As the second anniversary of the announcement that COVID-19 had reached the United States drew near in January, UC San Diego launched an online forum on December 2 that deals with the brief past, present, and possible future of the Disease concerned.
Under the direction of Kit Pogliano, Dean of the Department of Biosciences, “A Deep Look into COVID-19: Adapting to a COVID World” was presented by the medical professor Natasha Martin, the associate professor of life sciences Justin Meyer and the life sciences professor Elina Zuniga.
The panel looked at topics such as SARS-CoV-2, the coronavirus that causes COVID-19, has evolved and spread through the community, the current variants, what scientists are learning about how to fight the virus, and much more.
The past
“I think one of the most annoying parts of this whole pandemic has been that the advice on how to deal with the pandemic has changed over time,” Meyer said. “And yes, sometimes official communications are poor, but the changing advice really has a lot to do with the fact that the virus we are dealing with today is not the same virus that first emerged.”
He said the virus had evolved and adapted and could spread better in the human population than the version that emerged in late 2019 and soon shocked the world.
“That summer, when the Delta variety began to spread, it dominated and outperformed all other varieties,” said Meyer. “As it started to spread, it sparked this massive wave in the United States and around the world.”
Meyer said that changes in the proteins at the edge of the virus “play a large role in the ability of the virus to spread. If it can improve its ability to do so through mutation, the virus can spread faster and faster. “
The Delta variant is 2.2 times more transferable than the original, he said.
The mutations can also hinder our immune system’s ability to fight them, Meyer said. “But that doesn’t mean the vaccines aren’t effective; they are really still very effective. ”
The gift
Meyer recorded his portion of the forum on November 29, shortly after news broke about the Omicron variant of the virus.
“We don’t have a lot of data on its properties,” said Meyer. “I hope science will reveal more in the days to come.”
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Speaking to the science her laboratory deals with, Zuniga focused her talk on the role of interferons and plasmacytoid dendritic cells (PDCs) in fighting viral infections.
“In addition to the great suffering that COVID has inflicted on people around the world, it has also brought the importance of understanding antiviral defenses to the fore, as it can only be done through a deep understanding of how our bodies are before us protects viral infection that we can develop rational therapies, “said Zuniga.
Interferons, she said, are proteins with different “flavors” that, when activated, can signal an antiviral response. PDCs are “the most powerful interferon-producing cell; they are like interferon factories. “
“Almost every cell is able to produce interferons in response to a viral infection,” said Zuniga. “When a virus infects a cell, it exposes the viral RNA or DNA, which is then perceived by selected receptors that trigger a signal cascade that leads to the activation of this interferon gene.”
This will trigger another cascade of signals that will activate another group of genes that create an antiviral state in the cells where the interferon receptor is active, she said. “This prevents or severely restricts the growth of the virus in the infected cells.”
COVID-19 is susceptible to interferons and interferon-stimulated genes that limit the growth of SARS-CoV-2 or prevent infection of uninfected cells, Zuniga said.
The good news, she said, is, “We have these cells” [PDCs] that produce a phenomenal amount of interferons and are less susceptible to the antagonistic effects of viruses. … The bad news is that it’s not as good as it could be because after interferon production, PDCs become dysfunctional. “
Since the lab began studying the role of interferons and PDCs, “we have improved our understanding of the mechanisms and this PDC dysfunction,” Zuniga said. “Our laboratory has identified several genes that are downregulated in these dysfunctional PDCs, and we recently demonstrated that by restoring at least one of these genes and restoring its expression, we can restore interferon production capacity in these otherwise dysfunctional PDCs.”
When asked by the audience about integrating interferons into therapies, Zuniga replied that some therapies that use interferons are showing “promising results”, although she hopes to see more data.
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Martin spoke about UC San Diego’s “Return to Learn” program, which was launched earlier this year to conduct rigorous coronavirus tests and screenings for people on campus.
“In general, the campus is really well positioned to meet the challenges of Omicron,” said Martin. “We have well-vaccinated students, faculty and staff. We have a robust testing program and a really dedicated student body that has participated in our initiatives. ”
She added that a “Chancellor Challenge” aims to booster 10,000 students by Jan 1.
The future
Although not much is known about the future of COVID-19, Meyer said that mathematical models suggest that “it will be very difficult for us to achieve herd immunity … and get enough vaccinations and enough resistance to eradicate this virus . … What it means is that this virus will continue to exist for a while and we will have to adjust the way we fight disease and change our behavior in the future. “
“Coronavirus is likely to remain and be a new seasonal respiratory disease similar to influenza,” he added. “The good news is that the more vaccinated it becomes, the more difficult it is to spread, and with the number of people infected each year, it will behave more like the flu. There should also be fewer deaths and fewer illnesses as we have some level of immunity to vaccines and natural exposure. “
Meyer said he didn’t expect the general public to need an annual vaccination, “but it’s hard to know what exactly to expect as this is changing.” ◆
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