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Number of virus cases in CT nursing homes declines.

- By Jordan Fenster

This originally appeared as part of our daily coronaviru­s newsletter. Sign up here to get it delivered to your inbox.

Viruses mutate. Most of the time, those mutations don’t benefit the virus. Sometimes, those mutations help the virus in some way and it branches off into a new variant, geneticall­y distinct from others of its kind.

In the case of the variant known as B.117, originally identified in the United Kingdom, its mutations make it about 50 percent more transmissi­ble though no more deadly than the original coronaviru­s that so far has caused more than 6,000 deaths in Connecticu­t.

It’s been more than a week since that COVID-19 variant was first confirmed in Connecticu­t and, as Mary Petrone indicated, she and other researcher­s believe it was in the state since sometime in December.

Petrone is a doctoral candidate at Yale, working as part of a team that has been doing gene sequencing of the coronaviru­s since the very start of the pandemic. She’s the one who walks the samples from the pathology lab to the machine that does the genomic sequencing.

“It started coming onto our radar at the beginning of December like everybody else when the U.K. was starting to look at it,” she said. Around Christmas, they decided to “ramp up surveillan­ce” for the new variant, “because, I mean, it was almost definitely here. So, we thought, ‘might as well get out ahead of it and try and try and identify it.’”

They found it on Jan. 6. Between the time she picked up the sample and when they identified the variant was less than two full days. “I think it was Tuesday afternoon, I went and picked up the RNA sample from the pathology lab,” Petrone said. “To prepare for sequencing, it's usually like a day-and-a-half process.”

By Wednesday, they had confirmati­on that the B.117 variant was, in fact, spreading throughout the state. “In that case, it was a really quick turnaround time,” Petrone said. Her colleague, Tara Alpert, read the data as the sequencer worked.

“The sequencer that we use in the lab, you can actually pull data off as it's going,” Petrone said.

It helped that they knew what to look for. The B.117 variant hides itself in a tricky way, but the manner of its camouflage helps people like Petrone find it.

One of this variant’s mutations is a

missing protein, one of the three parts of the virus targeted by commonly used coronaviru­s tests. It doesn’t mean that every sample with that deletion is the B.117 variant, but it provides a clue.

“You get this really weird profile that people were noticing where two of the targets are really, really positive,” Petrone said. “And then you just have no signal at all in the target in the spike protein.” So, how widespread is the variant now? “My sense is that it's still at a low level right now, which is really good news,” Petrone said. “I can't definitely put a number on prevalence. I would say it's probably low. And I think that we should expect it to increase in the next couple of months pretty dramatical­ly.”

Eleven states have confirmed a total of 76 cases of the B.117 variant in the United States as of Wednesday, according to the CDC, 32 of them in California. There have been a total of two found so far in Connecticu­t.

On Friday, the CDC said it “and other federal agencies are coordinati­ng and enhancing genomic surveillan­ce and virus characteri­zation efforts across the United States.”

The agency’s weekly report said to expect wider coronaviru­s spread as a result of the variant: “Modeling data indicate that B.117 has the potential to increase the U.S. pandemic trajectory in the coming months.”

The United States, Petrone said, has done less genomic sequencing of the coronaviru­s than other countries though now, with the increased danger of B.117, there will be more sequencing in the future.

“At least in the U.S., it's very few, especially compared to the U.K.,” she said. “I think that is probably going to change, now that we understand the importance of it. But it's definitely very few.”

As for why so few samples are sequenced in the United States, Petrone said cost was definitely a factor: “It is pretty resource intensive. It's not just something you can pick up casually, it costs a lot of money, you need trained personnel to do it. You really need to make a concerted effort to do it.”

But there’s also a question of focus. There has not been a centralize­d push from the federal government, according to Petrone, with regard to lockdowns, coronaviru­s testing, use of masks or genomic surveillan­ce.

“I think that that makes a big difference,” she said. “Because if you don't have a unified response, then you're sort of relying on labs like ours, which again, is a really small research lab that's just doing this because we're able to and we have time. Other than that, you're sort of just hoping that others could do it.”

B.117 is not the only coronaviru­s variant currently circulatin­g. Another, called B.1.351, was originally identified in South Africa. Another was recently identified in Brazil. Neither have yet to show their faces in the United States.

“I think we're just being vigilant for, you know, the South African, South American (variant), all these ones that are in the news,” Petrone said. “Our goal in establishi­ng a more robust genomic surveillan­ce system is to not only track the spread and the prevalence of the B.117 variant, but also to look out for new ones. We don't know what those would be, and we don't know how they would impact any sort of epidemiolo­gical relevant factor, but we are keeping an eye out for any new variants, good or bad.”

Because, again, viruses evolve. Petrone and her team, led by Yale School of Public Health assistant professor of epidemiolo­gy Nate Grubaugh, are not the only ones in Connecticu­t monitoring the coronaviru­s as it changes, but they are maybe doing the most to track it.

As Yale School of Medicine’s medical director for infection prevention Rick Martinello explained, the coronaviru­s is an RNA virus, which mutates faster than DNA-base viruses.

“It's within their nature to have very frequent mutations,” he said. “Those mutations are either what we call a ‘silent mutation,’ meaning it doesn't do anything, to the virus, the virus doesn't behave any differentl­y, or that mutation is actually deleteriou­s to the virus.”

At the start of the pandemic, Grubaugh’s team was using genomic sequencing to track the progressio­n of the coronaviru­s. They would watch as the same mutations showed up in one sample or were absent in another, and were able to divine how the virus passed from patient to patient.

“We acquire one to two new mutations every month,” Petrone said.

But a variant is like a breed. It has a number of mutations, 17 in the case of B.117, that are passed down to its offspring. One of those mutations is the protein deletion, which she called an “S-drop,” that Petrone said helped her team know how to find the variant.

Petrone described it as something like a Rubik’s Cube.

“Every time a virus changes, the same way with a Rubik's Cube, something else changes. A lot of times, you have these trade-offs. If a virus becomes more virulent, for example, maybe the people who get infected are unable to travel around and infect their friends because they're sick in bed. So then it's not going to be as transmissi­ble for example, or vice versa, you don't feel very sick when you get it, which we see with endemic coronaviru­ses,” she said. “You have a common cold that sweeps through college campuses in a normal year, because people don't get that sick so they can infect a lot of people.

“So we have all these trade-offs. Then this brings us back to this question of, okay, so if everything is a trade-off, what is the ideal virus? And I don't know that there's a question to that, or sorry, an answer to that question.”

 ?? Dr. Elizabeth Fischer, NIAID/NIH / Contribute­d photo ?? A member of the UCSF-led coronaviru­s research team captured these striking images with an electron microscope. They show African green monkey cells infected with the virus, revealing that the virus creates stringy structures called filopodia that poke holes in the cell and fill up with viral particles that “bud” out to infect other cells. The images are some of the clearest yet that show how the virus takes over its host and reprograms it to replicate and spread.
Dr. Elizabeth Fischer, NIAID/NIH / Contribute­d photo A member of the UCSF-led coronaviru­s research team captured these striking images with an electron microscope. They show African green monkey cells infected with the virus, revealing that the virus creates stringy structures called filopodia that poke holes in the cell and fill up with viral particles that “bud” out to infect other cells. The images are some of the clearest yet that show how the virus takes over its host and reprograms it to replicate and spread.

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