What Scientists Know About the COVID-19 Virus

What the novel coronavirus tells us and what is yet to be learned

What Scientists Know About COVID-19

Verywell / Bailey Mariner

By now, most people are aware that COVID-19—short for "coronavirus disease 2019" (the year the virus was first identified)—is a type of coronavirus that can be spread from person to person and cause respiratory illness, sometimes severe. Beyond that, there remains a lot of confusion about what COVID-19 is and how it has been able to create a global crisis unseen since the emergence of AIDS in the 1980s or the polio pandemic of the 1950s.

There remains a lot that scientists need to learn about COVID-19 before an effective vaccine can be developed to not only treat the current type but genetic variations that are likely to emerge. With that said, there are things that researchers understand about COVID-19 based on observations of other coronaviruses with similar characteristics.

What Is a Coronavirus?

Coronaviruses are a group of related viruses that cause disease in humans, birds, and mammals. In humans, coronaviruses cause respiratory illness ranging from mild to severe. Some types of coronavirus are relatively harmless, causing nothing more than a mild cold, while others are more serious and associated with a high rate of fatality.

There are seven major strains of coronavirus. Between 10% and 15% of all common colds can be attributed to four specific strains, with most infections occurring in a seasonal pattern with increases during winter months. These milder strains are known as:

  • Human coronavirus 229E (HCoV-229E)
  • Human coronavirus HKU1 (HCoV-HKU1)
  • Human coronavirus OC43 (HCoV-OC43)
  • Human coronavirus NL63 (HCoV-NL63)

Meanwhile, there are three other strains of coronavirus that are potentially severe:

COVID-19 was first identified on December 31, 2019, in Wuhan, China. It was on March 13, 2020 that a state of emergency regarding COVID-19 was declared in the United States, just 73 days later.

How Does COVID-19 Differ From SARS and MERS?

Even though COVID-19 is closely related to SARS-CoV-1 and MERS-CoV, it would be a mistake to assume that it will act in the same ways or have the same infection patterns.

SARS-CoV-1 was the first of these severe strains to be identified back in 2002 when it swept through parts of southern China and Asia, infecting around 8,000 people and causing 774 deaths (a 9.6% fatality rate).

MERS-CoV was identified in 2012 and has since caused two additional outbreaks in 2015 and 2018, primarily affecting the Middle East but also reaching as far as the United States and the United Kingdom. While there were less than 500 deaths as a result of the three outbreaks, the rate of fatality was alarming, hovering around 35%.

What makes COVID-19 unique is its high rate of transmissibility. While SARS-CoV-1 affected just over 8,000 people (and only eight in the United States) and all three MERS outbreaks affected just over 2,000 people (two in the United States), COVID-19 has proven to be more transmissible, spreading in a way that is similar to the common cold (via respiratory droplets and possibly by contact with contaminated surfaces).

Given that these are the early days of the COVID-19 pandemic, it is unclear what the actual fatality rate of COVID-19 is since testing efforts in the United States have so far been mainly reserved for symptomatic patients.

It is currently unknown how many asymptomatic cases (those without symptoms) or subclinical cases (those without readily observable symptoms) will test positive, and what percentage of the total infected population they will represent.

As such, it is far too early to even suggest what the actual fatality rate of COVID-19 is. The World Health Organization (WHO) currently estimates that around 3–4% of all reported infections worldwide have died. However, the rate will almost certainly vary from one region to the next and may, in some cases, fall well above or well below the WHO estimates.

Clearly, the biggest factor in "flattening the curve" between the appearance and resolution of infections is the speed and scope of a government's response. Even with the 2003 SARS-CoV-1 outbreak, rapid response by the Centers for Disease Control and Prevention (CDC), which activated an emergency response center with pandemic planning on March 14, 2003, ensured that the spread of the virus in the United States was effectively halted by May 6 with few infections and no deaths.

Epidemiologic modeling will hopefully shed some light on the actual impact of COVID-19 once infection rates begin to decline.

Where Did COVID-19 Come From?

It is believed that COVID-19 jumped from bats or some other animals to humans. Early studies have found genetic evidence, albeit sparse, that pangolins (a type of anteater found in Asia and Africa) served as an interim host between bats and humans. This kind of zoonotic (animal-to-human) jump is not uncommon, and it oversimplifies the issue to suggest that COVID-19 is caused by the consumption of wild animals.

Lyme disease, cat scratch fever, bird flu, HIV, malaria, ringworm, rabies, and swine flu are just some of the diseases considered zoonotic. In fact, around 60% of human diseases are caused by organisms shared by animals and humans.

As human populations increase and infringe on animal populations, the potential for zoonotic diseases increases. At some point, a disease-causing organism like a virus will suddenly mutate and be able to infect a human host either directly (say, through someone eating an animal) or indirectly (via an insect bite or other interim host). But that is only part of the reason why these novel viruses like COVID-19 develop.

Understanding RNA Viruses

With coronaviruses, the potential for mutation is high, due in part to the fact that they are RNA viruses.

RNA viruses are those that carry their own genetic material (in the form of RNA) and simply "hijack" an infected cell to take over its genetic machinery. By doing so, they can turn the cell into a virus-producing factory and churn out multiple copies of itself. Examples of RNA viruses include the common cold, influenza, measles, hepatitis C, polio, and COVID-19.

However, the process of viral transcription—translating the new genetic coding into an infected host—is prone to errors. While many exact copies of the virus will be made, there will also be a multitude of mutated ones, most of which are non-viable and will quickly die.

On rare occasions, however, there will be a viral mutation that not only thrives but, in some case, become more virulent and effective in its ability to infect.

With that said, there is evidence that COVID-19 doesn't mutate as quickly or as often as influenza. According to evidence published in the journal Science, COVID-19 accumulates about one to two mutations per month, around two to four times slower than influenza.

If this evidence holds up, it may suggest that COVID-19 is able to remain more stable over time and not require a new vaccine every season like influenza viruses do.

Why Does COVID-19 Spread So Easily?

From a virologic standpoint, SARS-CoV-1 and MERS-CoV aren't transmitted as effectively as COVID-19. It's not entirely clear why this is and what factors, virological or environmental, may contribute to the efficient spread of COVID-19.

Currently, COVID-19 is believed to be transmitted by respiratory droplets released into the air while coughing. It is also possible that the virus can infect when aerosolized—think a fog rather than a spritz—but only appears to be transmitted effectively this way during prolonged exposure in confined spaces.

The current body of evidence, while sparse, suggests that close contact is needed to effectively spread COVID-19 and that symptomatic people are far more likely to transmit the virus.

This shouldn't suggest that asymptomatic people are inherently "safe"—there is no evidence to suggest that—or that certain environmental factors may enable the distant spread of viral particles.

Role of Temperature and Humidity

While it may seem fair to assume that COVID-19 is influenced by seasons—with decreases in summer and increases in winter—the four coronavirus strains associated with the common cold are known to circulate continuously, albeit with seasonal and geographical variations.

A study from the Massachusetts Institute of Technology (MIT) suggests that COVID-19 acts similarly and is susceptible to warm temperatures and high humidity in the same way as cold viruses.

According to the MIT researchers, COVID-19 infections occur most commonly between 37° F and 63° F (3° C and 17° C), while only 6% occurred at temperatures over 64° F (18° C). High humidity also appears to play a part by saturating the protein shell of the virus, effectively weighing it down and reducing its ability to travel far in the air.

What this suggests is that high temperatures and humidity during the summer may slow the spread of COVID-19 but not stop it immediately; neither will they reduce the risk of complications in vulnerable populations.

Research from Wuhan, China—where the pandemic began—showed that people infected with COVID-19 transmitted the virus to an average of 2.2 other people until aggressive government action was taken to stop the infection.

Is COVID-19 Deadlier Than SARS or MERS?

Again, it's too early to say how "deadly" COVID-19 is. It has certainly caused more deaths worldwide than SAR-CoV-1 or MERS-CoV combined, but that is related in large part to the exponentially increased rate of infections worldwide.

The symptoms of each of these coronaviruses are largely based on how and where they cause infection in the human body.

From a virological standpoint, COVID-19 and SARS-CoV-1 are both believed to attach to the same receptor on human cells, called angiotensin-converting enzyme 2 (ACE2) receptors. ACE2 receptors occur in high density in the respiratory tract, particularly the upper respiratory tract.

COVID-19 appears to have a greater affinity to ACE2 receptors than SARS-CoV-1, meaning that it can attach to target cells more easily. This would explain, at least in part, why COVID-19 spreads through communities more aggressively.

For its part, MERS-CoV is believed to attach to another receptor in the lungs called dipeptidyl peptidase 4 (DPP4) receptors. DPP4 receptors occur in higher density in the lower respiratory tract as well as in the gastrointestinal tract. This may explain why more severe and persistent lower respiratory symptoms (such as bronchiolitis and pneumonia) are common with MERS along with gastrointestinal symptoms (such as severe diarrhea).

On the flip side, because a MERS infection occurs deeper in the lungs, not as many viral particles are excreted during a cough. This may explain why it is harder to catch MERS, despite there being a higher risk of severe illness and death.

COVID-19 and Age

While the current evidence suggests that the risk of fatality from COVID-19 increases with age, it is worth noting that the mean age of those who died in the 2003 SARS outbreak was 52. In China particularly, around 9% of deaths occurred in people under 50 (with only a spattering occurring in under-30s).

A similar pattern was seen with COVID-19 in Wuhan, in which early research suggests that 9% of deaths occurred in people under 50 (albeit mainly between the ages of 40 and 49).

When Will a Vaccine Be Ready?

While there has been much talk about a COVID-19 vaccine being ready by the end of 2020, there remain significant challenges to developing a vaccine that is effective, safe, and readily distributed to a worldwide population.

Unlike SARS—which faded away in 2004 and has not been seen since—COVID-19 is a hearty virus that is likely here to stay. In order for an effective vaccine to be developed, it needs to induce an immune response—typically neutralizing antibodies and "killer" T-cells—that is robust enough to control the infection. No one assumes that producing this will be easy or that any vaccine will provide 100% protection—even the flu vaccine cannot do that.

On the plus side, scientists have begun to map the genome of COVID-19, allowing them to design vaccines that are more likely to work based on what they know about other coronaviruses. On the downside, scientists have yet to crack the code on the development of an effective MERS vaccine.

One of the challenges impeding the development of a MERS vaccine has been the inability to activate immunity in the mucosal tissues that line the respiratory tract.

Given these realities, the public will need to be on alert for future outbreaks of COVID-19 once the current crisis passes. Even if a vaccine is not yet available, a rapid response by public health officials and the public-at-large is more likely to bring an outbreak under control until a longer-term solution can be found.

A Word From Verywell

It is understandable to feel moments of panic when watching the around-the-clock news reports about the COVID-19 pandemic, which tend to focus on worst-case scenarios.

While it is imperative to remain on alert and adhere to public health guidelines, it is also important to recognize that we have much to learn about COVID-19. Some of the findings may be less-than-favorable but others may end up not being not as bad as you assume.

Instead of succumbing to dread or falling prey to misinformation on social media, focus on keeping yourself safe from infection or preventing others from becoming sick if you develop symptoms of COVID-19. By doing your part, efforts to contain COVID-19 can be achieved, allowing funding to be redirected to the development and distribution of a vaccine.

Feelings of fear, anxiety, sadness, and uncertainty are normal during the COVID-19 pandemic. Being proactive about your mental health can help keep both your mind and body stronger. Learn about the best online therapy options available to you.

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