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Gain-Of-Function Experiments At Boston University Create A Deadly New Covid-19 Virus. Who Thought This Was A Good Idea? – Forbes

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After all the controversy over the past few years about gain-of-function research on viruses, especially the Covid-19 virus, I thought this kind of work was on hold, at least in the U.S. Indeed, the controversy grew so hot that NIH issued a statement in May of 2021 declaring that it wouldn’t support such work.

Nonetheless, some scientists continue to pursue gain-of-function work. In a new study, just released on the preprint server bioRxiv, a group of virologists at Boston University did the following. They took the Spike protein from the Omicron BA.1 strain of SARS-CoV-2 (that’s the strain that spread throughout the world last winter, often slipping past the protection offered by vaccines) and combined it with an early 2020 strain of the Covid-19 virus.

This experiment gave them a brand-new, never-before-seen strain of Covid-19. Was it more deadly? You bet!

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In their experiments, the BU scientists infected laboratory mice with the original Omicron virus, which caused “mild, non-fatal infection.” But when they infected mice with their new, recombinant virus, which they called Omi-S, 80% of the mice died. To quote from their article:


“the Omicron S-carrying virus inflicts severe disease with a mortality rate of 80%.”


Well, that’s just great. Making matters worse, the researchers found that the new recombinant virus also replicated much faster in mice: “Omi-S-infected mice produced 30-fold more infectious virus particles compared with Omicron-infected mice.” Yes, you read that right: Omi-S might grow 30 times faster than the garden-variety Omicron strain.

This, dear readers, is what we mean by “gain of function” research. The scientists took sequences from two different strains of the Covid-19 virus, one of which was relatively mild, and created a new strain that is far more infectious and far more deadly. As many scientists (and others) have pointed out, research like this carries great risks, foremost among them the chance that an accidental lab leak could create a new pandemic, killing millions of people.

And the benefits? There must some pretty major benefits to offset this risk, right? Well, not exactly. The researchers say that these experiments show that the pathogenicity of the Covid virus is determined primarily by something other than the Spike protein. That’s a pretty narrow finding, and the authors don’t seem to consider that they might have learned this without creating an entirely new, more-lethal virus.

Does this work violate NIH policies? The NIH director has stated that “neither NIH nor NIAID have ever approved any grant that would have supported ‘gain-of-function’ research on coronaviruses that would have increased their transmissibility or lethality for humans.” First, let me point out that this is a very narrow statement: the NIH doesn’t deny that it funds gain-of-function work on viruses, because it does. They even put a “pause” on such work for 3 years, but they lifted it (regrettably) in 2017. I wrote about that at the time (“NIH Re-opens the Door to Creation of Super-Viruses,” December 2017).

Second, the NIH policy carefully says they don’t support work that would make viruses more deadly for humans. The BU study only looked at mice, so one might argue that it wasn’t making the viruses more deadly in humans–but there’s simply no way we can tell that, not unless we intentionally infect someone. Having read the paper, this work seems to me to be a clear violation of NIH rules.

Boston University and the researchers who led the study disagree. In a statement issued last week, BU officials wrote: “First, this research is not gain-of-function research, meaning it did not amplify the Washington state SARS-CoV-2 virus strain or make it more dangerous.”

Let’s take a look at this denial, shall we? First, let me reiterate that the new experiments combined 2 strains of the Covid-19 virus: the Omicron strain, which has been the main strain infecting humans since last winter, and an earlier strain that was collected from a patient in Washington state in 2020. The Omicron strain causes only mild infections in mice, but the new Omi-S strain–the one that Boston University scientists created in their lab–kills 80% of them. The Washington state strain, which is no longer circulating in people and thus isn’t a current threat, kills 100% of mice.

So that is the BU argument: because Omi-S is less deadly than one of its parental strains, the research doesn’t meet the definition of gain-of-function.

Sorry, but this argument is just nonsense. You don’t get to redefine gain-of-function in the same sentence where you’re denying you’ve done it. These experiments created a brand-new, recombinant strain of Covid-19, and that strain was much more infectious and much more deadly than Omicron, which is one of the strains it was created from. This is precisely what most scientists mean when they describe gain-of-function research and the risks that it carries.

Furthermore, we have no idea how this virus will behave in humans. It might be far more deadly than Omicron in people. Let’s hope we never find out.

And what about that 80% mortality rate? According to Prof. Ronald Corley, Director of BU’s National Emerging Infectious Diseases Laboratories (NEIDL), “This was a statement taken out of context for the purposes of sensationalism, and it totally misrepresents not only the findings, but [also] the purpose of the study.”

Out of context? Well, here’s what the scientists themselves wrote in the very first paragraph (the abstract) of their paper: “We generated chimeric recombinant SARS-CoV-2 encoding the S gene of Omicron in the backbone of an ancestral SARS-CoV-2 isolate and compared this virus with the naturally circulating Omicron variant…. In K18-hACE2 mice, while Omicron causes mild, non-fatal infection, the Omicron S-carrying virus inflicts severe disease with a mortality rate of 80%.”

That’s the scientists’ own statement, and it’s not out of context. The authors themselves were emphasizing this dramatic mortality rate.

The experiments also present another problem for BU. Despite being funded by multiple NIH grants, neither the scientists themselves nor Boston University appears to have informed NIH about this work, which is a requirement for gain-of-function research.

BU officials addressed this problem by stating, first, that the NIH funds only supported some of the underlying “tools and platforms,” and that NIH funds did not directly support the research. Really, BU? How stupid do you think we are? Money, as we all know, is fungible.

Second, according to BU, “there was no gain of function with this research. If at any point there was evidence that the research was gaining function, under both NIAID and our own protocols we would immediately stop and report.” (Read the full BU statement here.)

Well, I would say that when those mice started dying, you had some pretty good evidence that “the research was gaining function.”

I’ve been in touch with multiple virologists who take a similar view. Simon Wain-Hobson, an Emeritus Professor at the Pasteur Institute, wrote to tell me that the BU research “is a GOF outcome in that the recovered virus is more pathogenic than the parental (backbone) virus, albeit in a transgenic mouse setting.” Prof. Wain-Hobson also pointed out that this work “provides a road map to [creating] a virus that might be dangerous to man. By posting this, these authors are making life easier for the next person or copycat.”

Another virologist, Dr. Valentin Bruttel of the University of Würzburg, pointed out the same problems and more, writing that:

  • [the experiments] could have produced a virus that is “way more lethal” than the original SARS-CoV-2 strain
  • “the study is useless for the general population, because the chance that exactly this Omi-Spike [would] recombine with an extinct variant [the Washington state strain] are zero,”
  • “the chimeric virus could cause more severe disease in humans than estimated from mouse data.”

Like Prof. Wain-Hobson, Dr. Bruttel also pointed out that “any terrorist group could copy the BU group’s protocols.”

What does NIH think? They don’t appear convinced by the BU denials. According to an article in The Hill, “NIH is examining the matter to determine whether the research” fits the definition of gain-of-function. And as reported by Helen Branswell in Stat last week, an NIAID official said that NIH should have been informed, at a minimum so that they could determine whether or not the research was permitted under NIH’s gain-of-function rules.

I contacted the lead author of the study to get his response, but he did not reply.

The bottom line here is that some virologists (by no means a majority) believe that conducting gain-of-function research on the Covid-19 virus is just fine. Many other scientists disagree, and strongly. Some have pointed out that this work is qualitatively no different from biowarfare research. I’ve been warning about the risks for years, and I’m certainly not the only one.

Merely requiring scientists to inform the government, which is the current NIH policy, is not enough. We need to shut this research down and take a long, hard look at it before any such experiments can go forward again.

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HIV/AIDS progress in Brazil

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03:08

December 1 is World AIDS Day,  a time to raise awareness and show support for those living with AIDS or HIV, the virus that causes AIDS.

Treatment of HIV/AIDS has come a long way since the first cases became public in the 1980s.

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And Brazil is one country that led the way; its pioneering programs to identify and treat patients recognized the world over.

In recent years, however, the country’s progress has shown to be slipping.

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Early RSV season primarily impacts infants

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Dear Doctors: What can I do to protect my baby from RSV? What are the symptoms? People are talking about a “tripledemic,” and it has my husband and me worried. We’re both vaccinated for the flu and COVID-19, and we are being super careful when we’re out and about. What else can we do?

Dear Reader: RSV is short for respiratory syncytial virus. It’s a common winter virus that can affect people of any age. In most cases, RSV infection causes mild symptoms similar to the common cold. However, infants and children younger than 2, whose immune systems are still developing, are at increased risk of becoming seriously ill.

RSV is the most common cause of pneumonia in infants and young children in the United States. It is also the leading cause of bronchiolitis in that age group. That’s a lung infection in which the smallest airways become inflamed and swollen, and an increase in mucus production impedes air flow into and out of the lungs.

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This year, as with the flu, RSV season has arrived early. Hospitals throughout the U.S. are reporting a surge of serious infections among infants and younger children.

The virus enters the body through the airways and the mucous membranes. It can remain viable on hard surfaces — such as a doorknob, night table or dinnerware — for several hours. It can also persist on softer surfaces, such as a tissue or the skin. Someone can become infected by breathing in the viral particles that remain airborne following a cough or a sneeze, or by touching their mouth, nose or eyes after direct contact with contaminated droplets.

Someone who is sick with RSV typically remains contagious for between four and eight days. However, due to their still-developing immune systems, it’s possible for infants to continue to spread the virus for several weeks, even after symptoms of the disease have abated. There is no vaccine for this virus, and no targeted treatments. Prevention relies on the same precautions you use to avoid any respiratory illness. That is, keep your baby away from people who are ill, avoid close contact with people outside your home and be vigilant about hand hygiene.

Symptoms of RSV arise between three and six days after infection. They can include a runny nose, sneezing and coughing, fever, a decrease in appetite and lung congestion that can cause wheezing. These symptoms tend to be progressive, arriving in stages as the body mounts its attack against the virus. But in very young patients, the first, and sometimes only noticeable, symptoms of RSV can be increased fussiness, a decrease in activity and difficulty breathing.

Treatment for RSV consists of managing symptoms. The specific avenue of care depends on a child’s age, general health and symptoms. In infants, treating RSV includes a focus on adequate hydration and remaining alert for any signs of problems with breathing. The majority of RSV infections run their course in a week to 10 days. Parents of younger infants should check with their pediatricians for guidance on treatment, particularly medications. If your child has difficulty breathing, isn’t drinking enough fluids or has worsening symptoms, call your health care provider right away.

Eve Glazier, M.D., MBA, is an internist and associate professor of medicine at UCLA Health. Elizabeth Ko, M.D., is an internist and assistant professor of medicine at UCLA Health. Send your questions to askthedoctors@mednet.ucla.edu, or write: Ask the Doctors, c/o UCLA Health Sciences Media Relations, 10960 Wilshire Blvd., Suite 1955, Los Angeles, CA, 90024. Owing to the volume of mail, personal replies cannot be provided.

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AIDS Memorial Quilt comes to Palm Beach County

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PALM BEACH COUNTY, Fla. — The largest piece of community folk art in the world, a tribute to victims of AIDS, is on display in Palm Beach County.

Now through Dec. 15, three different panels of the NAMES Project AIDS Memorial Quilt, often known as the AIDS Quilt, will be on display at three different Palm Beach County Public Library locations.

The quilt is a giant tribute to the lives of people who have died due to AIDS or AIDS-related causes.

The quilt weighs around 54 tons and was started in the 1980s during the early years of the AIDS pandemic.

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Three different panels of the AIDS Quilt will be on display at three different Palm Beach County Public Library locations through Dec. 15.

The AIDS Memorial Quilt is comprised of nearly 50,000 panels containing 91,000 names of the men, women and children who lost their lives to the immune system disease.

The blocks, which make up the panels, are stitched by individuals in communities across the nation, including one librarian right in Palm Beach County.

Katrina Brockway, a librarian at the Hagen Ranch Road Branch Library, said she feels it brings tragedy a bit closer to home.

Katrina Brockway, librarian at the Hagen Ranch Road Branch Library discusses the AIDS Quilt visit
Librarian Katrina Brockway explains the impact of seeing the AIDS Quilt in person.

“It becomes so much more personal when you see these quilt panels and all of these people who were loved and didn’t have the same opportunity to escape this,” Brockway said. “So you can remember them, what they went through, and what their loved ones have gone through.”

Visitors can see the quilt panels during normal library hours at the library’s main branch on Summit Boulevard at the Jupiter branch and at the west Boca Raton branch.

Click here for the library’s hours and more information on upcoming AIDS events at the library.

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