Coronavirus: A Potential Genetic Link

DNA sleuths read the coronavirus genome, tracing its origins – STAT

Coronavirus: A Potential Genetic Link

As infectious disease specialists and epidemiologists race to contain the outbreak of the novel coronavirus centered on Wuhan, China, they’re getting backup that’s been possible only since the explosion in genetic technologies: a deep-dive into the genome of the virus known as 2019-nCoV.

Analyses of the viral genome are already providing clues to the origins of the outbreak and even possible ways to treat the infection, a need that is becoming more urgent by the day: Early on Saturday in China, health officials reported 15 new fatalities in a single day, bringing the death toll to 41. There are now nearly 1,100 confirmed cases there.

Reading the genome (which is made of RNA, not DNA) also allows researchers to monitor how 2019-nCoV is changing and provides a roadmap for developing a diagnostic test and a vaccine.


“The genetics can tell us the true timing of the first cases” and whether they occurred earlier than officials realized, said molecular biologist Kristian Andersen of Scripps Research, an expert on viral genomes.

“It can also tell us how the outbreak started — from a single event of a virus jumping from an infected animal to a person or from a lot of animals being infected.

And the genetics can tell us what’s sustaining the outbreak — new introductions from animals or human-to-human transmission.”

Scientists in China sequenced the virus’s genome and made it available on Jan. 10, just a month after the Dec. 8 report of the first case of pneumonia from an unknown virus in Wuhan.

In contrast, after the SARS outbreak began in late 2002, it took scientists much longer to sequence that coronavirus.

It peaked in February 2003 — and the complete genome of 29,727 nucleotides wasn’t sequenced until that April.

Since the sequencing of the first 2019-nCoV sample, from an early patient, scientists have completed nearly two dozen more, said Andrew Rambaut of the University of Edinburgh, an expert on viral evolution. That pace is “unprecedented and completely unbelievable,” said Andersen, who worked on sequencing the Ebola genome during the 2014 outbreak. “It’s just insane.”

The genome of the Wuhan virus is 29,903 bases long, one of many clues that have led scientists to believe it is very similar to SARS.

By comparing the two dozen genomes, scientists can address the “when did this start” question.

The 24 available samples, including from Thailand and Shenzhen as well as Wuhan, show “very limited genetic variation,” Rambaut concluded on an online discussion forum where virologists have been sharing data and analyses. “This is indicative of a relatively recent common ancestor for all these viruses.”

Given what’s known about the pace at which viral genomes mutate, if nCoV had been circulating in humans since significantly before the first case was reported on Dec.

8, the 24 genomes would differ more. Applying ballpark rates of viral evolution, Rambaut estimates that the Adam (or Eve) virus from which all others are descended first appeared no earlier than Oct.

30, 2019, and no later than Nov. 29.

The progenitor virus itself was almost certainly one that circulates harmlessly in bats (as SARS does) but has an “intermediate reservoir” in one or more animals that come into contact with people, Andersen said.

Presumably, that reservoir is one of the species of animals at the Wuhan market thought to be ground zero for the outbreak.

The ancestor of 2019-nCoV existed in that species for some unknown time, never infecting people, until by chance a single virus acquired a mutation that made it capable of jumping into and infecting humans.

The genome sequences suggest that was a one-time-only jump. “The genomes [from the 24 samples] are very uniform,” Andersen said. “If there had been multiple introductions,” including from many different animals, “there would be more genomic diversity. This was a single introduction.”

That means that what’s sustaining the spread is human-to-human transmission (suggesting that closing Wuhan’s animal market is very much an after-the-horse-has-fled-the-barn reaction).

Unfortunately, genetic analysis can’t identify what animal species the coronavirus jumped from into humans.

But an analysis by a team from the Wuhan Institute of Virology, posted to the preprint server bioRxiv, determined that the genome of this coronavirus (the seventh known to infect humans) is 96% identical to that of a bat coronavirus, suggesting that species is the original source.

(Writing in the New England Journal of Medicine on Friday, another team of scientists in China reported that the new coronavirus is 86.9% identical to the bat SARS- coronavirus.)

Virologists differ on whether it’s possible to read out viral properties from just the genome sequence, such as whether the microbe is spread by coughing, sneezing, touching, or merely breathing.

But the analysis by the Wuhan Institute team found that it enters human cells using the same doorway that SARS did.

Called angiotensin converting enzyme 2 (ACE2), the door is a receptor to which a “spike protein” on the virus’s surface first attaches and then enables the virus to fuse with the host cell.

If ACE2 is “druggable,” blocking it could conceivably treat 2019-nCoV. “It should be expected and worth to test if ACE2 targeting … drugs can be used for nCoV-2019 patients,” the scientists wrote.

The genome sequences have more to give. They “will be crucially important for development of diagnostics [and] vaccines,” said biologist Richard Ebright of Rutgers University.

For instance, the genome-editing technology CRISPR is the basis for Cambridge, Mass.-based startup Sherlock Biosciences’ diagnostics, which promise to slash how long it takes to make a definitive identification.

In the U.

S, that’s now done only by sending samples to the Centers for Disease Control and Prevention, which uses a technology invented in the 1980s, polymerase chain reaction or PCR, to identify the presence of coronavirus.

“Our vision is that our [CRISPR-based] SHERLOCK and INSPECTR platforms are tailor-made for outbreaks coronavirus,” said Sherlock CEO Rahul Dhanda, who declined to discuss “specific plans related to coronavirus.”

And as scientists keep adding 2019-nCoV genome sequences to their collection, they could get an early glimpse of whether the virus is mutating in a way that could make it more dangerous or more transmissible. “You need continuous sequencing,” Andersen said.

Correction: This story has been corrected to make clear that the coronavirus genome is made of RNA, not DNA.


Did pangolins spread the China coronavirus to people?

Coronavirus: A Potential Genetic Link

Pangolins are scaly creatures often used in traditional Chinese medicine.Credit: Frans Lanting/National Geographic

Researchers in Guangzhou, China, have suggested that pangolins — long-snouted, ant-eating mammals often used in traditional Chinese medicine — are the probable animal source of the coronavirus outbreak that has infected more than 30,000 people and is wreaking havoc worldwide.

Scientists say that the suggestion, a genetic analysis, seems plausible — but caution that the researchers’ work is yet to be published in full. “This is an extremely interesting observation.

Although we need to see more details, it does make sense as there are now some other data emerging that pangolins carry viruses that are closely related to 2019-nCoV,” says Edward Holmes, an evolutionary virologist at the University of Sydney, Australia.

The identity of the animal source of the coronavirus, named nCoV-2019, has been one of the key questions that researchers have been racing to answer.

Coronaviruses are known to circulate in mammals and birds, and scientists have already suggested that nCoV-2019 originally came from bats, a proposal the similarity of its genetic sequence to those of other known coronaviruses.

But the virus was probably transmitted to humans by another animal. The coronavirus that caused severe acute respiratory syndrome, or SARS, spread from bats to civet cats to humans.

Now, the South China Agricultural University in Guangzhou says that two of its researchers, Shen Yongyi and Xiao Lihua, have identified the pangolin as the potential source of nCoV-2019 on the basis of a genetic comparison of coronaviruses taken from the animals and from humans infected in the outbreak and other findings. The sequences are 99% similar, the researchers reported at press conference on 7 February.

A good candidate

Previously, researchers have noted that coronaviruses are a possible cause of death in pangolins1, and that nCoV-2019 and coronaviruses from pangolins use receptors with similar molecular structures to infect cells.

Even before today’s announcement, pangolins were a good candidate for being an intermediate species for the virus, so it’s very interesting that the researchers have found such a close sequence, says David Robertson, a computational virologist at the University of Glasgow, UK.

Pangolins are protected animals, but illegal trafficking is widespread, and some species are critically endangered.

They are sold, controversially, for their meat and scales, and for use in traditional Chinese medicine, in which parts of the animal are used to treat ailments such as skin diseases, menstrual disorders and arthritis.

Chinese law states that people selling pangolins can be punished by 10 years or more in prison.

The coronavirus emerged in the Chinese city of Wuhan in December, and is thought to have leapt to humans at a seafood and wild-animal market, where many of the first people to become infected worked. Pangolins were not listed on an inventory of items sold at the market — although the illegality of trading pangolins could explain this omission.

Last month, scientists in Beijing claimed that snakes were the source of nCoV-2019, but that theory was dismissed by other researchers.

Shen and Xiao did not immediately respond to Nature’s requests for comment, but Liu Yahong, president of the South China Agricultural University, told the press conference that the results would be published soon to help efforts to control the coronavirus.

Scientists hope that the paper will offer details including where the team found the pangolins with the similar virus.

Arinjay Banerjee, a coronavirus researcher at McMaster University in Hamilton, Canada, says that another crucial detail is where in pangolins the researchers found the virus — for example, whether it was isolated from blood samples or rectal swabs.

This will help to determine how it might have been passed to humans and how such transmission could be prevented in the future.

“I can definitely believe it could be true,” says Kristian Andersen, an immunologist and computational biologist at Scripps Research in La Jolla, California. Andersen says he has compared publicly available sequences of pangolin viruses and found that they are similar to that of nCoV-2019. “I look forward to the published report and data.”


Coronavirus’s Genetics Hint at its Cryptic Spread in Communities

Coronavirus: A Potential Genetic Link

When Emma Hodcroft read that, seemingly nowhere, a rash of cases of the novel coronavirus had popped up in Britain in late January, she started collecting media reports on them, searching the articles for clues as to how it had moved to the island nation.

Early reports suggested that a lone traveler from Singapore, who was unaware he was infected with virus, had visited a French chalet for a few days and had spread the virus to others at the ski resort.

This intrigued Hodcroft, who is half British and a postdoctoral researcher in evolutionary biologist Richard Neher’s lab at the University of Basel in Switzerland, where she uses genetics to study and track diseases. She took notes on the cases that were associated with the infected traveler.

“At first, there wasn’t that much information and the story was simple,” she tells The Scientist. But more and more cases kept appearing, and she found it hard to keep track of who had traveled to which country and when they were diagnosed.

Hodcroft decided to generate an infographic showing the connections between the traveler from Singapore and the other coronavirus cases emerging in Europe. “I thought, I’ll make an image and see if anyone else finds this useful,” she says.

She posted the image on , and “somewhat unexpectedly, it got a lot of attention,” she says. “People were definitely really, really interested in this. So I kept that image updated over the next week or so.

” As she updated it, the graphic showed that at least 21 people were exposed to the virus at the ski resort the traveler from Singapore visited; 13 of those people ended up developing COVID-19, the disease caused by the virus.

After she’d finished the preliminary work, a colleague of Hodcroft saw it and suggested she write it up for publication. She posted the paper on February 26; the next day it appeared in Swiss Medical Weekly.

Hodcroft talked with The Scientist about the work, how its conclusions have been supported by genetic testing of viral strains from patients, and what it tells us about the spread of the virus, SARS-CoV-2, in other countries.

The Scientist: What are the main takeaways from your paper?

Emma Hodcroft: Firstly, that it seems so many people [at least 13] could be infected by a single person. It seems they were infected by the man who traveled from Singapore.

So that’s quite a lot of forward transmission on his part in a fairly short time period; he was only in France for about four days.

Of course, this could be some unusual event that doesn’t normally happen, but it lets us put an outer bound on what is possible even if it is not common.  

The other thing that’s surprising is that, according to the patient statement that he released, the focal patient never had any symptoms. In his own words, he never felt sick.

So he did all of this transmission without ever having any indication that he was unwell or that he should be taking any precautions to modify his behavior.

It tells us that some infections might be from people who never even know that they’re sick. 

Text continues below infographic

Contact tracing showing the spread of SARS-CoV-2 in a particular cluster of patients in Europe.

TS: Were the cases in this cluster severe or mild?

EH: As far as we can tell, no one from this cluster had severe symptoms. It seems some people did have some symptoms, but they were never serious.

And that’s also interesting because it shows that if we didn't know about this outbreak, it’s pretty ly that these people would have kind of written this off as a bad cold or the flu. None of them would have ended up going to hospital or significantly changing their behavior.

And again, this indicates that it might be quite hard, and it is becoming quite hard, to contain this virus because some people don't feel very unwell, such that they would change their behavior or go for testing.

TS: The number of cases has been skyrocketing in several countries, the US included. How does your work on this cluster connect with genetic data being reported on about this spike in cases?

EH: In the US, from the information available, it still doesn’t seem the US has really ramped up testing.

We don’t know the number of tests that have been performed because it’s come down off of the CDC website, which is a little concerning.

But at least the last reports that were given to us show the US was really lagging behind most countries in the number of tests that it had done. 

See “Coronavirus’s Genetics Reveal Its Global Travels”

A few days ago, the research group called the Seattle Flu Study, which is designed to take community samples from random people who have any kind of cough, runny nose, or cold- symptoms and look for the flu—they pivoted and started testing some of the samples for coronavirus.

They found a case in the Seattle area and sequenced the viral genome of the infected person [posted on NextStrain] and showed it links very closely with another case in the Seattle area that’s from mid-January.

And so this strongly suggests (though we don’t yet know for certain) that there has been ongoing undetected transmission in Seattle since mid-January and wasn’t picked up because we weren’t looking for it.

This has become clearer in the last few days, as more cases and even deaths have been reported in Washington State. That tells us the virus hasn’t just appeared in the last few days in the area.

Text continues below graphic

The viral genome of the first case in Washington (USA/WA1/2020) is identical to Fujian/8/2020. The genome of the virus from a second case in Washington (USA/WA2/2020) is identical to the first Washington case, except it has three additional mutations. This suggests WA1 was a traveler from China bringing the virus to Snohomish County, Washington in mid-January, where the virus circulated undetected for about five weeks, a timespan that explains why WA2 is so similar genetically, with a few mutations. The graphic shows the connection to the other cases with viral sequences now available.

TS: How do the deaths indicate that the virus has been there for weeks?

EH: This virus causes respiratory illness, which can make you feel unwell for a few days and then you get better or it can progress. If the illness progresses it can cause lung damage that makes the person more susceptible to other illnesses, such as bacterial infection.

This can be treated too and for many people that treatment turns the course of the infection, but some don’t and the effort can essentially delay their death. So the infection may have occurred weeks [before a person dies]. This is not something intrinsic to this virus, however.

With respiratory illness, it’s usually something that takes a substantial amount of infection and lung damage before you succumb to it. 

EH: Sequencing can tell us a lot about what is happening with the virus right now. The Washington samples are a perfect example. . . .

Without having these genomes, we never would have seen this signal of ongoing transmission, which we saw just before the case explosion in Washington. And on the flip side we can tell when cases are coming in from other countries.

We have another genome from Washington State that’s grouping with genomes that we know have a travel history to Italy—so it seems this could be a case where [an infected person] came back from Italy. 

When you have a very small number of cases of a disease, you can do this just through epidemiological contact tracing: you can go to everyone and ask questions and find out the connections between the cases. As the case numbers scale up, this becomes very hard to do.

With genetic sequencing, we can do this without having to go and try and figure out where everyone was at the time of infection. We’ve had an influx of sequences from Brazil, Switzerland, Mexico, Scotland, Germany.

These have clustered with sequences from Italy and have a travel history from Italy and so from that we can show that Italy really is now exporting cases around the world to multiple countries. 

TS: How might public health officials use this information? Is it applicable to making decisions about containment or air travel?

EH: There’s been a lot of modeling, not only with genetics but epidemiologically in the last few weeks, and we had pretty strong indications that circulation was wider than publicly thought. At the time, we did try to some extent to get this message out to government health agencies and the public in general.

I do think that in the future, incorporating a little bit more of that scientific expertise perhaps into the public dialogue and government decision-making could make a big difference. The earlier that you can act in an epidemic, you have more effect you can have, because one person goes on to infect a few more people who go on to infect a few more people.

It’s much harder once that has gone up to 10 [infected] people, than if you can stop with person one.

One thing I would note is that studies have shown that limiting transportation really doesn’t make much of an impact for outbreaks.

Quarantining particular cities, if they seem to be epicenters, can work as a preventive measure, but as the epidemic scales up, you move past being able to contain it in this sense, [and] what you end up doing is just disrupting supply routes, interrupting business, making all of these things much harder.

Editor’s note: This interview has been edited for brevity. 

Ashley Yeager is an associate editor at The Scientist. Email her at Follow her on @AshleyJYeager.


The Coronavirus Outbreak

Coronavirus: A Potential Genetic Link
Continue reading the main story

Researchers who have examined the genomes of two coronavirus infections in Washington State say the similarities between the cases suggest that the virus may have been spreading in the state for weeks.

Washington had the United States’ first confirmed case of coronavirus, announced by the Centers for Disease Control and Prevention on Jan. 20. an analysis of the virus’s genetic sequence, another case that surfaced in the state and was announced on Friday probably was descended from that first case.

The two people live in the same county, but are not known to have had contact with one another, and the second case occurred well after the first would no longer be expected to be contagious.

So the genetic findings suggest that the virus has been spreading through other people in the community for close to six weeks, according to one of the scientists who compared the sequences, Trevor Bedford, an associate professor at the Fred Hutchinson Cancer Research Center and the University of Washington.

Dr. Bedford said it was possible that the two cases could be unrelated, and had been introduced separately into the United States. But he said that was unly, however, because in both cases the virus contained a genetic variation that appears to be rare — it was found in only two of the 59 samples whose sequences have been shared from China, where the virus originated.

A scientist who was not involved in the analysis said he agreed with the conclusion that the second case was connected to the original Washington case.

“I think he’s right,” said Andrew Rambaut, professor of molecular evolution at the University of Edinburgh, referring to Dr. Bedford. “It’s extremely unly that two viruses coming from outside the U.S.A.

independently would arrive in the same geographical area and be genetically related unless they were connected.”

State and local health officials have been hamstrung in their ability to test widely for the coronavirus. Until very recently, the C.D.C. had insisted that only its test could be used, and only on patients who met specific criteria — those who had traveled to China within 14 days of developing symptoms or had contact with a known coronavirus case.

If the virus has been spreading undetected in Washington since mid-January, that could mean that anywhere from 150 to 1,500 people may have it, with about 300 to 500 people the most ly range, said Dr.

Mike Famulare, a principal research scientist at the Institute for Disease Modeling in Bellevue, Wa., who performed the analysis.

These people “have either been infected and recovered, or currently are infected now,” he said.

Many of those people would now be in the early stages of incubating the virus, and might not yet be contagious, Dr. Famulare said.

Dr. Famulare’s estimate was a simulation using what scientists have learned about the incubation period and transmissibility of the virus. He called his figures a “best guess, with broad uncertainty.

” Another method, the size of the local population, the number of tests performed and the proportion of those that were positive, produced similar estimates of how widely the virus may have spread in the community.

The scientists immediately reported the genomic sequence and their findings to state and federal health officials.

Dr. Scott Lindquist, the state epidemiologist for communicable diseases with the Washington State Department of Health, said on Sunday that though Dr. Bedford’s laboratory had “very limited” data to work with, “I would not be surprised if there was transmission and these two were related.”

Dr. Lindquist said more would be known when genetic sequences from the state’s other cases have been similarly analyzed. “Seeing how they all relate to each other will be the real answer to the question of, has it been circulating,” he said. “I imagine within the week we should have some of these answers.”

Heather Thomas, a spokeswoman for the Snohomish Health District, said in a statement that the district was aware of the preliminary findings suggesting that coronavirus had been spreading for close to six weeks.

She said that it was important to remember that national testing capabilities have only been available for about six weeks, and in Washington, health personnel have only had the ability to test locally for a few days. “It is definitely possible that Covid-19 has been circulating, with people experiencing mild symptoms just the flu,’’ she said.

The C.D.C. did not respond to a request for comment.

The first patient, a man in his 30s, has recovered after being treated in a hospital isolation unit. The later patient, a teenager, had a mild enough illness to recuperate at home.

According to a statement by the Snohomish Health District, the teenager was unaware that he was being tested for the coronavirus. His case came to light on Friday because he went to a clinic on Feb. 24 to be tested for the flu, and his sample was shared with the Seattle Flu Study, which tested it for a variety of pathogens including the new coronavirus.

Tests have been performed on about 1,000 samples from the study, Dr. Lindquist said, with only one positive result thus far. “So it’s not it’s super prevalent,” he said of the virus.

“I do think, as more community cases start popping up in the United States, this approach and technique could prove very useful to figuring out the extent of community transmission we currently are having,” Dr. Bedford said of the genetic analysis.

Similar analyses have helped public health officials trace cases and fight outbreaks of Ebola in West Africa and the Democratic Republic of Congo.

On Saturday, local health officials in Seattle said that delays in being able to test for the virus had slowed identification of community cases, meaning those who did not travel to places with major outbreaks or have contact with known patients. “If we had the ability to test earlier, I’m sure we would have been able to identify patients earlier,” said Dr. Jeffrey Duchin, health officer for Seattle and King County.

Two more confirmed cases in the state were announced on Sunday.

The genomic technique used to compare the viruses is akin to constructing a family tree. “As a virus passes from person to person, there will be errors that occur” as copies of the virus are made, Dr. Bedford said. To explain, he compared the tiny mutations in the genetic sequence to mistakes made during a game of telephone. “Those can link up,” he said.

The first case had one genetic difference from the original virus that was detected in Wuhan. The new case had that mutation, plus three additional ones. More than 125 genomes derived from samples taken from coronavirus patients around the world have been shared among scientists thus far, providing data for the analysis.

In the first case in Washington, the man in his 30s had been traveling in Wuhan, China, and returned home to Snohomish County, Wash., on Jan. 15. He sought medical care a few days later after developing symptoms and suspecting that he might have the coronavirus, officials have said, and tests later came back positive.

Health officials then scrambled to retrace his history, tracking down eight people he had socialized with at a group lunch and 37 more who were in the clinic when he showed up for medical help. They also reached out to people on his flight back to the United States.

But as the man remained in hospital isolation, and then later returned home, officials reported no new cases in Washington state. They tested two dozen people over a span of five weeks, and all came back negative.

That changed this week, when the state laboratory became able to test for the virus. Officials reported two new confirmed cases Friday night, and then more, including the first patient to die of the virus in the United States. They are now working to trace how the cases in the state might be linked, and who else might have been exposed.

Two cases have been detected at a skilled nursing facility in Kirkland, Wash., where officials said dozens of other people also had symptoms that could be a sign of coronavirus infection but could also be symptoms of flu.

Gov. Jay Inslee of Washington has declared a state of emergency, and said officials may need to take steps canceling sporting events and closing schools to slow the spread of the virus in the community.

  • Updated March 14, 2020
    • What is a coronavirus? It is a novel virus named for the crown spikes that protrude from its surface. The coronavirus can infect both animals and people and can cause a range of respiratory illnesses from the common cold to lung lesions and pneumonia.
    • How contagious is the virus? It seems to spread very easily from person to person, especially in homes, hospitals and other confined spaces. The pathogen can travel through the air, enveloped in tiny respiratory droplets that are produced when a sick person breathes, talks, coughs or sneezes.
    • Where has the virus spread? The virus, which originated in Wuhan, China, has sickened more than 154,800 in at least 130 countries and more than 5,700 have died. The spread has slowed in China but is gaining speed in Europe and the United States. World Health Organization officials said the outbreak qualifies as a pandemic.
    • What symptoms should I look out for? Symptoms, which can take between two to 14 days to appear, include fever, a dry cough, fatigue and difficulty breathing or shortness of breath. Milder cases may resemble the flu or a bad cold, but people may be able to pass on the virus even before they develop symptoms.
    • What if I’m traveling? The State Department has issued a global Level 3 health advisory telling United States citizens to “reconsider travel” to all countries because of the worldwide effects of the coronavirus. This is the department’s second-highest advisory.
    • How long will it take to develop a treatment or vaccine? Several drugs are being tested, and some initial findings are expected soon. A vaccine to stop the spread is still at least a year away.

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Coronavirus: A Potential Genetic Link

This article is for informational purposes only. The current coronavirus outbreak is an ongoing event and certain details may change as new information comes to light.

None of the information here should be taken as medical advice. If you suspect you may have any kind of infection, seek medical help immediately.

This article will focus on genetic factors that may affect the body’s response to COVID-19. For more information on the disease, including symptoms and prevention, check out these resources from the Centers for Disease Control and Prevention.

The current outbreak of coronavirus disease, better known as COVID-19, is a disease caused by an infection of a virus called SARS-CoV-2 (formerly known as 2019-nCoV) [1].

Generally speaking, the large majority of COVID-19 cases are mild and involve cold- symptoms [1].

However, about 14% of cases are considered severe and 5% of cases result in critical illness, according to preliminary data from Chinese centers [2].

The World Health Organization estimates that about 3.4% of COVID-19 cases have resulted in death globally [3].

While these numbers will ly change as we learn more about the disease, it appears that COVID-19 may affect certain groups of people differently.

Initial research suggests that age, gender, geographic location, and underlying health conditions may all influence the severity and susceptibility to COVID-19 [1, 2].

Interestingly enough, there is some evidence that genetics may also play a role in disease severity. More specifically, the ACE2 gene may have important interactions with the coronavirus [4, 5].

Coronavirus and ACE2

Coronavirus actually refers to a group of viruses, including SARS, MERS, and SARS-CoV-2 (the virus that is responsible for the current outbreak of COVID-19) [6].

Viruses, in general, work by invading the body’s own cells and using the components inside to help replicate and spread.

The SARS-CoV-2 virus, in particular, appears to enter human cells by attaching to the ACE2 receptor, which serves as an entry point for the virus [6].

Normally, the ACE2 receptor plays an important role in regulating the body’s blood pressure and fluid balance [7].

ACE2 receptors can be found in the body’s airways, making them a target for several types of viruses [7].

One recent study suggests there may be a connection between genetics and the body’s response or susceptibility to SARS-CoV-2 [4].

Researchers from this study identified a number of ACE2 variants that are significantly more common in East Asian populations compared to other groups.

Some of these variants (also known as SNPs) include rs4646127, rs2158082, rs5936011, rs6629110, rs4830983, and rs5936029 [4].

In all these variants, the major allele (more common variant) is present in over 95% of people from East Asian populations [4].

In contrast, less than 65% of European populations carry this major allele [4].

The major allele in all these variants is associated with greater expression of ACE2, which researchers theorize may increase susceptibility or severity of COVID-19 because this genetic variant potentially provides more entry points for the virus [4].

However, further research is required to confirm a link between the ACE2 gene and COVID-19.

Researchers from this study also tried to identify any ACE2 gene variants that may prevent the virus from attaching to the body’s cells, but no evidence was found [4].

Treatment of COVID-19: Ongoing Research

Currently, a strong effort is being made by researchers to identify potential agents for the prevention or treatment of COVID-19 [8, 9].

In particular, the ACE2 receptor has received attention because of its potential as an entry point for SARS-CoV-2. Researchers are exploring treatments that block the binding of viruses to the ACE2 receptor [8].

One example are treatments that block TMPRSS2, an enzyme that facilitates the binding process between the ACE2 receptor and SARS-CoV-2. Preliminary cell studies of TMPRSS2 inhibitors have shown promising results [10, 8].

Other potential treatments include other agents that can block the ACE2 receptor or the development of vaccines [11, 8].

However, these treatments are all in very early stages of research and it remains to be unseen which may be effective.