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By: Joseph Osmundson
Last updated: August 3, 2020


MYTH: The vast majority of people recover from COVID-19 without consequences
FACT: There are increasing concerns about long-term complications of COVID-19

By Richard Jefferys
From the inception of the COVID-19 pandemic, there has been misinformation and disinformation circulating regarding the seriousness of the disease. A common fallacy is to compare with seasonal flu, despite the greater risk of hospitalization and death. As more has been learned about COVID-19, the breadth and duration of the potential negative health consequences has become clearer. That hasn’t stopped the President of the U.S. recently claiming erroneously that “99 percent [of cases] are totally harmless.”

The reality is that there are increasing concerns about the potential for long-term complications from COVID-19. A research study published in JAMA reported that 87.4% of 143 participants experienced the persistence of at least one symptom (most commonly fatigue and difficulty breathing) an average of 60 days after the onset of their first symptom. More than half reported persistence of three or more symptoms.

The U.S. Centers for Disease Control and Prevention (CDC) has described follow up of individuals with COVID-19 who were never sick enough to be hospitalized, and 35% had not returned to normal health two to three weeks after testing positive. A study in Ireland found that more than half of the 128 participants reported persistent fatigue an average of 10 weeks after initial COVID-19 symptoms.

In addition to these formal reports, many news articles have described similar anecdotes from individuals continuing to experience symptoms long after acute COVID-19, leading to the term “long haulers” to describe the phenomenon.

Studies are also uncovering evidence of persistent organ damage related to the inflammation associated with COVID-19. Recent papers from German researchers revealed a high prevalence of damage to the heart. There are similar concerns about potential long-term neurological problems.

Scientists and advocates are drawing parallels with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases and a member of the White House Coronavirus Task Force, has repeatedly stated to the public that what COVID-19 patients are experiencing is highly suggestive of ME/CFS. Advocates are stressing the importance of supporting and broadening investigation of all possible forms of post-viral illness as part of the COVID-19 research agenda.


MYTH: Face masks are a COVID-19 silver bullet that are the single or best tool for preventing SARS-CoV-2 transmission.

FACT: Face masks are an essential component of a broad array of non-pharmaceutical interventions (NPIs) that prevent the spread of SARS-CoV-2 and include physical distancing, work from home, limiting large group gatherings (particularly indoors), and increased hygiene and sanitation, in addition to widespread and correct face mask usage.

Face masks are routinely worn in some countries during cold and flu season to prevent transmission of these seasonal viruses. Early in the global COVID-19 pandemic, many countries mandated or encouraged the use of surgical or cloth face masks to slow or prevent transmission in the community. In the U.S., the Centers for Disease Control and Prevention (CDC) and federal officials initially dismissed face mask usage outside of the typical hospital setting before reversing course.

As face mask usage in the U.S. apparently increased, some initial hotspots (such as New York City) were able to control the initial COVID-19 spike. This, along with correlative data between countries with a low rate of COVID-19 infection and a high rate of mask wearing, led to the theory that masks are the most effective tool, or perhaps even are uniquely able, to stop SARS-CoV-2 transmission.

In a recent (and hotly contested) PNAS paper, Renyi Zhang et al., from Mario Molina’s research laboratory at University of California San Diego argue that most COVID-19 transmission is primarily through aerosols and that masks prevent this transmission. In a widely popular Twitter thread, Jeremy Howard analyzed published and unpublished data to come to the same conclusion. The thread was based mostly on optical images of droplets from breath, but did not consider whether any of these droplets contain infectious SARS-CoV-2 particles, leading to widespread criticism that these data were being overinterpreted.

While mask wearing is clearly an important component of a broad COVID-19 response, it’s not yet clear how effective masks (either surgical or cloth) are at preventing SARS-CoV-2 transmission or what the effect of widespread mask wearing is on COVID-19 at a population and epidemiological level. Various mask types have shown a wide (5-95%) range of protection against the spread of various sizes of liquid droplets. Also still unclear are the size of liquid droplet most likely to carry SARS-CoV-2 virions (viral particles) and how many virions are required to initiate a COVID-19 infection.

In the absence of clear causative data, there remains strong indications that widespread mask wearing is a crucial component of a responsible response to the COVID-19 pandemic. However, in this time of diminished trust between scientists, public health officials, and the general public, we must not overinterpret data or make conclusive claims unless they are built upon a foundation of clear and quality data.


MYTH: Hydroxychloroquine is a safe and effective treatment and prophylaxis for COVID-19
FACT: There is no evidence from high quality clinical trials that hydroxychloroquine is effective in treating or preventing COVID-19, and it is associated with a significant number of adverse effects, including death

Early in the COVID-19 pandemic, there were reports from small clinical studies that the anti-malaria drug hydroxychloroquine, alone or in combination with an antibiotic such as azithromycin, was an effective treatment for SARS-CoV-2 (the virus that causes COVID-19). Hydroxychloroquine modulates the immune system by increasing the pH of lysosomes, which are enzyme filled spheres that break down pathogens in immune system cells, decreasing the immune cells’ activity. Early hypotheses about COVID-19 suggested that altering the biology of lysosomes in this way may also inhibit the ability of SARS-CoV-2 to enter cells.

The use of hydroxychloroquine for COVID-19 treatment became frequent in critical care situations, and researchers in India began testing its effectiveness as prophylaxis.

However, as soon as larger clinical trials with control groups were published or the original data were reanalyzed, it became clear that hydroxychloroquine did not decrease the likelihood of death or shorten the duration of symptoms. Meta-analysis recently confirmed the lack of significant effect. Moreover, hydroxychloroquine was associated with adverse effects, including heart complications such as de-novo ventricular arrhythmia, leading to death.

Both the World Health Organization’s Solidarity trial and the United Kingdom’s RECOVERY trial have ceased evaluation of hydroxychloroquine after results demonstrated it was ineffective. Published results from a postexposure prophylaxis study also showed no efficacy. The use of hydroxychloroquine for treatment or prophylaxis of COVID-19 is not supported by science.


MYTH: People testing positive on RNA tests are infectious
FACT: Viral SARS-CoV-2 RNA does not equal infectious virus

Most of the tests used to identify SARS-CoV-2 don’t look for the actual virus at all. They look instead for little bits of the viral genes, small pieces of RNA that are necessary for viral replication. SARS-CoV-2 encodes its genome in RNA, not DNA like living cells.

Viral RNA is not sufficient for the virus to replicate. Infectious virus is needed for that. For virus to be infectious,  the RNA must be long and packaged, not just in a membrane, but with surface proteins that will help it bind to human cells.

SARS-CoV-2 viral RNA seems to be ubiquitous on, around, and in infected people. Studies have found viral RNA in patients’ stool samples, all through their hospital rooms, on doctors’ shoes, in the air, and on surfaces on cruise ships up to 17 days after people with COVID-19 are gone.

It remains unclear what relationship there is – if any – between the amount of viral RNA detected in a sample and how much infectious virus is present.

The virus might well survive in some of these places for a time, up to two days, but very limited research has actually been done toward answering these questions.

Studies that look at how much infectious virus is found in various places are fairly rare because BSL-3 lab facilities are required to test viral growth. Viral RNA on a surface or in a sample simply does not mean infectious virus is present. In stool – for example – abundant SARS-CoV-2 RNA can be detected, but scientists have shown mixed results on whether this RNA is due to infectious virus or not, and epidemiologists see no evidence for fecal transmission of COVID-19

Viral RNA does not indicate infectious virus. The viral RNA is necessary for infection but – in itself – not sufficient.


MYTH: SARS-CoV-2 was invented in a lab
FACT: All available evidence indicates SARS-CoV-2 evolved naturally in animals before infecting humans 

One of the enduring conspiracy theories that has emerged since COVID-19 spread around the world is that the virus did not evolve naturally to enter human hosts, but that it was a product of purposeful laboratory design and/or an accidental release from a coronavirus research lab.

All current evidence points to these theories being false. The sequence of the SARS-CoV-2 virus, which causes COVID-19, is closely related (97% identical) to another coronavirus that resides in bats, a known coronavirus reservoir. It’s much more related to this naturally existing virus than to either SARS-CoV-1 or the MERS virus, which we know can transmit in humans. Any likely research or development of a virus for transmission in humans would not use a distant relative of a bat coronavirus, but would likely begin with a virus known to transmit in humans.

While it’s more difficult to rule out an accidental lab release, a recent study identified a virus in pangolins that has 100% match for one proteins in SARS-CoV-2, suggesting that SARS-CoV-2 arose from co-infection and recombination of a pangolin and bat virus. Previous research on bat coronaviruses would therefore not be a possible source for a lab leak of SARS-CoV-2.

Further, researchers looked directly at this question and determined that the only explanation for the evolution of the viral spike protein, which binds to human receptors, was through natural selection. This rules out the possibility of bioengineering to develop the SARS-CoV-2 virus now spreading worldwide. In the case of SARS-CoV-2, the most cruel designer of a deadly virus is evolution itself.


MYTH: There are multiple strains of SARS-CoV-2
FACT: There are not multiple strains of SARS-CoV-2

Some research pre-prints claim that there are multiple SARS-CoV-2 strains circulating in different geographical regions. One study appeared to show that various mutations in the SARS-CoV-2 genome caused a 270-fold decrease in viral replication. These studies were widely reported in the media, stoking fears about COVID-19 in New York differing substantially from more virulent or benign strains in Singapore, China, Europe, and the West Coast. This would make vaccine development more difficult and raises the horrifying spectre of SARS-CoV-2 evolving to become more pathogenic and deadly or more transmissible.

To our best scientific understanding, there is currently only one SARS-CoV-2 strain circulating worldwide, and there is no good evidence for differences in COVID-19 disease pathology along geographical lines or due to changes in viral RNA sequence.

Coronaviruses have a slow rate of mutation due to an exonuclease (error checking) domain in the viral RNA polymerase. There are currently thousands of SARS-CoV-2 viruses that have been sequenced from patient samples worldwide. Across the 30,000 base genome, these viruses differ by 25 individual mutations at most. This is likely not sufficient genetic variation to create separate strains of the virus. Further, there is no evidence that different viruses – by sequence or geography – have different disease outcomes. Because SARS-CoV-2 evolves so slowly and has only been transmitting in the human population for months, it is entirely inaccurate to denote separate strains of the virus without in vivo data showing varying disease severity.

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