There are ways to keep symptoms to a minimum and avoid complications that may lead to a bad end
The best defense is to maintain an optimized immune system AND make sure you have an adequate supply of natural anti-pathogens on hand. You won’t be able to prevent the virus if you’re exposed to it (this is a brand new virus, and no human being has any immunity to it), but it is possible to keep the viral load to a minimum so that it doesn’t progress into a cytokine storm, pneumonia, or acute respiratory distress syndrome (ARDS). If you do that, symptoms are likely to be mild.
But, for those of you who understand that knowledge is power, here’s the underlying story.
What Exactly is the Coronavirus?
Coronaviruses are not a single virus, but rather, a large family of viruses that mostly infect bats, pigs, and small mammals. However, a handful can infect humans and cause illness ranging from the common cold (about 20% of all colds are the result of coronaviruses) to more severe diseases such as SARS, MERS, and the new coronavirus. They are named for the crown-like spikes on their surface. And no, the fact that 20% of all colds are caused by a mere four of the many coronaviruses does not mean that the current coronavirus outbreak is nothing more than a common cold as some have proposed.1 Rush Limbaugh. “Overhyped Coronavirus Weaponized Against Trump. The Rush Limbaugh Show. Feb 24, 2020. (Accessed 25 Feb 2020.) https://www.rushlimbaugh.com/daily/2020/02/24/overhyped-coronavirus-weaponized-against-trump/ And even more confusingly, some of those same people have also theorized that it’s probably a “laboratory experiment that is in the process of being weaponized.” How it’s both a nothing-to-worry-about common cold AND a weaponized virus at the same time I’ll leave to brighter minds than mine to explain.
And speaking of conspiracy theories, over two dozen scientists, health experts and epidemiologists, in an open letter published in The Lancet, disputed Rush’s conspiracy theory that the virus is a bioweapon made in a lab near Wuhan.2 Charles Calisher, Dennis Carroll, Rita Colwell, et al. “Statement in support of the scientists, public health professionals, and medical professionals of China combatting COVID-19.” The Lancet. February 19,2020. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30418-9/fulltext And I quote, “We stand together to strongly condemn conspiracy theories suggesting that COVID-19 does not have a natural origin. Scientists from multiple countries have published and analyzed genomes of the causative agent…and they overwhelmingly conclude that this coronavirus originated in wildlife as have so many other emerging pathogens.” Yes, they could be lying or mistaken, but probably not.
Before COVID-19, only six coronaviruses had been known to be responsible for human diseases. Two are zoonoses (diseases which are transmitted to humans from animals). These would be SARS and MERS, both of which can be fatal. The remaining four viruses are widespread in human society, causing the common cold. COVID-19, the seventh such virus seems to borrow from both groups. It originally was a zoonotic disease, likely jumping from animals to humans in a Chinese Seafood Wholesale Market. Very quickly, it showed a facility to readily and rapidly spread from human to human, while still maintaining its zoonotic ability to kill people. The natural animal host of COVID-19 is undetermined, but the closest animal-coronavirus by genetic-sequence is a bat-coronavirus, and this is the likely ultimate origin of the virus,3 Chen Y, Liu Q, Guo D. “Emerging coronaviruses: genome structure, replication, and pathogenesis.” (2020) Journal of medical virology. https://pubmed.ncbi.nlm.nih.gov/31967327-emerging-coronaviruses-genome-structure-replication-and-pathogenesis/ , 4 Heymann DL, Shindo N. “COVID-19: What Is Next for Public Health?” (2020) Lancet. https://pubmed.ncbi.nlm.nih.gov/32061313-covid-19-what-is-next-for-public-health/ , 5 Ng LFP, Hiscox JA. “Coronaviruses in animals and humans.” (2020) BMJ (Clinical research ed.). 368: m634. https://pubmed.ncbi.nlm.nih.gov/32075782-coronaviruses-in-animals-and-humans/ although it seems the disease can also be transmitted by snakes.6 Yueying Pan, Hanxiong Guan, Shuchang Zhou, et al. “Initial CT findings and temporal changes in patients with the novel coronavirus pneumonia (2019-nCoV): a study of 63 patients in Wuhan, China.” (2020) European Radiology. https://pubmed.ncbi.nlm.nih.gov/32055945-initial-ct-findings-and-temporal-changes-in-patients-with-the-novel-coronavirus-pneumonia-2019-ncov-a-study-of-63-patients-in-wuhan-china/
So, this particular strain is brand new and has never previously been identified in humans, which again is why no human being on the planet has any immune system memory of it—and therefore no immunity. It was first named the 2019 novel coronavirus.7 Na Zhu, Dingyu Zhang, Wenling Wang, et al. “A Novel Coronavirus from Patients with Pneumonia in China, 2019.” (2020) New England Journal of Medicine. https://pubmed.ncbi.nlm.nih.gov/31978945-a-novel-coronavirus-from-patients-with-pneumonia-in-china-2019/ , 8 Perlman S. “Another Decade, Another Coronavirus.” N Engl J Med. 2020;382(8):760–762. https://pubmed.ncbi.nlm.nih.gov/31978944-another-decade-another-coronavirus/ It was then named COVID-19 by the World Health Organization (short for Corona Virus Disease, 2019). Around the same time, the Coronavirus Study Group of the International Committee on Taxonomy of Viruses named the virus SARS-CoV-2 (short for “Severe Acute Respiratory Syndrome coronavirus 2).9 Alexander E. Gorbalenya, Susan C. Baker, Ralph S. Baric, et al. “Severe acute respiratory syndrome-related coronavirus – The species and its viruses, a statement of the Coronavirus Study Group.” bioRxiv 2020.02.07.937862; https://www.biorxiv.org/content/10.1101/2020.02.07.937862v1 , 10 Enserink, M. (2020). “Update: ‘A bit chaotic.’ Christening of new coronavirus and its disease name create confusion.” Sciencemag.org. Feb. 12, 2020. (Accessed 25 Feb 2020.) In the end, COVID-19 seems to have won out.
The first cases were seen in the city of Wuhan, China in December 2019 (how far we have come in such a short time) and have been linked to the Huanan Seafood Wholesale Market.11 Na Zhu , 12 Perlman , 13 Hui DS, I Azhar E, Madani TA, et al. “The continuing 2019-nCoV epidemic threat of novel coronaviruses to global health – The latest 2019 novel coronavirus outbreak in Wuhan, China.” Int J Infect Dis. 2020;91:264–266. https://pubmed.ncbi.nlm.nih.gov/31953166-the-continuing-2019-ncov-epidemic-threat-of-novel-coronaviruses-to-global-health-the-latest-2019-novel-coronavirus-outbreak-in-wuhan-china/ Person-to-person transmission readily occurs, and no effective treatment or vaccine currently exists.14 “Coronavirus Disease (COVID-19): Prevention & Treatment.” CDC February 15, 2020 (Accessed 27 Feb 2020.) https://www.cdc.gov/coronavirus/2019-ncov/about/prevention-treatment.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fcoronavirus%2Fabout%2Fprevention.html
Incidence and Distribution of the Virus
According to a Johns Hopkins online virus tracker, as of March 18, 2020, over 205,000 cases of COVID-19 have been confirmed worldwide, with the majority in China. However, Italy is also very high. (Sometimes the internet is astounding.)
On January 13, 2020, the first confirmed case outside China was diagnosed, a Chinese tourist in Thailand.15 Hui DS On 20 January, the first infected person in the United States was confirmed to be a man in the State of Washington who had recently returned from a visit to Wuhan.16 Holshue ML, DeBolt C, Lindquist S, et al. “First Case of 2019 Novel Coronavirus in the United States.” [published online ahead of print, 2020 Jan 31]. N Engl J Med. 2020;10.1056/NEJMoa2001191. https://pubmed.ncbi.nlm.nih.gov/32004427-first-case-of-2019-novel-coronavirus-in-the-united-states/ The disease has now been diagnosed in 33 territories, including Macau and Hong Kong, in five continents.17 Johns Hopkins , 18 Wang D, Hu B, Hu C, et al. “Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China.” [published online ahead of print, 2020 Feb 7]. JAMA. 2020;10.1001/jama.2020.1585. https://pubmed.ncbi.nlm.nih.gov/32031570-clinical-characteristics-of-138-hospitalized-patients-with-2019-novel-coronavirus-infected-pneumonia-in-wuhan-china/
In the largest study to date, a paper published by the Chinese Center for Disease Control and Prevention (CCDC) analyzed all the cases diagnosed up to 11 February 2020, which came to 44,672 cases. Of these, 1.2% were asymptomatic and 80.9% were classed as “mild”. The overall mortality rate was found to be 2.3%.19 Perlman , 20 Johns Hopkins , 21 “Novel Coronavirus Pneumonia Emergency Response Epidemiology Team.” Zhonghua Liu Xing Bing Xue Za Zhi. 2020;41(2):145–151. https://pubmed.ncbi.nlm.nih.gov/32064853-the-epidemiological-characteristics-of-an-outbreak-of-2019-novel-coronavirus-diseases-covid-19-in-china/ Now, a 2.3% mortality rate doesn’t sound like a lot (just ask Rush Limbaugh), but it is. In fact, it’s huge. The Spanish Flu of 1919 had an almost identical mortality rate of 2.5%. The standard flu has a mortality rate of about 0.1% and that kills about 56,000 every year in the US (last year it was 80,000) and somewhere between 291,000 to 646,000 worldwide.22 “Seasonal flu death estimate increases worldwide.” CDC December 13, 2017. (Accessed 25 Feb 2020.) https://www.cdc.gov/media/releases/2017/p1213-flu-death-estimate.html Now here’s the fly in the ointment. Two percent may be small, but it’s 20 times bigger than 1/10 of one percent. Do the math (multiply the numbers above by 20) and you’re looking at the potential for some very large numbers. So yes, it’s “potentially” a big deal—although it’s highly unlikely to play out like that. More on that in a bit. (Note: ultimately, as more people are tested, the real mortality rate will probably end up somewhat less that 2.3%, but it is still likely to be several times higher than the numbers for seasonal flu.)
COVID-19 is primarily transmitted in a similar way to the common cold, that is face to face, either from sneezing/coughing or close contact with infected individuals’ bodily secretions.23 Heymann Think, family, friends, coworkers, buses, planes, trains, movie theaters, concerts, etc. Additionally, coronaviruses can survive for up to nine days on surfaces such as doorknobs and shopping cart handles.24 Rebecca Blankenship. “How long does coronavirus live on surfaces?” Medical News Bulletin. February 11, 2020. (Accessed 26 Feb 2020.) https://medicalnewsbulletin.com/how-long-does-coronavirus-live-on-surfaces/ Touch the surface anytime during those nine days and then touch your eyes, nose or mouth, and you have the possibility of infection. [Newer studies now say that COVID-19 lasts up to three days on surfaces and up to 30 minutes in the air when someone sneezes or coughs.]
The infection was declared a Public Health Emergency of International Concern (PHEIC) on 30 January 2020 by the WHO.25 “Statement on the second meeting of the International Health Regulations (2005) Emergency Committee regarding the outbreak of novel coronavirus (2019-nCoV)”. Who.int, 2020. https://www.who.int/news-room/detail/30-01-2020-statement-on-the-second-meeting-of-the-international-health-regulations-(2005)-emergency-committee-regarding-the-outbreak-of-novel-coronavirus-(2019-ncov)
Coronavirus: Initial Symptoms and Pathology
The evidence suggests that when COVID-19 enters the body—primarily through droplets in the air—it attaches to a particular receptor found in lung tissue.26 Zhao, Yu; Zhao, Zixian, Wang, Yujia, et al. “Single-cell RNA expression profiling of ACE2, the putative receptor of Wuhan 2019-nCov.” bioRxiv 2020.01.26.919985. https://www.biorxiv.org/content/10.1101/2020.01.26.919985v1.full From there, the virus “hijacks” the host cell’s mechanisms to make more copies of itself. Tissue damage happens as a result of viruses taking over the cell completely, causing it to die, or when immune cells mount a defense against the viral infection, leading to cell death.
If large numbers of cells die, then the affected organ—in this case, the lung— can’t function effectively.
Typically, coronaviruses in humans cause mild respiratory infections such as the common cold. COVID-19, on the other hand, has demonstrated an ability in some patients to go beyond mild symptoms and develop into ALI and ARDS, which is more typical of pneumonias. (Note: Acute lung injury (ALI) is a more recently coined term that includes ARDS but also milder degrees of lung injury.) ALI and ARDS always result from another severe underlying disease. ARDS is the acronym to remember, though, since it’s respiratory failure or cardio-respiratory issues resulting from ARDS that lead to patients dying.
Then again, some people can have the virus and yet present no symptoms while the virus is in incubation. Symptoms of COVID-19 may appear in as few as two days or take as long as 14 days after exposure to appear. And this part is particularly worrisome—the carriers of the virus are highly infectious even while demonstrating no symptoms of infection. Think millions of Typhoid Mary‘s walking around, completely asymptomatic, infecting everyone they come in contact with—even if just for a moment.
Some individuals, especially young children, may remain asymptomatic for the entire course of their illness. And many other individuals may demonstrate, at most, mild upper respiratory tract symptoms. Other symptoms can include fever, aches and pains, fatigue, chest pain, and a dry cough. All these people that we’ve just mentioned are the 98% who will survive COVID-19 illness without any problems. For a small handful, however, the course of the disease is quite different—fatal. In fact, there are two paths to death.
- Some people are young, with strong immune systems. For them, the problem is that the virus overstimulates their immune system, triggering a cytokine storm in which a person’s own immune system attacks the lungs, leading to a large release of fluid in the lungs (ARDS), eventually leading to that person “drowning” in their own lung fluids.
- The second group tends to be older, with weakened immune systems, and lungs already compromised by disease (think COPD and emphysema). For them, the virus can weaken the immune system even more, to the point that pneumonia takes hold. Severe pneumonia has multiple paths to death including ARDS, heart failure, and sepsis.
According to the Chinese Center for Disease Control, 81% of cases are mild, 14% are severe, and 5% are critical.27 The Novel Coronavirus Pneumonia Emergency Response Epidemiology Team. “Vital Surveillances: The Epidemiological Characteristics of an Outbreak of 2019 Novel Coronavirus Diseases (COVID-19.” China CDC Weekly. 2020, 2(8): 113-122. http://weekly.chinacdc.cn/en/article/id/e53946e2-c6c4-41e9-9a9b-fea8db1a8f51 And about half of those who go critical die.
Keeping in mind that patients can be infected for anywhere from two to 14 days before they exhibit symptoms (infecting everyone they meet the entire time), here’s how symptoms progress among typical patients once they first manifest:
- The first symptoms, if any, are likely to be a fever, fatigue, and myalgia (muscle pain)
- This might be followed by difficulty breathing, especially if the patient is older or has a preexisting condition.
- Most people start to feel better after about a week. But about 20% will elevate to either a cytokine storm or pneumonia, both of which can lead to Acute Respiratory Distress Syndrome and require hospital admittance. (And now let’s talk about ARDS.)
- The lungs are highly vascularized. There’s a lot of blood flow in the lungs, because that’s where carbon dioxide is removed from your blood and replaced by oxygen, which is required by every cell in your body. Normally, you want your airways to be relatively dry so that you can breathe in air from which the oxygen gets transferred to red bloods cells and carried to the rest of body. ARDS occurs when fluid leaks from small blood vessels and collects in the tiny air sacs in your lungs so they can’t fill with enough air. That build-up of fluid in the lungs is what can cause breathing distress, because now lungs aren’t exchanging carbon dioxide for oxygen very efficiently. In addition to your lungs being compromised, organs such as your kidneys or brain might begin to malfunction, or even shut down if they do not receive enough oxygen.
- ARDS/ALI typically occurs in people who are already critically ill or who have significant injuries. Severe shortness of breath—the main symptom of ARDS—usually develops within a few hours to a few days after the precipitating infection. But as we’ve seen with COVID-19, that timeframe can stretch out as long as two weeks.
- ARDS is characterized by an acute inflammatory response triggered by immune cells followed by a chronic fibroproliferative phase marked by progressive collagen deposition in the lung.28 Tisoncik JR, Korth MJ, Simmons CP, Farrar J, Martin TR, Katze MG. Into the eye of the cytokine storm. Microbiol Mol Biol Rev. 2012;76(1):16–32. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294426/ Pathogen-induced lung injury can progress into ALI or its more severe form, acute respiratory distress syndrome (ARDS), as was seen with SARS, more aggressive flu virus infections, and now COVID-19. Interlukin-1β is a key cytokine driving proinflammatory activity in bronchoalveolar fluid washing out of patients with lung injury.
- About 4% of all those infected will continue to worsen and require admittance to an ICU
- ARDS is usually treatable, and most people normally survive. But when the underlying trigger for the condition is strong enough, as with COVID-19, only about half of people who develop ARDS survive. The risk of death increases with age and the severity of illness. HOWEVER, sometimes people with strong immune systems also succumb. And the reason is that once a cytokine storm is unleashed, the stronger your immune system, the stronger the storm. In effect, young healthy people can die because their immune systems are so strong. (There is a way to mitigate this without compromising your immune system, and we will talk about why that’s not a good idea later.) Of the people who do survive ARDS, some recover completely while others experience lasting damage to their lungs.
- Over the next week of infection (from day 10-17) about half of those admitted to ICU will recover. The other half will not.
Treatment and Prognosis
Currently, no specific treatment or vaccine exists for COVID-19, which is why most efforts have been made to contain the virus and prevent infected people from spreading the disease. This includes personal hygiene, fitted masks, and the avoidance of large crowds and crowded environments.29 Chen
In healthcare facilities, it is crucial to diagnose COVID-19 as rapidly as possible, quarantine infected cases, and provide effective supportive therapies including antibiotics, antivirals, steroids and supportive measures. Oxygen and the use of a ventilator have also been used when necessary.
While no specific antiviral therapies for COVID-19 currently exist, the combination of the protease inhibitors ritonavir and lopinavir (or a triple combination of these antiviral agents with the addition of ribavirin) showed some success in the treatment of SARS,30 Zhang L, Liu Y. “Potential Interventions for Novel Coronavirus in China: A Systematic Review [published online ahead of print, 2020 Feb 13].” J Med Virol. 2020;10.1002/jmv.25707. https://pubmed.ncbi.nlm.nih.gov/32052466-potential-interventions-for-novel-coronavirus-in-china-a-systematic-review/ and early reports suggest similar efficacy in the treatment of COVID-19.31 Lim J, Jeon S, Shin HY, et al. “Case of the Index Patient Who Caused Tertiary Transmission of COVID-19 Infection in Korea: the Application of Lopinavir/Ritonavir for the Treatment of COVID-19 Infected Pneumonia Monitored by Quantitative RT-PCR.” J Korean Med Sci. 2020;35(6):e79. Published 2020 Feb 17. https://pubmed.ncbi.nlm.nih.gov/32056407-case-of-the-index-patient-who-caused-tertiary-transmission-of-covid-19-infection-in-korea-the-application-of-lopinavirritonavir-for-the-treatment-of-covid-19-infected-pneumonia-monitored-by-quantitative-rt-pcr/
Vaccines for the coronaviruses have been under development since the SARS outbreak, but none are yet available for human patients.32 Chen , 33 Ng LFP A phase I trial in humans of a potential vaccine against MERS-CoV has already been performed in the UK.34 Ng LFP It is possible that an effective MERS vaccine might also have some applicability to COVID-19, but that’s purely speculative at the moment.
The key to the higher mortality rate for COVID-19 is the cytokine storm. A cytokine storm is triggered when the body perceives that a viral attack is more than it can handle through a normal response. This can happen in several different ways.
- A virus can be so virulent that its assault on the body is so great it triggers a cytokine storm. A normal immune system protects against invaders, but an immune system driven into over-active by an aggressive virus can not only damage the lungs but also other organs, including the kidneys, liver and heart.
- A virus can be so new (unlike most flus or colds) that the body has no memory of it, or any virus like it. This means your immune system can’t rely on its best, most trained defenders, the B-Cells and especially the T-Cells. Instead, it must turn to the extremely aggressive, but untrained, shock troops of the immune system, the macrophages and dendritic cells. They are powerful; they are quick; and they are aggressive. But being untrained, their attack may not be so precise. In other words, they can cause collateral damage. This is the pathway that can lead healthy, young people into the critical stages of illness.
- A virus by itself may not be strong enough to trigger a cytokine storm, but it may trigger a secondary infection (usually pneumonia) which, when combined with the initial infection, produces enough viral overload to trigger a cytokine storm. Any respiratory virus, including flu, respiratory syncytial virus, human metapneumovirus, and now COVID-19 can lead to pneumonia. This is how seasonal flu kills over 600,000 people a year. People don’t die from the flu, they die from the storm unleashed by the pneumonia, which was brought on as a secondary infection. Seniors with weakened immune systems are particular vulnerable to this pathway if they are infected with COVID-19, and the majority of deaths so far have come through this scenario—mostly involving older men.
However the storm is triggered, it causes your immune system to go nuts, whipping itself into a frenzy in response to the invading virus/viruses. A biochemical cascade of immune cells and immune system bio-chemicals such as interferon, interleukin, and monokines—collectively known as cytokines—literally pours into the lungs bringing macrophages and dendritic cells along with them. The subsequent damage to the lung tissue caused by these cells and biochemicals leads to ARDS that can literally chew up a person’s lung tissue, causing fluid to pour into the lungs, ultimately causing the victim to suffocate as a result of their own disease-fighting chemistry. The patient literally drowns in their own body fluids.
Most common flu’s do not produce cytokine storms. Most flu’s that kill people usually do so to those who have weak immune systems by eventually opening the door for pneumonia, which subsequently triggers a cytokine storm. That’s why health authorities specify that the very old and the very young are prime candidates for annual flu vaccines (even though they don’t work very well). But swine flu, avian flu, the great flu pandemic of 1918, and now COVID-19 are different animals. Yes, they can follow the same path in seniors with weakened immune systems. But because they are so virulent, and because human immune systems have no memory of them, they don’t need pneumonia to kill you. They can kill you by directly unleashing a cytokine storm, which means that it is your own, healthy immune system that kills you. And this means that although the most vulnerable are the very old (especially those with weak immune systems and/or underlying health conditions), healthy adults and pregnant women and people who have very strong immune systems are not free of risk, even if that risk is low. Curiously, at least to this point, young children do not seem to be particularly vulnerable.
To translate that into English, in a cytokine storm, the immune system overacts to the invasion of pathogens, and it’s the immune system itself that damages the lungs, not the virus. Think of it like using a sandblaster to scratch an itch instead of your finger. There’s going to be collateral damage. It’s the cytokine storm that made both SARS and MERS, along with the bird flu, so deadly. An important difference between those infections and COVID-19, though, is that almost all infections with those diseases were from animal to human. Human to human infection, when it occurred, was both rare and difficult. What sets COVID-19 apart is how easily it transmits between humans. Add in the fact that humans can be highly infectious for up to two weeks without displaying a single symptom, and you have a concerning situation.
Looking to the Future
On Friday, Feb 21st, the World Health Organization director general, Tedros Adhanom Ghebreyesus, said that there was still a chance to contain the virus, “but the window of opportunity is narrowing.” Just four days later, that optimistic projection was fading. On Tuesday, Feb 25th, American health authorities said they ultimately expect the virus to spread throughout the United States and are urging local governments, businesses, and schools to develop plans like canceling mass gatherings or switching to teleworking. As Dr. Nancy Messonnier, a senior official with the CDC said in a telebriefing, “Ultimately, we expect we will see community spread in this country. It’s not so much a question of if this will happen anymore but rather more a question of exactly when this will happen and how many people in this country will have severe illness.”35 “Transcript for the CDC Telebriefing Update on COVID-19.” CDC February 26, 2020. https://www.cdc.gov/media/releases/2020/t0225-cdc-telebriefing-covid-19.html Messonnier went on to say: “We are asking the American public to prepare for the expectation that this might be bad.” And finally, she pointed out, there are concerns that the outbreak poses a threat to the security of the US drug supply chain because a high proportion of ingredients used to make medicine is made in China, where the virus is causing massive disruption.
The headline in an article in The Atlantic says it all: “You’re Likely to Get the Coronavirus.”36 James Hamblin. “You’re Likely to Get the Coronavirus.” The Atlantic. February 24, 2020. (Accessed 26 Feb 2020.) https://www.theatlantic.com/health/archive/2020/02/covid-vaccine/607000/ In the article, James Hamblin writes:
“The Harvard epidemiology professor Marc Lipsitch is exacting in his diction, even for an epidemiologist. Twice in our conversation he started to say something, then paused and said, ‘Actually, let me start again.’ So, it’s striking when one of the points he wanted to get exactly right was this: ‘I think the likely outcome is that it will ultimately not be containable.’
“Lipsitch predicts that within the coming year, some 40 to 70 percent of people around the world will be infected with the virus that causes COVID-19. But, he clarifies emphatically, this does not mean that all will have severe illnesses. “It’s likely that many will have mild disease, or may be asymptomatic,” he said. As with influenza, which is often life-threatening to people with chronic health conditions and of older age, most cases pass without medical care.”
And that, of course, is precisely why COVID-19 is likely to be unstoppable. Viruses like SARS, MERS, and the bird flu were eventually contained in part because:
- They weren’t infectious before symptoms appeared.
- They were more intense and had a higher fatality rate. In other words, once you had symptoms, you were too sick to be out and about and mingling with people.
- And if you were going to die, you tended to die pretty quickly.
But because the current coronavirus can be asymptomatic, or at least very mild, there’s a better chance people will be going about their day as normal unknowingly spreading infection. Additionally, because people won’t know when they started spreading infection, it will be that much harder to trace and prevent the disease from spreading to others.
The Atlantic reports Lipsitch is definitely not alone in his prediction. There’s an emerging consensus that the outbreak will eventually morph into a new seasonal disease, which, per The Atlantic, could one day turn “cold and flu season” into “cold and flu and COVID-19 season.”
And one final reminder. Although Professor Lipsitch said “it’s likely that many will have mild disease,” that also means that some will not. And a small percentage applied to 40 to 70 percent of the world’s population is a very, very large number.
Now let’s talk about you can avoid being one of them.
What to Do? What to Do? What to Do?
- First of all, reassurances from government officials that COVID-19 is not going to hit the United States are nonsense, but don’t panic. Despite the fact that it looks like this virus is going to spread far and wide, for “most” people, symptoms will be mild or even non-existent. But also understand that, as I just mentioned, small percentages of people being critically ill and dying works out to be very large numbers if applied across enough people.
- Look to the future. Time is your best friend. The longer you can go without getting infected, the better your chances will be of never getting infected or surviving any infection you do get. As the pool of “once infected people” grows, the ability of the virus to spread diminishes. In other words, your chances of getting COVID-19 will follow a bell curve. For the next 12 months or so, they will increase dramatically, and then begin to fade—eventually getting very low. (Note: there may be a slow down to the curve as warmer months appear since early evidence indicates that, like the flu virus, COVID-19 thrives in cold, dry weather VS hot, moist weather. If so, things will accelerate again as the colder fall months arrive.)
- Also, over time, medical researchers will develop proven treatments that go far beyond mere palliative care. It’s worth noting—for those of you who have not been paying attention—that even Ebola is no longer incurable. Recently, Ebola treatments have been successful 90 percent of the time when symptoms were detected early.
- Speaking of which, an alternative that might speed things up is that, instead of creating brand new drugs to combat COVID-19, researchers are looking at the possibility of repurposing already existing drugs. For example, researchers have found that both remdesivir (one of the drugs currently be used to combat Ebola in Africa) and chloroquine (a widely used and FDA approved anti-malarial and autoimmune disease drug) were both effective in stopping COVID-19 from replicating in a lab dish. 37 Wang, M., Cao, R., Zhang, L. et al. Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCoV) in vitro. Cell Res (2020). https://doi.org/10.1038/s41422-020-0282-0 Also, both drugs were effective at low concentrations, and neither drug is considered particularly toxic to human cells. But fully testing both drugs on humans for use against COVID-19 and gearing up production for these drugs to be used on a massive scale will still take time, and the coronavirus is spreading at exponential speed. Also, it probably—and unfortunately—should be mentioned that if it’s decided to use these drugs for COVID-19, they will simply shift supplies currently being used in Africa to fight Ebola and malaria, to more politically “favorable” locations in the world, at least until production ramps up.
- And keep in mind that, given enough time, a vaccine will be developed. For example, and most people are not aware of this, the newly developed Ebola vaccine is proving highly effective in preventing at-risk people in the Democratic Republic of Congo from becoming infected. As for COVID-19, researchers are already working on a vaccine based on the one used for Ebola. Claims by some in the government that it is nearly finished are, at best, wishful thinking. However, within the next 24 months, we are likely to see a vaccine that is at least “mostly” effective and with “minimal” side effects.
- And if you want to be proactive, use natural immune boosters to keep your immune system optimized. Yes, under one set of circumstances, a strong immune system increases the risk of a cytokine storm. But under most scenarios, having a strong immune system will hold the viral level down enough so that you can’t develop a cytokine storm. Remember, although some healthy people are getting critically ill, the vast majority of those suffering from acute symptoms and dying are those with compromised immune systems.
- But most important of all, keep a supply of natural antipathogens on hand and begin taking them hard and strong at the first sign of symptoms, or if you believe you have been in contact with an infected person. Again, it’s not about curing the disease. All you need to do is support your body’s ability to hold the viral load down low enough so that you never develop pneumonia, or your immune system never kicks into a cytokine storm followed by ARDS. The bottom line is that if you prevent COVID-19 from initiating a cytokine storm, its symptoms are pretty mild for most people–much less than the flu or even most colds. Do that; keep the viral load down, and you can be like Mad Magazine’s Alfred E. Newman. “What, me worry?”
PS: Many people use elderberry extract for dealing with the flu, but it should be noted that it does so, as do many immune boosters, by increasing the cytokine response,38 Barak V, Halperin T, Kalickman I. “The effect of Sambucol, a black elderberry-based, natural product, on the production of human cytokines: I. Inflammatory cytokines.” Eur Cytokine Netw. 2001;12(2):290–296. https://pubmed.ncbi.nlm.nih.gov/11399518-the-effect-of-sambucol-a-black-elderberry-based-natural-product-on-the-production-of-human-cytokines-i-inflammatory-cytokines/ which means you probably want to use it in concert with natural antipathogens.
Editor’s Note: On 3/12/20, Jon posted a follow up to this newsletter answering all the questions that arose in the days since this newsletter was first released: COVID-19: There’s No Need for Panic
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|↑2||Charles Calisher, Dennis Carroll, Rita Colwell, et al. “Statement in support of the scientists, public health professionals, and medical professionals of China combatting COVID-19.” The Lancet. February 19,2020. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30418-9/fulltext|
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|↑4||Heymann DL, Shindo N. “COVID-19: What Is Next for Public Health?” (2020) Lancet. https://pubmed.ncbi.nlm.nih.gov/32061313-covid-19-what-is-next-for-public-health/|
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|↑17, ↑20||Johns Hopkins|
|↑18||Wang D, Hu B, Hu C, et al. “Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China.” [published online ahead of print, 2020 Feb 7]. JAMA. 2020;10.1001/jama.2020.1585. https://pubmed.ncbi.nlm.nih.gov/32031570-clinical-characteristics-of-138-hospitalized-patients-with-2019-novel-coronavirus-infected-pneumonia-in-wuhan-china/|
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|↑22||“Seasonal flu death estimate increases worldwide.” CDC December 13, 2017. (Accessed 25 Feb 2020.) https://www.cdc.gov/media/releases/2017/p1213-flu-death-estimate.html|
|↑24||Rebecca Blankenship. “How long does coronavirus live on surfaces?” Medical News Bulletin. February 11, 2020. (Accessed 26 Feb 2020.) https://medicalnewsbulletin.com/how-long-does-coronavirus-live-on-surfaces/|
|↑25||“Statement on the second meeting of the International Health Regulations (2005) Emergency Committee regarding the outbreak of novel coronavirus (2019-nCoV)”. Who.int, 2020. https://www.who.int/news-room/detail/30-01-2020-statement-on-the-second-meeting-of-the-international-health-regulations-(2005)-emergency-committee-regarding-the-outbreak-of-novel-coronavirus-(2019-ncov)|
|↑26||Zhao, Yu; Zhao, Zixian, Wang, Yujia, et al. “Single-cell RNA expression profiling of ACE2, the putative receptor of Wuhan 2019-nCov.” bioRxiv 2020.01.26.919985. https://www.biorxiv.org/content/10.1101/2020.01.26.919985v1.full|
|↑27||The Novel Coronavirus Pneumonia Emergency Response Epidemiology Team. “Vital Surveillances: The Epidemiological Characteristics of an Outbreak of 2019 Novel Coronavirus Diseases (COVID-19.” China CDC Weekly. 2020, 2(8): 113-122. http://weekly.chinacdc.cn/en/article/id/e53946e2-c6c4-41e9-9a9b-fea8db1a8f51|
|↑28||Tisoncik JR, Korth MJ, Simmons CP, Farrar J, Martin TR, Katze MG. Into the eye of the cytokine storm. Microbiol Mol Biol Rev. 2012;76(1):16–32. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294426/|
|↑30||Zhang L, Liu Y. “Potential Interventions for Novel Coronavirus in China: A Systematic Review [published online ahead of print, 2020 Feb 13].” J Med Virol. 2020;10.1002/jmv.25707. https://pubmed.ncbi.nlm.nih.gov/32052466-potential-interventions-for-novel-coronavirus-in-china-a-systematic-review/|
|↑31||Lim J, Jeon S, Shin HY, et al. “Case of the Index Patient Who Caused Tertiary Transmission of COVID-19 Infection in Korea: the Application of Lopinavir/Ritonavir for the Treatment of COVID-19 Infected Pneumonia Monitored by Quantitative RT-PCR.” J Korean Med Sci. 2020;35(6):e79. Published 2020 Feb 17. https://pubmed.ncbi.nlm.nih.gov/32056407-case-of-the-index-patient-who-caused-tertiary-transmission-of-covid-19-infection-in-korea-the-application-of-lopinavirritonavir-for-the-treatment-of-covid-19-infected-pneumonia-monitored-by-quantitative-rt-pcr/|
|↑33, ↑34||Ng LFP|
|↑35||“Transcript for the CDC Telebriefing Update on COVID-19.” CDC February 26, 2020. https://www.cdc.gov/media/releases/2020/t0225-cdc-telebriefing-covid-19.html|
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|↑38||Barak V, Halperin T, Kalickman I. “The effect of Sambucol, a black elderberry-based, natural product, on the production of human cytokines: I. Inflammatory cytokines.” Eur Cytokine Netw. 2001;12(2):290–296. https://pubmed.ncbi.nlm.nih.gov/11399518-the-effect-of-sambucol-a-black-elderberry-based-natural-product-on-the-production-of-human-cytokines-i-inflammatory-cytokines/|