The Lambda Coronavirus Variant Has Arrived In Australia Here’s What We Know So Far

We’ve seen the Alpha, Kappa and Delta variants cross our borders, but it turns out another strain of the virus that causes COVID-19 has reached our shores.

The variant, named Lambda by the World Health Organization (WHO) last month, was detected in an overseas traveller who was in hotel quarantine in New South Wales in April, according to national genomics database AusTrakka.

Some reports suggest the new variant could be fast spreading and difficult to tackle with vaccines. So what sets this variant apart from others and should we be concerned?

Here’s what we know so far.

Where did it originate?

Previously known as C.37, Lambda was first detected in Peru in December 2020. Since then, it’s spread to 29 countries, seven of which are in South America.

In April and May this year, Lambda accounted for over 80 per cent of COVID-19 cases in Peru, with a high proportion of cases also in Chile, Argentina, and Ecuador.

On 14 June, Lambda was listed as a ‘variant of interest’ by the World Health Organization due to its vast spread in South America.

Variants of interest are listed as such because they have the potential to be more infectious and severe, but haven’t yet had the devastating impact of those listed as variants of concern.

On 23 June, Public Health England classified it as a ‘variant under investigation’, after six cases were detected in the UK to date, which were all linked to overseas travel.

What makes it different from other variants?

There are now 11 official SARS-CoV-2 variants listed by the WHO.

All SARS-CoV-2 variants are distinguished from one another by mutations in their spike proteins — the components of the virus that allow it to invade human cells.

For instance, the Delta variant first detected in India has two key spike protein mutations — T478K and L452R  — that allow it to infect cells more easily and evade the body’s immune response.

According to research published last week but yet to be peer reviewed,  Lambda has seven unique spike protein mutations.

A Chilean team of scientists analysed blood samples from health workers in Santiago who had received two doses of the CoronaVac vaccine developed by Sinovac Biotech in China.

They found  the Lambda variant has a mutation called L452Q, which is similar to the L452R mutation seen in the Delta and Epsilon variants.

As the L452R mutation is thought to make Delta and Epsilon more infectious and resilient against vaccination, the team concluded that Lambda’s L452Q mutation might also help it spread far and wide.

While it’s possible that Lambda is indeed more infectious than other variants, it’s too early to know for sure, said Kirsty Short, a virologist at the University of Queensland.

“It’s very preliminary,” said Dr Short, who was not involved in the study.

“It’s a good starting point, but I certainly wouldn’t infer anything from that into the clinic.”

Are vaccines still effective against the Lambda variant?

The study also found signs that Lambda’s unique spike mutations could help it slip past the body’s immune response.

The results of the study suggested that the CoronaVac vaccine produces fewer neutralising antibodies — proteins that defend cells against infections — in response to the Lambda variant.

But according to Paul Griffin, who specialises in infectious diseases and vaccines at the University of Queensland, it’s important to remember that these antibodies are just one aspect of immunity.

“We know that [neutralizing antibodies] only tell a part of the story,” said Dr Griffin, who was not involved in the study.

“If that further immunity remains intact, then even with a reduction in neutralizing antibodies, sometimes that protection can still be enough.”

It’s also worth remembering that different vaccines work in different ways to respond to the virus and its variants.

“You can’t really extrapolate from one vaccine,” Dr Short said.

CoronaVac uses inactive versions of SARS-CoV-2 to kick the immune system into gear.

On the other hand, Pfizer contains a single strand of the genetic code that builds the virus’s spike proteins, while AstraZeneca contains a double-strand.

Dr Griffin said that more traditional inactivated vaccines like CoronaVac have proven to be less effective overall than others.

“As a broad category, the inactivated ones have been a little bit underwhelming, particularly compared to others that have such high rates of efficacy,” said Dr Griffin, who was not involved in the study.

While not much is known about how effective the Pfizer and AstraZeneca vaccines are against Lambda, their response to the Delta variant can offer clues.

A recent study from the UK found that two doses of either Pfizer or AstraZeneca are over 90 per cent effective at preventing hospitalisation due to the Delta variant.

Should Australia be worried?

While there has only been one case of Lambda recorded in hotel quarantine in Australia so far, it’s worth keeping an eye on the emergence and spread of SARS-CoV-2 variants around the world, Dr Short said.

“There’s a reason why it’s a variant that we’re watching and looking into more, but it’s certainly not at a point of panic or anything like that.”

Dr Griffin added that Lambda would need to out-compete Delta to become a major concern. “That’s certainly not what we’re seeing,” he said.  But as more people get infected, the more chance the virus has to evolve into new variants, Dr Short said.

The best way to tackle this is to focus on getting more people vaccinated, not just in Australia, but globally. “What this should emphasise to everyone is that we need global effort in the vaccination campaign,” Dr Short said.

 By: ABC Health & Wellbeing Gemma Conroy

Source: The Lambda coronavirus variant has arrived in Australia. Here’s what we know so far – ABC News

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The Cancer Custodians Hidden Truths

woman-with-headscarf-getting-chemo-treatment-article

Part of Dennis Plenker’s daily job is growing cancer. And a variety of different ones, too. Depending on the day and the project, different tumors may burgeon in the petri dishes stocked in the Cold Spring Harbor Laboratory where Plenker works as a research investigator. They might be aggressive breast cancers.

They might be glioblastomas, one of the deadliest brain tumors that rob patients of their ability to speak or read as they crowd out normal cells. Or they might be pancreatic cancers, the fast and vicious slayers that can overtake a healthy person within weeks or even days.

These tiny tumor chunks are transparent and bland—they look like little droplets of hair gel that accidentally plopped into a plastic dish and took hold. But their unassuming appearance is deceptive. If they were still in the human bodies they came from, they would be sucking up nutrients, rapidly growing and dodging the immune system defenses.

But in Plenker’s hands—or rather in the CSHL’s unique facility—these notorious killers don’t kill anyone. Instead, scientists let them grow to devise the most potent ways to kill them. These tumor chunks are called organoids. They are three-dimensional assemblages of malignant growths used to study cancer behavior and vulnerability to chemotherapy and the so-called “targeted drugs”—the next generation therapies.

Scientists used to study tumors at a single-cell level, but because tumors grow as cell clusters in the body, it proved to be inefficient. The three-dimensional structures make a difference. For example, chemo might destroy the tumor’s outer cell layer, but the inner ones can develop resistance, so where single cells may die, a 3D mass will bounce back. Organoids can provide a window into these little-known mechanisms of drug resistance.

They can reveal how normal tissues turn malignant and where the cellular machinery goes off-track to allow that to happen. As their name suggests, organoids are scientists’ windows into organs, whether healthy or stricken with disease. You need to know your enemy to beat it, Plenker says, and cancer organoids offer that opportunity.

Taken from patients currently undergoing cancer treatments, these tumor chunks will reveal their weaknesses so scientists can find the cancers’ Achilles’ heel and devise personalized treatments. “Organoids are essentially patients in a dish,” Plenker says. Only unlike real patients, the organoids can be subjected to all sorts of harsh experiments to zero in on the precise chemo cocktails that destroy them in the best possible way.

And they will likely provide a more realistic scenario than drug tests in mice or rats, as animal models aren’t perfect proxies for humans.

These notorious killers don’t kill anyone. Instead, scientists devise the most potent ways to kill them.

The way that cancer proliferates in the body is hard to reproduce in the lab. Stem-cell research made it possible. After scientists spent a decade understanding how various cells multiply and differentiate into other cell types based on molecular cues and nourishment, they were able to make cells grow and fuse into tissues.

To stick together like bricks in a nicely laid wall, cells need a biological scaffold that scientists call an extracellular matrix or ECM, which in the body is made from collagen and other materials. Today, the same collagen scaffolds can be mimicked with a gooey substance called Matrigel—and then seeded with specific cells, which take root and begin to multiply.

Some tissue types were easy to grow—Columbia University scientists grew viable bones as early as 2010.1 Others, like kidney cells, were trickier. They would grow into immature tissues incapable of performing their job of cleaning and filtering blood. It took scientists time to realize that these cells wanted more than scaffolding and food—they needed to “feel at home,” or be in their natural habitat. Kidney cells needed the feeling of liquid being washed over them, the Harvard University group found, when they first managed to grow functioning kidney tissue in 2018.2

Cancers have their own growth requirements. In the body, they manage to co-opt the organism’s resources, but keeping them happy in a dish means catering to their dietary preferences. Different cancers need different types of molecular chow—growth factors, hormones, oxygen and pH levels, and other nutrients. Pancreatic adenocarcinoma thrives in low-oxygen conditions with poor nutrients.3 Glioblastomas feed on fatty acids.4 These nutrients are delivered to organoids via a specific solution called growth medium, which the lab personnel regularly doles out into the dishes.

Plenker is charged with keeping this murderous menagerie alive and well. He is the one who designs the cancers’ dietary menu, a specific protocol for each type. And while his official title is facility manager and research investigator who works closely with David Tuveson, director of the CSHL’s Cancer Center, he is essentially a cancer custodian, a curator of a unique collection that aims to change the paradigm of cancer treatment.

Plenker’s research area is pancreatic cancer—one of the most notorious killers known. Often diagnosed late and resistant to treatment, it is essentially a death sentence—only 8 to 10 percent of patients remain alive five years after diagnosis. The chemo drugs used to treat it haven’t changed in 40 years, Plenker says. In the past decade, physicians tried combining multiple drugs together with relative success. Identifying winning combos can save lives, or at least prolong them—and that’s what the organoids will help clinicians do better.

In a groundbreaking clinical trial called PASS-01 (for Pancreatic Adenocarcinoma Signature Stratification for Treatment), Plenker’s team collaborates with other American and Canadian colleagues to identify the most effective chemo cocktails and to understand the individual patients’ tumor behaviors, which would lead to more personalized treatments.5

Scientists know the same cancer types behave differently in different patients. Typically, all malignancies have the so-called “driver mutation”— the cancer’s main trigger caused by a mutated gene. But tumors also often have “passenger mutations” that happen in nearby genes. These additional mutated genes can generate various proteins, which may interfere with treatment.

Or not. Scientists call these mutated gene combinations tumor mutational signatures, which can vary from one patient to the next. With some cancers, doctors already know what mutations signatures they may have, but with pancreatic cancer they don’t have good tale-telling signs, or biomarkers. “There aren’t many biomarkers to help clinicians decide which chemo may be better for which patient,” explains oncologist Grainne O’Kane, who treats pancreatic cancer patients at the Princess Margaret Hospital in Toronto, Canada.

That’s the reason O’Kane participates in the PASS-01 trial—it will give doctors a better view into the exact specifics of their patients’ malignancies. As they take their patients’ biopsies, they are sending little cancer snippets to the CSHL to be grown into organoids, which will be subjected to chemo cocktails of various combinations to design more personalized regiments for them.

The hospital treats all patients with the so-called standard of care chemotherapy, which is more of a one-size-fits-all approach. Some patients will respond to it but others won’t, so the goal is to define the second line of chemo defense in a more personalized fashion. “That’s where the biopsies we send to Tuveson’s lab might be useful,” O’Kane says. “They can help us find something to benefit patients after the first line of chemo stopped working.”

Organoids are patients in a dish. Unlike real patients, organoids can be subjected to experiments.

Scientists can try all kinds of combos on the tumorous organoids, which they can’t do in living people. “You can treat 100 organoids with 100 different compounds and see which one works, or which compound does a good job and which ones don’t work at all,” Plenker says. That would also allow scientists to define the precise amount of chemo, so doctors wouldn’t have to over-treat patients with harsh drugs that create sickening side effects. Ultimately, organoids should take a lot of guesswork out of the process.

With about 150 patients’ adenocarcinomas already collected, the team hopes to come up with some answers. O’Kane says her team already has three patients for which they were able to design the more personalized second line of defense chemo, based on what their organoids revealed. They haven’t yet tried it, because the trial has only started recently, but this would be the next step.

“Being able to piece all this information together in real time as patients are moving through their therapies can really improve the outcomes,” O’Kane says. And while they may not be able to save all of those who graciously donated their biopsy snippets to science, it will help build better treatments in the future. “Even if we won’t be able to help these specific patients we’re hoping to use this info in the future clinical trials,” O’Kane says.

Organoids can also help understand how cancer develops. This is particularly true for breast cancers, says Camilla dos Santos, associate professor and a member of the CSHL Cancer Center. She studies the inner life of human mammary glands, more commonly referred to as breasts, and is also part of the cancer custodian crew. The hormonal changes that women go through during pregnancy subsequently modify breast cancer risk, sometimes lowering it and sometimes increasing—a complex interplay of the body’s chemicals.

“We know that women who get pregnant for the first time before they turn 25 years old, have a 30 percent decrease in breast cancer incidents later in life,” dos Santos says. “When they turn 60 or 70, 30 percent of them will not develop cancer.” On the contrary, those who are pregnant past 38 have a 30 to 50 percent increase in developing aggressive breast cancer types. Clearly, some molecular switches are involved, but they are very hard to study within the body. That’s where organoids can provide a window into the surreptitious process.

Using breast organoids, scientists can model the complex life of mammary glands at various stages of a woman’s life. And while most women wouldn’t want their breasts poked and pierced when they are pregnant or breastfeeding, many donate their tissues after breast reduction surgery or prophylactic mastectomy due to high-risk mutations like the BRCA gene.

That’s where organoids shine because scientists can not only grow them, but also give them the pregnancy hormonal cues, which will make cells generate milk, stop lactating, or do it again—and study the complex cellular interactions that take place in real life.

There’s a lot to study. At birth, mammary glands are similar in both genders—just little patches of the mammary epithelium tissue. But when puberty hits, the female glands fill up with the so-called mammary tree—a system of ducts for future milk production, which fully “blooms” in pregnancy.

“When a woman becomes pregnant, the duct tree expands, growing two types of cells—luminal and myoepithelial ones,” explains Zuzana Koledova, assistant professor of Masaryk University in Czech Republic who also uses organoids in her work. When the baby is born, the luminal cells, which line the inside of the ducts, produce the proteins that comprise milk.

The myoepithelial cells reside outside the ducts and work as muscles that squeeze the ducts to push milk out. Dos Santos likens this pregnancy mammary gland growth to the changes of the seasons. The images of sprouting ducts look like blossoming trees in the spring while later they shrivel like plants do in the fall.

The body governs these processes via the molecular machinery of hormones, which stimulate breast cells growth during pregnancy, and later cause them to die out. The two pregnancy-related hormones, prolactin and oxytocin, are responsible for milk production. Prolactin induces the luminal cells to make milk while oxytocin makes the myoepithelial cells contract. Once the baby is weaned, the levels of these hormones drop, causing cells to shrink back to their non-pregnant state.

With organoids scientists can observe these cellular dynamics at work. Koledova’s team had watched breast organoids secrete milk based on biological cues. They even recorded movies of cells pumping tiny milk droplets in the dish they were growing in. Using tiny snippets of donated breast tissue, the team grew the organoids inside the Matrigel matrix in the growth media and then added the two pregnancy hormones into the mix, explains Jakub Sumbal, a mammary gland researcher in Koledova’s group.

As they began to secret proteins that compose milk, the organoids, which looked like little domes inside the dish, changed from translucent to opaque. “At first, you can see through them, but then as they produce these proteins, they kind of darken,” Sumbal says. “And you can see them pushing out these little droplets.”

Cancer patients would no longer have to undergo chemotherapy by trial and error.

Dos Santos’s team, who also did similar work, outlined molecular changes that follow such dish-based hormonal cues in their recent study.6 In response to hormonal messages, cells produce proteins, which they display on their surfaces, like status symbols. During pregnancy the burgeoning cells prepping for milk production display the “proteins flags” that make them look important, attracting nourishment. When it’s time to die, they commit a cellular suicide.

They signal to the bypassing macrophages—immune system cleanup crew—to devour them. “They essentially say ‘come eat me!’ to the macrophages,” dos Santos says. “Because I’m no longer needed.”

The ability to mimic these processes in a dish, allows scientists to study the molecular switches that trigger breast cancer development—or minimize it. Scientists know that cancerous cells can hide from the immune system and even co-opt it into protecting themselves. They do it by displaying their own “do not eat me” protein flags on the surface and avoid destruction.

“Sometimes cancer cells can recruit specific types of immune cells to protect them,” dos Santos says. “They can not only say ‘do not eat me,’ but say ‘come hang out with me’ to the macrophages, and the macrophages will send suppressive signals to the B-cells or T-cells, the body defenders.” It is as if the cancer requests protection—a crew of guardians around it to defend against other cells that would otherwise wipe it out.

Scientists can’t telescope into the body to peek at these interactions, but they now can watch these stealth battles unfolding in a dish. “Right now we are looking at the proteins that are secreted by the organoids—the proteins that go on the surface of the organoids’ cells and what they would communicate to the immune system,” dos Santos says.

“Even when there’s no immune system surrounding them, they would still be doing that.” There’s a way to mimic the immune system, too. Scientists can add B-cells, T-cells, macrophages, and other players into the growth medium and watch the full-blown cellular warfare in action. “That’s the next step in our research,” dos Santos says.

Understanding what hormonal fluxes trigger breast cancer, and how it recruits other cells for safekeeping, can give scientists ideas for pharmaceutical intervention. “We can find drugs that pharmacologically turn off the switches that trigger cancer or interrupt its signaling for protection,” dos Santos says. “That opens novel ways to treat people.”

Can organoid research lead to a new standard of care for cancer patients? That’s the ultimate goal, researchers say. That’s why Plenker works at keeping his collection of cancer glops alive and well and thriving—he calls it a living biobank. And he keeps a stash in the cryogenic freezer, too.

He is also developing protocols that would allow commercial companies to grow organoids the same way chemical industries make reagents or mice suppliers grow rodents for research. A benefit of organoid experiments is they don’t involve animals at all.

Hospitals may one day start growing organoids from their patients’ biopsies to design and test personalized chemo cocktails for them. Once science crosses over to that reality, the entire treatment paradigm will change. Cancer patients won’t have to undergo chemotherapy by trial and error.

Instead their cancer organoids will be subjected to this process—knocked out by a gamut of drug combinations to find the winning one to use in the actual treatment. Plenker notes that once enough data is gathered about the tumors’ mutational signatures, scientists may create a database of tumor “mugshots” matching them to the chemo cocktails that beat them best.

And then just sequencing a biopsy sample would immediately inform oncologists what drug combo the patient needs. “We may be about 10 years away from that,” Plenker says, but for now there’s a lot more research to do. And a lot more cancers to grow.

By: Lina Zeldovich

Lina Zeldovich grew up in a family of Russian scientists, listening to bedtime stories about volcanoes, black holes, and intrepid explorers. She has written for The New York Times, Scientific American, Reader’s Digest, and Audubon Magazine, among other publications, and won four awards for covering the science of poop. Her book, The Other Dark Matter: The Science and Business of Turning Waste into Wealth, will be released in October 2021 by Chicago University Press. You can find her at LinaZeldovich.com and @LinaZeldovich.

Source: The Cancer Custodians – Issue 102: Hidden Truths – Nautilus

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Critics:

Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. These contrast with benign tumors, which do not spread. Possible signs and symptoms include a lump, abnormal bleeding, prolonged cough, unexplained weight loss, and a change in bowel movements. While these symptoms may indicate cancer, they can also have other causes. Over 100 types of cancers affect humans.

Tobacco use is the cause of about 22% of cancer deaths. Another 10% are due to obesity, poor diet, lack of physical activity or excessive drinking of alcohol. Other factors include certain infections, exposure to ionizing radiation, and environmental pollutants. In the developing world, 15% of cancers are due to infections such as Helicobacter pylori, hepatitis B, hepatitis C, human papillomavirus infection, Epstein–Barr virus and human immunodeficiency virus (HIV).

These factors act, at least partly, by changing the genes of a cell. Typically, many genetic changes are required before cancer develops. Approximately 5–10% of cancers are due to inherited genetic defects. Cancer can be detected by certain signs and symptoms or screening tests. It is then typically further investigated by medical imaging and confirmed by biopsy.

Most cancers are initially recognized either because of the appearance of signs or symptoms or through screening. Neither of these leads to a definitive diagnosis, which requires the examination of a tissue sample by a pathologist. People with suspected cancer are investigated with medical tests. These commonly include blood tests, X-rays, (contrast) CT scans and endoscopy.

The tissue diagnosis from the biopsy indicates the type of cell that is proliferating, its histological grade, genetic abnormalities and other features. Together, this information is useful to evaluate the prognosis and to choose the best treatment.

Further reading

New Covid Strain: How Many Variants of Coronavirus Are There

The emergence of variants is linked to ongoing surges since infections give viruses the chance to mutate and spread.

Many variants of the coronavirus are circulating around the world, but scientists are primarily concerned about three. How many variants of the coronavirus are there?

There are many circulating around the world, but health experts are primarily concerned with the emergence of three. As a virus infects people, it can mutate as it makes copies of itself. Some mutations can be harmful to a virus, causing it to die out. Others can offer an advantage and help it spread.

“Not every mutation is created equal,” said Dr. Mary Petrone, who studies infectious diseases at Yale University. “The virus is going to get lucky now and again.”Monitoring variants is important because of the possibility that they could make vaccines and treatments less effective, or change the way they infect people.

A mutation early in the pandemic fueled the spread of the virus around the world, but there had been no notable changes since — until recently, said Ohio State University biologist Daniel Jones.

One of the three main variants experts are watching was discovered in the United Kingdom late last year and has been detected in dozens of countries since. Health officials initially said it didn’t seem to cause worse disease, but some newer information suggests it might — that remains unknown at the moment. It does appear to spread more easily, which could lead to more hospitalisations and deaths.

The variant might become dominant in the US by March, according to the Centers for Disease Control and Prevention. Other variants first detected in South Africa and in Brazil also appear more contagious, experts say.

Data so far suggests current vaccines should still protect against these variants, though there’s some concern their effectiveness may be slightly diminished. There is some evidence that some antibody treatments may be less effective against certain variants.

There are ways to adjust vaccines and treatments to maintain their effectiveness, said Dr. Anthony Fauci, the top US infectious disease expert.The emergence of variants is linked to ongoing surges since infections give viruses the chance to mutate and spread. It’s another reason experts stress the importance of mask wearing and social distancing.

“The fewer humans carrying the virus, the fewer opportunities it has to mutate,” Jones said.The announcement that the coronavirus strain sweeping Britain could be more deadly as well as more transmissible has raised fresh concerns about the variant that has spread to dozens of countries.

Initially British experts said that their evidence suggested the new strain circulating in the UK — one of several to have emerged internationally in recent months — was between 50 per cent and 70 per cent more transmissible.On Friday, however, the government said the new variant could also be 30-40 percent more deadly, although it stressed the assessment relied on sparse data.

What has changed?

In mid-January, two separate studies by London School of Hygiene and Tropical Medicine and Imperial College London were presented to Britain’s New and Emerging Respiratory Virus Threats Advisory Group (NERVTAG).They linked data from people who tested positive for the virus in the community — rather than in hospital — with death data and found a roughly 30 percent increase in the risk of death associated with the new strain.

The groups used slightly different methods, but both matched people with the new variant to those with the older variants, taking into account other variables like age and location and controlling for hospitals being under pressure.Other studies by Exeter University and Public Health England also found higher deaths and both came up with even higher figures.

Based on these analyses, NERVTAG said there was “a realistic possibility” that infection with the new variant is associated with an increased risk of death compared with previously circulating variants.The increase in transmissibility associated to the variant was already causing alarm, because the more people the virus infects the more people will suffer serious illness and the risk of death.

“Unfortunately, it looks as if this virus might be both” more infectious and potentially more deadly, John Edmunds, a professor in LSHTM’s Centre for the Mathematical Modelling of Infectious Diseases, told a press briefing Monday”So it’s really a serious turn for the worse unfortunately,” he said.

How reliable are the findings?

Researchers said there were still uncertainties in the data and said the picture would become clearer in the next few weeks.Edmunds said the findings were “statistically significant”.But he said while the studies used information from those tested in the community, most people who die of Covid-19 go straight to hospital and are tested there.

Researchers do not yet have that hospital information.NERVTAG said this lag in data could be why the studies did not find evidence of an increase in hospitalisations of people with the new variant, which seems at odds with the findings of increased severity of disease.

It also said the mortality data used in the research only covers eight percent of the total deaths during the study period and said the results “may therefore not be representative of the total population”.

Why more deadly?

Researchers think it could be the same set of mutations that has made it more infectious — although all stress more study is needed.One mutation in particular increases the virus’ ability to latch on more strongly to human cells and NERVTAG head Peter Horby, an emerging infectious disease professor at Oxford University, said evidence suggests this means it could make it easier to become infected.

“If it’s then able to spread between cells much quicker within the lungs, that may increase the rate of disease and the rate of inflammation, which may then progress quicker than your body can respond to, so it could explain both characteristics of the virus,” he said.Bjorn Meyer, virologist at France’s Institut Pasteur, told AFP that the issue could be viral load.

“The virus might not have evolved to be more deadly as such, but it might have evolved to grow more or better, which could cause more damage in a patient overall,” he said.

Does this affect treatments?

Horby, who also leads the Recovery trial — which identified the steroid dexamethasone as effective for severely ill hospital patients — said there was “no evidence” that treatments would work less well. Anti inflammatories such as dexamethasone “should work equally as well because it’s not related to the virus, it is related to the host response”, he said.

Horby said overall improvements in therapies and treatments — including things like better strategies for hospital respiratory support — have brought down case fatality rates since the first wave and could even “offset any difference with this new variant”.

As for the vaccines, a preliminary study this month from Britain and the Netherlands found the variant would not be able to evade the protective effect of current vaccines. Pfizer/BioNTech and Moderna have also released early research suggesting their vaccines would still be effective against the strain.

Don’t viruses weaken as they spread?

Scientists have sought to challenge the belief that the virus will become get less virulent as it evolves to become more infectious. The virus that causes Covid-19 is already “very good at its job of getting transmitted” said Emma Hocroft, an epidemiologist at the University of Bern.

“So I don’t think that we can make this assumption that it wants to be less severe. I don’t want to downplay that it is severe for many people, but for the majority of people, it’s not severe,” she told AFP. She said the ability to transmit before it kills was “a really low bar”, citing diseases like measles and HIV that have remained as dangerous.

Graham Medley, a professor of Infectious Disease Modelling at the LSHTM, told the Monday press briefing that despite uncertainties in the new studies on the new variant in the UK, they should dispel the idea that it would become less virulent. “It’s certainly not the case that this is a more benign virus,” he said.

By: https://www.khaleejtimes.com/

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Professor Shane Crotty, Ph.D. explains recent coronavirus mutations and how they might impact COVID 19 vaccines and transmission. COVID-19 research of Prof. Crotty and his team was published Jan. 6, 2021, in the prestigious Journal Science: https://science.sciencemag.org/conten… Prof. Shane Crotty is a Professor at the La Jolla Institute for Immunology, Center for Infectious Disease and Vaccine Research, Crotty Lab. Prof. Crotty also has an academic appointment with the University of California San Diago. See his full bio here: https://www.lji.org/labs/crotty/#over… Prof. Crotty on Twitter: https://twitter.com/profshanecrotty Interviewer: Kyle Allred, Physician Assistant, Producer and Co-Founder of MedCram.com TOPICS DISCUSSED IN THIS VIDEO INCLUDE: 0:00 Intro 0:08 SARS-CoV-2 / COVID 19 mutations (UK variant etc.) and implications for COVID-19 vaccines 10:58 How to test if coronavirus variants can escape immunity 12:28 How have mutations made this virus more transmissible? 17:44 Could mutations make vaccines less than 50% effective? 24:15 Possible changes to vaccine schedules (one dose, half dose)? 35:34 Could alternate COVID-19 vaccine schedule make mutations more likely? 38:29 What is next for Prof. Crotty and his team? (This video was recorded on January 5, 2021) PREVIOUS DISCUSSION WITH PROF. CROTTY (Dec 16, 2020): https://youtu.be/eK0C5tFHze8 REFERENCES: Viral mutations may cause another ‘very, very bad’ COVID-19 wave, scientists warn (Science) | https://www.sciencemag.org/news/2021/… Vaccine Tracker (Bloomberg) | https://www.bloomberg.com/graphics/co… FDA Statement on Following the Auth. Dosing Schedules for COVID-19 Vaccines | https://www.fda.gov/news-events/press… S-variant SARS-CoV-2 is assoc. with sig. higher viral loads in samples tested by ThermoFisher TaqPath RT-QPCR (MedRxiv) | https://www.medrxiv.org/content/10.11… Human Leukocyte Antigen (HLA) System | https://www.merckmanuals.com/professi… UK reports new variant, termed VUI 202012/01 (GISAID) https://www.gisaid.org/references/gis… Covid-19 in South Africa: Scientists seek to understand new variant (BBC) | https://www.bbc.com/news/world-africa… Mutation Allows Coronavirus to Infect More Cells. Scientists Urge Caution (NY Times) | https://www.nytimes.com/2020/06/12/sc… The UK is delaying second vaccine shots and it’s proving controversial (CNBC) https://www.cnbc.com/2021/01/05/the-u… The receptor binding domain of the SARS-CoV-2 (News Medical Life Sciences) | https://www.news-medical.net/news/202… NY Times article highlighting Prof. Shane Crotty’s research: https://www.nytimes.com/2020/11/17/he… THE MEDCRAM WEBSITE: Visit us for videos on over 60 medical topics and CME / CEs for medical professionals: https://www.medcram.com SUBSCRIBE TO THE MEDCRAM YOUTUBE CHANNEL: https://www.youtube.com/user/MEDCRAMv… Get notified of new videos by hitting the bell icon! PREVIOUS / RECENT MEDCRAM COVID-19 INTERVIEWS: Vitamin D and COVID 19: The Evidence for Prevention and Treatment of Coronavirus (SARS CoV 2) with Professor Roger Seheult, MD https://youtu.be/ha2mLz-Xdpg At Home COVID 19 Antigen Testing and Vaccine Update with Professor Michael Mina, MD https://youtu.be/CjphzlV5DYo All coronavirus updates are at MedCram.com ad-free (including more videos on RNA vaccines, BioNTech vaccine, vaccine side effects, AstraZeneca Oxford coronavirus vaccine, new strain of coronavirus, and more): https://www.medcram.com/courses/coron… We offer over 60 medical topics (ECG Interpretation, DKA, influenza, measles, mechanical ventilation, etc.) on our website and CME for clinicians. MEDCRAM WORKS WITH MEDICAL PROGRAMS AND HOSPITALS: MedCram offers group discounts for students and a variety of medical programs, hospitals, and other institutions. Contact us at customers@medcram.com if you are interested. MEDIA CONTACT: Media Contact: customers@medcram.com Media contact info: https://www.medcram.com/pages/media-c… Video Produced by Kyle Allred FOLLOW US ON SOCIAL MEDIA: https://www.facebook.com/MedCramhttps://twitter.com/MedCramVideoshttps://www.instagram.com/medcram DISCLAIMER: MedCram medical videos are for medical education and exam preparation, and NOT intended to replace recommendations from your doctor. #COVID19#SARSCoV2#Coronavaccine

Mutations In Father’s Sperm Can Predict Children’s Autism

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There’s no question that autism can be traced to a combination of genetic and environmental factors. One genetic contributor in particular has in recent years intrigued scientists studying autism: DNA mutations originating in fathers’ sperm.

Studies have linked autism risk to de novo mutations, or changes in DNA that arise spontaneously in sperm as the germline cell develops, or in the embryo after fertilization. Researchers estimate that such mutations might be involved in anywhere from 10% to 30% of autism cases, and that the older a father is at the time of conception, the higher the chance his sperm will result in de novo mutations that can contribute to autism spectrum disorder. In fact, with every decade of life, the number of de novo mutations in sperm doubles.

In a new study published in Nature Medicine, researchers led by a team at the University of California, San Diego (UCSD) set out to determine if they could match specific disease-causing genetic mutations in the DNA of children with autism to the same mutations in their fathers’ sperm.

The team analyzed DNA from eight sets of fathers and children. In the children, they looked for a phenomenon called mosaicism, which are genetic differences even among cells from the same person. Each time a cell divides, the process can generate mutations, or genetic mistakes—some can be harmful (for example, some can lead to cancer), but most are not because they occur outside of important genes in what are known as “DNA deserts.”

The researchers then matched these changes found in the children to those found in their fathers’ sperm. That confirmed that the de novo mutations were indeed playing some role in contributing to autism.

The researchers also determined what percentage of sperm produced by the father contained these de novo mutations. This knowledge, say the study authors, could potentially lead to a test that can help fathers of children with autism to know how likely they are to have another child affected by the condition.

Eventually, the genetic test could also tell parents-to-be if they are at increased risk of having a child with autism. The DNA sequencing technology used is basically the same as used for whole genome sequencing, and the price for that continues to drop, so this wouldn’t be an especially expensive tool.

Inhibitor CocktailsCurrently around 165 genetic mutations have been linked to autism, and conducting a deep analysis of a potential father’s sperm for some of these aberrations could let him know if he is at higher or lower risk of fathering a child who might be affected by autism. (The list of implicated genes continues to grow at a rapid pace, and at the time of the study, the scientists worked with a smaller number of culprit genetic variants).

In some of the eight fathers in the study, up to 10% of their sperm carried mutations; if these men decided to have more children, they would have the option of choosing whether they wanted to take measures to reduce the risk their children would be affected. Some, for example, might use IVF so they could screen their embryos for the mutations.

By Alice Park December 23, 2019

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Source: Mutations In Father’s Sperm Can Predict Children’s Autism

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Part of the joy and challenge of being a parent is making sacrifices so your children can hit traditional milestones: a high school graduation, going off to college, starting a life of their own. But for some parents – like Barbara Rivera, a mother of three with two autistic children – the sacrifices are far greater and the milestones far different than what she expected. (Caregiving; Season 2, Episode 8. Original Air Date: Saturday, December 20, 2014.)