The answers to the origin questions matter, if not simply for accountability, then for the sake of science and allaying a growing theory that perhaps we had created a monster and unleashed it on the world. The ensuing investigation (still technically ongoing), as with everything related to Covid, became a daunting, conspiracy-laden undertaking, riddled with misinformation, coverups, disclosures, and plenty of ass-covering. No one wants to be held accountable for global chaos and a mounting body count.

Two main theories evolved, and we will examine both. The first was that the virus was artificial or engineered and leaked from a laboratory in Wuhan, whether with nefarious intent or by accident. The second drew its basis from conventional science that the virus had crossed over from the animal population (a zoonotic origin), either a bat or another unfortunate animal sold in the Wuhan market and destined for dinner.

I have tried to eschew technical terms in the article in favor of plain English, and where it cannot be avoided, I have attempted to explain the science involved to the best of my limited abilities. The article is long and perhaps a tad tedious in places, but background matters if you are really looking to understand the two opposing arguments.

Before we look at the – what can only roughly be termed – “evidence” supporting both claims, a few things worth noting about any origin theory.

There is a third possible scenario related to the location of “patient zero” or the first person infected with the virus. There are research laboratories spread across the globe that engage in Gain of Function (GOF) research, something I’ll discuss further in the article. Essentially GOF is the process whereby a virus is engineered to be more deadly. For example, the virus’s ability to infect its host would be amplified with genetic manipulation. The laboratory in Wuhan would have shared its research with any of these institutions.

We only assume that Wuhan was the point of origin, but it is possible that the virus was circulating in the human population earlier than December 2019 in another location. Like either of the aforementioned scenarios, the waters surrounding this possibility are equally murky.

The real problem posed by the new Covid virus came down to one thing. How it attaches itself to its human host and exploits our ACE2 receptors. What follows is a bit technical and you can ignore it and skip on to the next paragraph, as a working understanding of the virus’s mechanism of action isn’t crucial to following the story

The SARS-CoV-2 genome contains typical coronavirus genes but the receptor binding domain (RBD) in the S protein is highly specific. The site for furin-like protease cleavage of the S protein into S1 and S2 subunits is also unique.

These specific and unique adaptations make the virus so at home in our bodies and fuel the artificial theory. They have also, to date, posed the most significant stumbling blocks to identifying a zoonotic (animal) origin.

Also, before we dive in, scientists have identified the sources for the zoonotic origin of the SARS-COV outbreak in 2002. It is a complicated and often painstakingly long process to track down a carrier, an animal providing a cross-over point from animals to humans. Similarly, MERS is passed to humans by dromedary. We live in proximity to these animals, and it is this proximity that adds to the risk of cross-over events. These viruses are the exception rather than the rule.

Theory 1. Animal infects man, man infects man, and the pandemic begins

I cannot, in all honesty, suggest that there can be many people, including leading scientists, who in 2023, still place much faith in this theory. It can only however be ruled out once a definitive answer is provided. So, let’s explore why the natural origin theory was promoted so vociferously and why, to prove the theory, an animal infected with the virus, sold in the markets in Wuhan, needed to be found.

How infectious are these new viruses that originate in animals?

What follows below may seem long winded, but it is a necessary preface for a very important point, one of transmissibility, and it’s an important point to grasp in the origin debate.

Luckily for us, novel viruses are rarely adept at person to person transmission. The process by which they escape their animal host and manage to infect a human host is usually a result of a new mutation of the virus, and most of the time, the genetic mechanisms the virus has evolved are not well enough developed to make it effective at jumping from one human host to another. Many of these terrifying new strains that pop up are self-limiting and relatively easy to contain.

That, from a public health point of view, is a huge blessing, but it is unfortunately not always the case. Take the Spanish or the Great Flu of 1918. The virus responsible for the outbreak (H1N1) originated in ducks or poultry, supposedly in the US, despite the term “Spanish Flu.” One of the first recorded cases was on March 11, 1918, at Fort Riley in Kansas. While there is some disagreement about the US as the point of origin, there is no doubt the original host was avian. This virus not only managed the cross-species jump, but it also proved a winner in the infectious stakes, moving with deadly ease from one person to another.

As an interesting aside, the H1N1 virus claimed more than 50 million lives out of an estimated 1.8 billion people alive in 1918 and disappeared as rapidly as it had emerged. Estimates vary, but figures suggest it claimed between 1 and 5% of the global population. The SARS-COV2 virus has killed 6.73 million globally out of a population of 7.7 billion, infecting, according to the WHO, 662 million, or roughly about 10 percent of the global population. Deaths only represent approximately 1% of the infected and 0.01% of the total population.

SARS-NCOV2 is very infectious and as it mutates and develops new strains, it follows a typical viral evolution, becoming less deadly in exchange for an increase in transmissibility. So, to the point. The novel virus first documented in Wuhan is immediately an outlier. Unlike most other novel viruses, it is perfectly adapted to infecting humans.

No prior recorded run-ins with the good folk of planet Earth, the virus simply appears out of the blue in 2019, perfectly adapted to infecting it’s human host and equally adept at passing from person to person, in other words, highly transmissible. Now while the odds of this occurring naturally cannot be ruled out, they are slim. Really slim. We encounter thousands of viruses in the course of our day to day lives with no ill effects.

The changes that enable a virus to cross over to humans from their animal hosts, are, as I discussed earlier, rare and often self limiting. The virus makes the jump, but is unable to spread itself effectively from human host to human host (low transmissibility). You may not be aware of this, but new pathogens emerge frequently and fortunately for us, aren’t sufficiently evolved to maintain a presence in their new hosts (us).

Also, the more deadly pathogens tend to kill off their victims before the person has the chance to spread the new disease very far., thereby also limiting the spread. There is a sweet spot for viruses that want to hit it off with mankind, and very few achieve it. From early analysis of the SARS-COV2 virus, it offered the perfect balance of transmissibility and lethalness.

A virus made for humanity, if you’ll excuse the phrase.

Tracking down the deadly courier

As members of the identified species responsible for the original SARS-COV virus outbreak in China in late 2002, bats and civets were immediately marked as prime suspects. In the 2002 outbreak, initial assessments determined that the virus crossed to human hosts from zoonotic reservoirs, including bats, Himalayan palm civets (Paguma larvata), and raccoon dogs (Nyctereutes procyonoides), sold in exotic animal markets in Guangdong Province.

Initial suspicion fell on the pangolin as the original reservoir for the SARS-COV2 virus and some even suggested that the virus may have evolved by combining pangolin and bat COV strains, a theory later dismissed as the virus was subsequently shown not to be recombinant (made of of two or more strains). Then, in October 2020, the pangolin was exonerated. It could not, it was shown, have been responsible for harboring the virus that infected us.

Science dug deeper. Setting aside the pangolin, SARS-CoV-2 was also reported to bind to ACE2 from Chinese horseshoe bats, civet, cat, turtle, ferret, monkey, dog, Chinese hamster, buffalo, cow, sheep, swine and even pigeon, but none proved feasible as either a reservoir or as an intermediary between the reservoir and man.

A lot hinged on the fact that we had an established pattern with SARS-COV that appeared to be repeating itself. In 2002 it had been the wet markets in Guangdong Province and the exotic animals traded there, now it was the wet markets in Wuhan, specifically the Huanan Seafood Wholesale Market, where the first cases were supposedly recorded. Appearances can however be deceptive.

What if the Huanan market had not been ground zero for Covid-19? Could that rule out a zoonotic reservoir? As early as May of 2020, papers began circulating, questioning the publicly accepted narrative of the market and pointing to earlier cases in Wuhan, unrelated to the market. The quote below is lifted directly from one such paper published in Frontiers of Medicine.

COVID-19 is officially considered to have emerged at the Huanan
seafood wholesale market (HSWM) in Wuhan in December, however, epidemiological data show that early cases of COVID-19 were not related to HSWM and thus that it is not the site of emergence. Phylogenetic studies suggest that SARS-CoV-2 might have circulated in Wuhan as early as October 2019 and that the virus then spread at low-level from person to person (the latency phase), before being imported to HSWM where it was detected in December 2019

Flaws in zoonotic theories for SARS and MERS predate SARS-COV2. Without getting into technical details (links included for those who wish to explore the topic in more depth) there are two basic models that allow a virus to jump species, the first being the spillover model and a second, referred to as the circulation model. In this model there is no requirement for zoonotic pressure or epizootic episode prior to the emergence of a human disease.

In layman’s terms, we (animals and humans) coexist with viruses (often shared) and are frequently infected with no ill effects. However, under the right conditions, one of these viral infections can mutate, perhaps in the presence of a host with a weakened immune system or genetic abnormality that predisposes the person to that specific virus’s genome. It is therefor possible that SARS-COV2 used a human chain as its intermediary and evolved in human hosts.

SARS-CoV2 is suggested to be one of nearly 900 zoonotic pathogens that have made the leap from nonhuman animals to human populations over millennia. Emerging evidence suggests we return the favor, according to  officially reported SARS-CoV-2 human infections in 23 nonhuman animal species, including not only big cats like tigers and lions but also domestic cats and dogs, gorillas, white-tailed deer, hamsters, farmed mink, otters, anteaters, manatees, hippopotamuses, and others, according to the World Organization for Animal Health.

There remains another issue, not frequently discussed. Technological advances in the sciences have outstripped our ability to fully comprehend what we can now observe and the intricate interdependencies of nature still elude us. A lot of what we see published is nothing more than an educated guess based on unfolding models. We may or may not be on the right track and the huge amount of conflicting opinion supports the fact that virology and its related fields are far from an exact science.

To date, no zoonotic reservoir or intermediary has been identified for the SARS-COV2 virus.

Theory 2. Man amplifies existing virus, dooms the world.

Subtitled: Wuhan, the Capital of Coincidences

I’ve written extensively on this topic during the last three years and you will find links to these articles interspersed below. For the sake of continuity, some of this older content is repeated, and has, where new information has emerged, been updated to reflect the ever evolving narrative. The information deals only with verifiable, known facts and where I digress into opinion, it will be clearly stated.

To fully understand what unfolds below, lets kick of with GOF research, as it plays an integral part of the man-made theory.

Gain of Function (GOF)

Gain-of-function research refers to the serial passaging of microorganisms to increase their transmissibility, virulence, immunogenicity, and host tropism by applying selective pressure to a culture. So in other words, in layman’s terms, it’s about creating something nastier, tougher, and more deadly than the original by manipulating it in a laboratory, for whatever purpose, military, scientific, or otherwise.

To level the playing field however, associating Gain of Function research as being mutually exclusive to influenza or coronaviruses is patently wrong. The field is immense and it is incorrect to equate GOF studies only with influenza transmission experiments. Virology is founded on adaptation approaches, and these have broad utility because they provide phenotypic evidence of a genotypic change when combined with a discriminatory biological assay.

Used responsibly, GOF is an incredibly useful and some would argue, essential tool in the virologists arsenal. Inadequate or flawed safety and ethics protocols are however commonplace in research laboratories where GOF is undertaken, particularly in countries like China. Without being dramatic, pursuing GOF research without properly ensuring its safety, could lead to an extinction-level event. Us being the species we wipe out. It’s an unlikely, but not impossible consequence.

For further reading, including the 2014 US moratorium on GOF, follow this link. Also you may be interested to know that another outbreak of the H1N1 strain in 1977 (the one that caused the Great Flu in 1918) was caused by a laboratory leak of the virus. You can read more about that here.

WIV or the Wuhan Institute of Virology

At the center of the web of coincidences surrounding the virus origin, sits the Wuhan Institute of Virology, or WIV, and one of it’s employees, a scientist affectionately known as batwoman. The WIV comes equipped with a biosafety laboratory, and of course, the facility works on coronaviruses, particularly the SARS-COV virus. That’s where batwoman comes into the picture.

Chinese virologist, Dr. Zheng-li Shi started out as a research assistant at the Wuhan Institute for Virology (WIV), with a focus on aquatic viruses. She trained in France and later pivoted to bats in 2004 after SARS broke out. She is widely recognized as a leader in the field and to facilitate her research, she has spent years collecting bats from caves across China, investigating how the coronavirus can jump from animal to human. Said bats are relocated to the Institute (where else) for further study.

Safety Levels in Laboratories handling Biohazards

SARS has not naturally recurred since 2003, but there have been six separate “escapes” from virology labs studying it: one each in Singapore and Taiwan, and in four distinct events at the same laboratory in Beijing.

Many instances involving the accidental release of pathogens have taken place in labs around the world. Hundreds of breaches have occurred in the U.S., including a 2014 release of anthrax from a U.S. government lab that exposed 84 people. The SARS virus escaped four times from the Chinese National Institute of Virology in Beijing causing four infections and one death and also escaped facilities in Singapore and Taiwan.

Despite our best efforts, we cannot ensure viruses used in GOF remain secure. China, unfortunately, has a reputation for lax safety protocols, and the WIV is no exception. In 2014 scientists calling themselves the Cambridge Working Group urged caution on creating new viruses. In what may have been prescient words, they specified the risk of creating a dangerous virus.

“Accident risks with newly created ‘potential pandemic pathogens’ raise grave new concerns,” they wrote. “Laboratory creation of highly transmissible, novel strains of dangerous viruses, especially but not limited to influenza, poses substantially increased risks. An accidental infection in such a setting could trigger outbreaks that would be difficult or impossible to control.”

If you’re thinking we ever learn, think again. In 2021 SARS-COV2 once again escaped from a high level biosecurity laboratory in Taiwan by infecting a laboratory worker. Clearly, we do not have sufficient technical prowess to deal safely with the viruses we create and collect.

Follow the Money

Did the NIH and the NIAID fund GOF research in Wuhan, or didn’t they? Enter the EcoHealth Alliance and Dr Peter Daszak, one of the strongest proponents (naturally) for the natural origin theory. More on that later. The short answer is an absolute, resounding yes. To avoid this article turning into a novel, you can reference the hard evidence in an article I published in 2021. Ironically, if you’re an American, your tax dollars may very well have contributed directly to the pandemic.

The referenced article does not deal with Dr Anthony Fauci’s role in this sordid saga, but given the volume of evidence that has emerged recently, you are free to draw your own conclusions regarding the extent of his involvement with EcoHealth Alliance and Peter Daszak.

That pesky Furin cleavage site

As discussed earlier, one of the most prominent features of the virus relates to its S protein, in particular, the furin cleavage site, that, and the receptor binding domain (RBD) in the S protein is highly specific. So specific in fact, that many virologists took one look at them and had the same thought. Engineered. Not by nature, but by a far more malicious entity, man.

And that brings us back nicely to our friend from EcoHealth Alliance, Peter Daszak. What follows is possibly either the greatest attempt to cover tracks in the history of science or intentional misdirection to further an alternate agenda. We may never know the true motivation, but we know the facts. Daszak lied.

On February 19th of 2020, a group of virologists and others published a letter in the Lancet on the origin, in their professional opinions, of the virus. This extract is taken directly from said letter.

“We stand together to strongly condemn conspiracy theories suggesting that COVID-19 does not have a natural origin,”

The author of this letter was none other than Peter Daszak and the signatories to it included Charles Calisher, Dennis Carroll, Rita Colwell, Ronald B Corley, Christian Drosten, Luis Enjuanes, Jeremy Farrar, Hume Field, Josie Golding, Alexander Gorbalenya, Bart Haagmans, James M Hughes, William B Karesh, Gerald T Keusch, Sai Kit Lam, Juan Lubroth, John S Mackenzie, Larry Madoff, Jonna Mazet, Peter Palese, Stanley Perlman, Leo Poon, Bernard Roizman, Linda Saif, Kanta Subbarao and Mike Turner (no relation).

Now under normal circumstances, this statement of support for their poor beleaguered Chinese colleagues would have been in good form, and the strongly worded endorsement of a natural origin for the virus, well within their rights, however, on the release of emails from the NIH and EcoHealth Alliance under a Freedom of Information request, it came to light that Peter Daszak (whom you will note declared no conflicting interests) was pursuing an alternative agenda. One he had coerced other signatories to agree to, amny of whom workerd for, or were involved with EcoHealth Alliance.

An article highlighting the extent of the coercion was published in the U.S. Right to Know website on the day the statement was published in the Lancet. Titled “EcoHealth Alliance orchestrated key scientists’ statement on “natural origin” of SARS-CoV-2” the article’s introduction leaves no doubt as to its intent.

Emails obtained by U.S. Right to Know show that a statement in The Lancet authored by 27 prominent public health scientists condemning “conspiracy theories suggesting that COVID-19 does not have a natural origin” was organized by employees of EcoHealth Alliance, a non-profit group that has received millions of dollars of U.S. taxpayer funding to genetically manipulate coronaviruses with scientists at the Wuhan Institute of Virology.

Now, if I am not mistaken, that looks pretty conflicted to me. The extent of the funding Peter Daszak and EcoHealth Alliance received can be viewed here. One of Dr Fauci’s last acts as director of the NIAID before retiring in late 2022 was to award one final lump sum to EcoHealth Alliance, despite dismal failures by the company to account for, or produce records relating to their involvement with WIV and the GOF research undertaken there.

Peter Daszak intentionally sought, and still seeks, to influence public and scientific opinion on the origins of the virus to deflect attention from the elephant in the room.

Since 2010, scientists, in particular, one Ralph. S Baric, had known that coronaviruses use the spike protein to gain a foothold in their human hosts. Baric published a paper in 2010 entitled “Recombination, reservoirs, and the modular spike: mechanisms of coronavirus cross-species transmission” and was widely recognized as one of the leading figures experimenting on modifying the spike protein.

No prizes for guessing where Baric found gainful employment. He has developed genetic techniques to enhance the pandemic potential of existing bat coronaviruses, working in collaboration with Dr. Zheng-li Shi at the Wuhan Institute of Virology and with the EcoHealth Alliance. Coincidence after coincidence.

Moderna and Pfizer drive the nail home

Lest we forget, both Moderna and Pfizer produced almost identical mRNA based vaccines in record time. In fact, Moderna had theirs ready to go on the 28th of January, 2020. Impressive you say, but what does this have to do with the virus origins? Perhaps nothing and perhaps everything.

We know Moderna was heavily invested in pursuing a vaccine for coronaviruses and was intimately familiar with the SARS-COV virus. The company would no doubt have been privy to the research being carried out in Wuhan and may well have met with early success against newly engineered strains, particularly if they knew specifically how these strains interacted with our bodies. Almost a case of putting the cart before the horse.

Pure conjecture on my part, of course, but far from unlikely.

Putting the facts aside

Given the unending list of coincidences surrounding Wuhan, it would seem statistically impossible for the virus to have originated anywhere else. If I were a betting man I would also most certainly place my cash on Theory 2, as each coincidence further reduces the likelihood of natural origin. Which then raises one final question which must be broached, as unpleasant as it may be.

If the virus did indeed originate from within the WIV, was it’s release into the wild intentional or accidental?

Profiteering and Smoking Guns

Perhaps the final straw on the wobbling camel-of-natural-origins back is provided by the billionaires, new and old, that profited immensely from the death and chaos that unfolded post 2019. How profitable was/is the pandemic? Here are a few eye watering numbers to make you wish you’d followed a career path in virology.

Now while every bloke is entitled to an honest days wage, whatever their profession, profiteering from a global event you may directly, or indirectly, have initiated tends to raise an eyebrow. It provides an excellent motive for aiding and abetting the virus’s escape and while the likelihood is that the leak was unintentional and purely down to poor security protocols, if there was indeed a leak, we cannot, until proven otherwise, dismiss any of the theories swirling around Wuhan.

Profit, of course is not the only motivating factor, as conspiracy theorists will be quick to point out. Population control on a global scale requires mass vaccination, which, of course is easily justified in the face of a global viral threat. Who would engage in such monstrous evils? Why the elites of course, with fingers pointing towards the likes of Klaus Schwab (chairman of the World Economic Forum, currently meeting in Davos as I write this, to plan their next move), Bill Gates and others.

There may very well be a “smoking gun” that will inadvertently turn up somewhere in the years that follow, a shooter emerging from the grassy knoll, that confirms finally, one way or another where SARS-COV2 originated. I suspect the virus itself will offer up the final answers. As our technology improves, definitively identifying natural and engineered viral sequences in minutes will become a reality. It will also make detailed analysis of the “vaccines” possible, essential for restoring trust in medicines we use to treat billions.

So to return to the original pandemic question. Where did our current coronavirus originate? We may never know with certainty, our best bet being an educated guess based on snippets we’re told are facts, buried in the shifting sands of political opinion and scientific agendas. I made a choice in 2021, to believe that when presented with coincidence upon coincidence, we’d be fools to try and disprove the obvious conclusions these coincidences point to. Let’s disprove the obvious first and then look to natural origin.

Perhaps after evaluating the history of the last three years, you’ll join me on that side of the wall.

Missed Part 4 of the Covid Files on When is a vaccine not a vaccine? Catch up here.

The post On the Origin of Covid. With Apologies to Darwin appeared first on Medika Life.

Coronaviruses are a large family of viruses that usually cause mild to moderate upper-respiratory tract illnesses, like the common cold. However, three new coronaviruses have emerged from animal reservoirs over the past two decades to cause serious and widespread illness and death.

There are hundreds of coronaviruses, most of which circulate among such animals as pigs, camels, bats and cats. Sometimes those viruses jump to humans—called a spillover event—and can cause disease. Four of the seven known coronaviruses that sicken people cause only mild to moderate disease.

Three can cause more serious, even fatal, disease. SARS coronavirus (SARS-CoV) emerged in November 2002 and caused severe acute respiratory syndrome (SARS). That virus disappeared by 2004. Middle East respiratory syndrome (MERS) is caused by the MERS coronavirus (MERS-CoV). Transmitted from an animal reservoir in camels, MERS was identified in September 2012 and continues to cause sporadic and localized outbreaks.

The third novel coronavirus to emerge in this century is called SARS-CoV-2. It causes coronavirus disease 2019 (COVID-19), which emerged from China in December 2019 and was declared a global pandemic by the World Health Organization on March 11, 2020. To date, at the time of this articles publication, it has infected more than 8 million people globally and killed over 400,000.

COVID-19, MERS & SARS

In January 2020, a novel coronavirus, SARS-CoV-2, was identified as the cause of an outbreak of viral pneumonia in Wuhan, China. The disease, later named coronavirus disease 2019 (COVID-19), subsequently spread globally. In the first three months after COVID-19 emerged nearly 1 million people were infected and 50,000 died.

The Centers for Disease Control and Prevention (CDC) developed a test to diagnose COVID-19 in respiratory and serum samples. The National Institute of Allergies and Infectious Diseases (NIAID) also is accelerating efforts to develop additional diagnostic tests for COVID-19. These tests are helping facilitate preclinical studies and aid in the development of medical countermeasures.

NIAID COVID-19 research efforts build on earlier research on severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), which also are caused by coronaviruses. MERS is a viral respiratory disease that was first reported in Saudi Arabia in September 2012 and has since spread to 27 countries, according to the World Health Organization. Some people infected with MERS coronavirus (MERS-CoV) develop severe acute respiratory illness, including fever, cough, and shortness of breath.

From its emergence through January 2020, WHO confirmed 2,519 MERS cases and 866 deaths (about 1 in 3). Among all reported cases in people, about 80% have occurred in Saudi Arabia. Only two people in the United States have tested positive for MERS-CoV, both of whom recovered. They were healthcare providers who lived in Saudi Arabia, where they likely were infected before traveling to the U.S., according to the CDC.

Infection with SARS coronavirus (SARS-CoV) can cause a severe viral respiratory illness. SARS was first reported in Asia in February 2003, though cases subsequently were tracked to November 2002. SARS quickly spread to 26 countries before being contained after about four months. More than 8,000 people fell ill from SARS and 774 died. Since 2004, there have been no reported SARS cases. 

Research evidence suggests that SARS-CoV and MERS-CoV originated in bats, and it is likely that SARS-CoV-2 did as well. SARS-CoV then spread from infected civets to people, while MERS-CoV spreads from infected dromedary camels to people. Scientists are trying to determine how SARS-CoV-2 spread from an animal reservoir to people.

Characterizing MERS and COVID-19 Disease

Since the emergence of MERS coronavirus (MERS-CoV) in 2012 and SARS-CoV-2 in 2019, NIAID scientists have advanced their understanding of how the viruses cause disease, focusing on developing animal models of disease and on countermeasures such as diagnostic tests and vaccine candidates. Research by NIAID scientists and others demonstrated that MERS-CoV and SARS-CoV-2 use their spike (S) protein to enter cells and initiate infection. After entering the cell, the viruses delay usual immune system responses, allowing the infection to gain a foothold. By the time the immune system responds, the infection has progressed and becomes much harder to fight.

Scientists also have characterized different strains of MERS-CoV and can determine through tests how those strains affect different animals. They also are studying how the form of the virus—liquid or aerosol—affects its stability. Using a monkey model of MERS, researchers have learned how the virus causes disease in people. For example, scientists at NIAID’s Rocky Mountain Laboratories (RML) demonstrated in a monkey model that clinical signs of MERS appear within 24 hours of infection. They also found that the virus causes disease deep within the lungs, leading to pneumonia. NIAID-funded researchers also have established several mouse models of infection that have been critical in developing MERS-CoV medical countermeasures.

A research group at RML also has developed a rhesus macaque model of SARS-CoV-2 to study COVID-19. The model mimics mild- to-moderate respiratory disease in people, including signs of pneumonia seen in an X-ray; this also is an important diagnostic feature in human patients. They also learned that the virus causes disease in the lungs, and that virus is shed from the nose, throat and rectum in a pattern similar to virus shedding in COVID-19 patients. The scientists are using this model to evaluate treatments and preventive vaccines. 

About Covid-19

COVID‑19 is the new respiratory disease spreading around the world and it is caused by a coronavirus. COVID‑19 is short for “coronavirus disease 2019.”

The virus is thought to spread mainly between people who are in close contact with one another (about 6 feet) and through respiratory droplets produced when an infected person coughs or sneezes.

• People are most contagious when they are the sickest. But those who don’t have a lot of symptoms can still pass the virus on to others.
• There is currently no vaccine or cure for COVID‑19 but researchers are working to find one.

What are COVID‑19’s symptoms?

The most common symptoms are very similar to other viruses: fever, cough, and difficulty breathing. Common symptoms of COVID‑19 are changing as more is learned about the disease.

The most common symptoms of COVID-19 are fever, dry cough, and tiredness. Other symptoms that are less common and may affect some patients include aches and pains, nasal congestion, headache, conjunctivitis, sore throat, diarrhea, loss of taste or smell or a rash on skin or discoloration of fingers or toes. These symptoms are usually mild and begin gradually. Some people become infected but only have very mild symptoms.

Most people (about 80%) recover from the disease without needing hospital treatment. Around 1 out of every 5 people who gets COVID-19 becomes seriously ill and develops difficulty breathing. Older people, and those with underlying medical problems like high blood pressure, heart and lung problems, diabetes, or cancer, are at higher risk of developing serious illness.  However, anyone can catch COVID-19 and become seriously ill. 

People of all ages who experience fever and/or  cough associated withdifficulty breathing/shortness of breath, chest pain/pressure, or loss of speech or movement should seek medical attention immediately. If possible, it is recommended to call the health care provider or facility first, so the patient can be directed to the right clinic.

Who is at high risk for COVID‑19?

Everyone is at risk of getting COVID‑19, but some people are at a higher risk of serious illness.

Asthma (moderate-to-severe)

Moderate-to-severe asthma may put people at higher risk for severe illness from COVID-19.

Actions to take

• Follow your Asthma Action Plan.
• Keep your asthma under control.
• Continue your current medications, including any inhalers with steroids in them (“steroids” is another word for corticosteroids).
• Know how to use your inhaler.
• Avoid your asthma triggers.
• If possible, have another member of your household who doesn’t have asthma clean and disinfect your house for you. When they use cleaning and disinfecting products, have them:
  • Make sure that people with asthma are not in the room.
  • Minimize use of disinfectants that can cause an asthma attack.
  • Open windows or doors and use a fan that blows air outdoors.
  • Always follow the instructions on the product label.
  • Spray or pour spray products onto a cleaning cloth or paper towel instead of spraying the product directly onto the cleaning surface (if the product label allows).

Why you might be at higher risk

COVID-19 can affect your respiratory tract (nose, throat, lungs), cause an asthma attack, and possibly lead to pneumonia and serious illness.

Chronic kidney disease being treated with dialysis

Chronic kidney disease being treated with dialysis may increase a person’s risk for severe illness from COVID-19.

Actions to take

• If you are on dialysis, you should NOT miss your treatments.
• Contact your dialysis clinic and your healthcare provider if you feel sick or have concerns.
• Plan to have enough food on hand to follow the KCER 3-Day Emergency Diet Plan for dialysis patients in case you are unable to maintain your normal treatment schedule.

Why you might be at higher risk

Dialysis patients are more prone to infection and severe illness because of weakened immune systems; treatments and procedures to manage kidney failure; and coexisting conditions such as diabetes.

Chronic lung disease

Chronic lung diseases, such as chronic obstructive pulmonary disease (COPD) (including emphysema and chronic bronchitis), idiopathic pulmonary fibrosis and cystic fibrosis, may put people at higher risk for severe illness from COVID-19.

Actions to take

• Keep taking your current medications, including those with steroids in them (“steroids” is another word for corticosteroids).
• Avoid triggers that make your symptoms worse.

Why you might be at higher risk

Based on data from other viral respiratory infections, COVID-19 might cause flare-ups of chronic lung diseases leading to severe illness.

Diabetes

Diabetes, including type 1, type 2, or gestational, may put people at higher risk of severe illness from COVID-19.

Actions to take

• Continue taking your diabetes pills and insulin as usual.
• Test your blood sugar every four hours and keep track of the results.
• Make sure that you have at least a two-week supply of your diabetes pills and insulin.
• Follow the sick day guidelines for people with diabetes.

Why you might be at higher risk

People with diabetes whose blood sugar levels are often higher than their target are more likely to have diabetes-related health problems. Those health problems can make it harder to overcome COVID-19.

Hemoglobin Disorders

Hemoglobin disorders such as sickle cell disease (SCD) and thalassemia may put people at higher risk for severe illness from COVID-19.

Actions to take

• Ask your healthcare provider about telemedicine or remote healthcare visits, and know when to go to the emergency department.
• Work with your healthcare provider to manage medications and therapies for your disorder (including hydroxyurea, chelation therapy, blood transfusions, and prescriptions for pain management) and any other health condition you may have (such as diabetes, high blood pressure, and arthritis).
• Try to prevent vaso-occlusive episodes or pain crises by avoiding possible triggers.

Why you might be at higher risk

Living with a hemoglobin disorder can lead to serious multi-organ complications, and underlying medical conditions (such as heart disease, liver disease, diabetes, iron overload, kidney disease, viral infections, or weakened immune system) may increase the risk of severe illness from COVID-19.

Immunocompromised

Many conditions and treatments can cause a person to have a weakened immune system (immunocompromised), including cancer treatment, bone marrow or organ transplantation, immune deficiencies, HIV with a low CD4 cell count or not on HIV treatment, and prolonged use of corticosteroids and other immune weakening medications. People who are Immunocompromised

Actions to take

• If you are immunocompromised, continue any recommended medications or treatments and follow the advice of your healthcare provider.
• Call your healthcare provider if you have concerns about your condition or feel sick.

Why you might be at higher risk

People with a weakened immune system have reduced ability to fight infectious diseases, including viruses like COVID-19. Knowledge is limited about the virus that causes COVID-19, but based on similar viruses, there is concern that immunocompromised patients may remain infectious for longer than other COVID-19 patients.

Liver disease

Chronic liver disease,  including cirrhosis, may increase risk for serious illness from COVID-19.

Actions to take

• Take your medications exactly as prescribed.

Why you might be at higher risk

Severe illness caused by COVID-19 and the medications used to treat some severe consequences of COVID-19 can cause strain on the liver, particularly for those with underlying liver problems. People living with serious liver disease can have a weakened immune system, leaving the body less able to fight COVID-19.

People aged 65 years and older

Older adults, 65 years and older, are at higher risk for severe illness and death from COVID-19.

Actions to take

• Take your medications for any underlying health conditions exactly as prescribed.
• Follow the advice of your healthcare provider.
• Develop a care plan that summarizes your health conditions and current treatments.
• Prepare yourself to stay home for long periods using this checklist.

Why you might be at higher risk

Although COVID-19 can affect any group, the older you are, the higher your risk of serious disease. Eight out of 10 deaths reported in the U.S. have been in adults 65 years or older; risk of death is highest among those 85 years or older. The immune systems of older adults weaken with age, making it harder to fight off infections. Also, older adults commonly have chronic diseases that can increase the risk of severe illness from COVID-19.

People who live in a nursing home or long-term care facility

Many cases of COVID-19 in the U.S. have occurred among older adults living in nursing homes or long-term care facilities

Actions to take

• Carefully follow your facility’s instructions for infection prevention.
• Notify staff right away if you feel sick.
• Ask your caretakers about the actions that are being taken at your nursing home or long-term care facility to protect you and your loved ones, including if and how they are limiting visitors.

Why you might be at higher risk

The communal nature of nursing homes and long-term care facilities, and the population served (generally older adults often with underlying medical conditions), put those living in nursing homes at higher risk of infection and severe illness from COVID-19.

Serious heart conditions

Serious heart conditions, including heart failure, coronary artery disease, congenital heart disease, cardiomyopathies, and pulmonary hypertension, may put people at higher risk for severe illness from COVID-19.

Actions to take

• Take your medication exactly as prescribed. Continue angiotensin converting enzyme inhibitors (ACE-I) or angiotensin-II receptor blockers (ARB) as prescribed by your healthcare provider for indications such as heart failure or high blood pressure.
• Make sure that you have at least a two-week supply of your heart disease medications (such as those to treat high cholesterol and high blood pressure).
• People with hypertension should continue to manage and control their blood pressure and take their medication as directed.

Why you might be at higher risk

COVID-19, like other viral illnesses such as the flu, can damage the respiratory system and make it harder for your heart to work. For people with heart failure and other serious heart conditions this can lead to a worsening of COVID-19 symptoms.

Severe obesity

Severe obesity, defined as a body mass index (BMI) of 40 or above, puts people at higher risk for complications from COVID-19.

 Actions to take

• Take your medications for any underlying health conditions exactly as prescribed.

Why you might be at higher risk

Severe obesity increases the risk of a serious breathing problem called acute respiratory distress syndrome (ARDS), which is a major complication of COVID-19 and can cause difficulties with a doctor’s ability to provide respiratory support for seriously ill patients. People living with severe obesity can have multiple serious chronic diseases and underlying health conditions that can increase the risk of severe illness from COVID-19.

What about COVID‑19, pregnancy, and newborns?

At this time, pregnant women reportedly have the same COVID‑19 risk as adults who are not pregnant. There is also no clear evidence that a fetus can be infected with COVID‑19 in the womb.

Pregnant women are known to have a higher risk of severe illness when infected with viruses from the same family as COVID‑19 and other viral respiratory infections. This is why pregnant women should take extra precautions to not get COVID‑19. Avoid those who have or who have been exposed to COVID‑19. Wash your hands often. Practice physical distancing. Clean and disinfect frequently touched surfaces daily

• During this time, it’s normal for care providers to change some prenatal visits to telemedicine.
• Ask if your delivering hospital has changed any rules, like if you’ll be asked to wear a face covering while giving birth or if there is a new visitor policy.
• Most babies born to people with COVID‑19 are not affected. However, once the baby is born, it is at risk for infection. New parents should take the same precautions to protect themselves from illness as pregnant women.
• So far, COVID‑19 has not been detected in breast milk. If you are sick, including with COVID‑19, wear a cloth face covering and wash your hands before each feeding. If pumping milk, do not share your pump with anyone else. Wash your hands before expressing milk or before touching the pump or bottle parts. Follow recommendations for cleaning the pump and parts after each use. If possible, have someone who is not sick feed the baby.
• Stay in touch with your care team if you feel sick or develop COVID‑19 symptoms.
• Pregnancy and postpartum can be stressful, and COVID‑19 can add to feelings of uncertainty, stress, anxiety, or depression. Talk with your care provider if you are feeling overwhelmed. Seek help if you are in crisis and feel like you may harm yourself or your baby.

When should I see a doctor?

Knowing when to see a doctor can keep medical care available for those who need it most.

Most mild symptoms can be treated at home. The most up-to-date way to assess your best next steps is to complete our Screening Tool.

• If you need to see your doctor, call the office before you go. Many physicians’ offices are doing virtual visits. They will tell you what to do based on your location.
• Testing is limited-availability across the country and is currently being prioritized for healthcare workers, emergency medical service providers, police, and other essential workers, so please consult your doctor for availability in your local area.
• If you develop emergency warning signs, call emergency services. Emergency warning signs include: severe, constant chest pain or pressure; extreme difficulty breathing; severe, constant lightheadedness; or serious disorientation or unresponsiveness.

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