#ace2 receptor

[covid-safer-hotties]

also preserved on our archive

By Erica Sloan

These days, it’s tempting to compare COVID-19 with the common cold or flu. It can similarly leave you with a nasty cough, fever, sore throat—the full works of respiratory symptoms. And it’s also become a part of the societal fabric, perhaps something you’ve resigned yourself to catching at least a few times in your life (even if you haven’t already). But let’s not forget: SARS-CoV-2 (the virus responsible for COVID) is still relatively new, and researchers are actively investigating the toll of reinfection on the body. While there are still a lot of unknowns, one thing seems to be increasingly true: Getting COVID again and again is a good deal riskier than repeat hits of its seasonal counterparts.

It turns out, SARS-CoV-2 is more nefarious than these other contagious bugs, and our immune response to it, often larger and longer-lasting. COVID has a better ability to camouflage itself in the body, “and it has the keys to the kingdom in the sense that it can unlock any cell and get in,” says Esther Melamed, PhD, an assistant professor in the department of neurology at Dell Medical School, University of Texas Austin, and the research director of the Post-COVID-19 program at UT Health Austin. That’s because SARS-CoV-2 binds to ACE2 receptors, which exist in cells all over your body, from your heart to your gut to your brain. (By contrast, cold and flu viruses replicate mostly in your respiratory tract.)

It only follows that a bigger threat can trigger an outsize immune response. In some people, the body’s reaction to COVID can turn into a “cytokine storm,” Dr. Melamed tells SELF, which is characterized by an excessive release of inflammatory proteins that can wreak havoc on multiple organ systems—not a common scenario for your garden-variety cold or flu. But even a “mild” case of COVID can throw your immune system into a tizzy as it works to quickly shore up your defenses. And each reinfection is a fresh opportunity for the virus to win the battle.

While you develop some immunity after a COVID infection, it doesn’t just grow with each additional hit. You might be thinking, “Aren’t I more protected against COVID and less likely to have a serious case after having been infected?” Part of that is true, to an extent. In the first couple years after COVID burst onto the scene, reinfections were generally (though not always) milder than a person’s initial bout of the virus. “The way we understand classic immunology is that your body will say to a virus [it’s seen before], ‘Oh, I know how to deal with you, and I’m now going to deal with you in a better way the second time around,’” says Ziyad Al-Aly, PhD, a clinical epidemiologist at Washington University in St. Louis School of Medicine and the chief of research and development at the Veterans Affairs St. Louis Health Care System.

But any encounter with COVID can also cause your immune system to “go awry or develop some form of dysfunction,” Dr. Al-Aly tells SELF. Specifically, “immune imprinting” can happen, where, upon a second (or third or fourth) exposure to the virus, your immune cells launch the same response as they did for the initial infection, in turn blocking or limiting the development of new antibodies necessary to fight off the current variant that’s stirring up trouble. So, “when you get hit an [additional] time, your immune system may not behave classically,” Dr. Al-Aly says, and could struggle with mounting a good defense.

Pair that dip in immune efficiency with the fact that your antibody levels also wane with time post-infection, and it’s easy to see how another hit can rock your body in a new way. Indeed, the more time that passes after any given COVID infection, the less of a “competitive advantage” you’ll have against any future one, Richard Moffitt, PhD, an associate professor at Emory University, in Atlanta, tells SELF. His research found that, while people who got sick initially during the delta phase were less likely to get reinfected during the first omicron wave (as compared to folks who were infected in a prior period), that benefit leveled off with following omicron variants.

There’s also the fact that no matter how your immune system has responded to a prior strain (or strains!) of the virus, it could react differently to a new mutation. “We tend to think of COVID as one homogeneous thing, but it’s really not,” Dr. Al-Aly says. So even if your body successfully thwarted one of these intruders in the past, there’s no guarantee it’ll do the same for another, now or in the future, he says.

Getting COVID again and again is especially risky if it previously made you very ill. Dr. Moffitt’s study above also found that the “severity of your first infection is very predictive of the severity of a reinfection,” he says. Meaning, you’re more likely to have a severe case of COVID—for instance, requiring hospitalization or intensive care, such as ventilation—when reinfected if you had a rough go of it the first time around.

It’s possible that some folks are more prone to an off-kilter immune response to the virus, which could then happen consistently with reinfections. The antibodies created in people who’ve had severe cases “may not function as well as those in folks who’ve had mild infections or were able to fight the virus off,” Dr. Melamed says. Though researchers don’t fully understand why, some people’s immune systems are also more likely to overreact to COVID (remember the cytokine storm?), which can cause serious symptoms—like fluid in the lungs and shortness of breath—whenever they’re infected.

Being over the age of 65, having a chronic illness or other medical condition, and lacking access to health care have all been shown to spike your risk of serious outcomes with a COVID infection, whether it’s your first or fifth fight with the virus.

But you’re not home free if you’ve only had, say, a brief fever or cough with COVID in the past; Dr. Moffitt points out that a small subset of people in his research who had minor reactions with their initial infection went on to be hospitalized with a repeat hit. The probability of that might be lower, but it’s still a possibility, he says.

Even if you’ve only had “mild” cases, each reinfection strains your body, upping your chances of developing long COVID. A 2022 study led by Dr. Al-Aly found that COVID reinfections also increase your risk of complications across the board, regardless of whether you recovered just fine in the past or got vaccinated. In particular, it showed that reinfection raises the likelihood that you’ll need hospitalization; have heart or lung problems; or experience, among other possible issues, GI, neurological, mental health, or musculoskeletal symptoms. “We use the term ‘cumulative effects,’” Dr. Al-Aly says, “so, multiple hits accrue and then leave the body more vulnerable to all the potential long-term health effects of COVID.”

That doesn’t mean your experience of a second (or third or fourth) infection will necessarily be worse, in and of itself, than what you felt during a prior case. But with each new hit, a fresh batch of the virus seeps into your system, where, even if you have a mild case, it has another chance to trigger any of the longer-term complications above. While the likelihood of getting long COVID (a constellation of symptoms lingering for three months or longer post-infection) is likely greatest after initial infection, “The bottom line is, people are still getting diagnosed with long COVID after reinfection,” Dr. Moffitt says.

Researchers don’t totally know why one person might deal with lasting health effects over another, but it seems that, in some folks, the immune system misfires, generating not only antibodies to attack the virus but also autoantibodies that go after the body’s own healthy cells, Dr. Al-Aly says. This may be one reason why COVID has been linked to the onset of autoimmune conditions like psoriasis and rheumatoid arthritis.

A different hypothesis suggests that pieces of the virus could linger in the body, even after a person has seemingly “recovered” (reminder that SARS-CoV-2 is scarily good at weaseling its way into all sorts of cells). “Maybe the first time, your immune system was able to fully clear it, but the second time, it found a way to hang around,” Dr. Al-Aly posits. And a third theory involves your gut microbiome, the community of microbes in your GI tract, including beneficial bacteria. It’s conceivable that “when we get sick with COVID, these bacteria do, too, and perhaps they recover [on initial infection], but not on the second or third hit,” he says, throwing off your balance of good-to-bad gut bugs (which can impact your health in all sorts of ways).

Another unnerving possibility: The shock to your system triggered by COVID may “wake up” a latent (a.k.a. dormant) virus or two lurking in your body, Dr. Melamed says. We all carry anywhere from eight to 12 of these undetected bugs at a time—things like Epstein-Barr, varicella-zoster (which causes chickenpox and shingles), and herpes simplex. And research suggests their reactivation could be a contributing factor in long COVID. Separately, the systemic inflammation often created by COVID may spark the onset of high blood pressure and increased clotting (which can up your risk of stroke and pulmonary embolism), as well as type 2 diabetes, Dr. Melamed says.

There’s no guarantee that any given COVID infection snowballs into something debilitating, but each hit is like another round of Russian roulette, Dr. Al-Aly says. From a sheer numbers standpoint, the more times you play a game with the possibility of a negative outcome, the greater your chances are of that bad result occurring. And because every COVID case has at least some potential to leave you very ill or dealing with a host of persistent symptoms, why take the risk any more times than you need to?

Bottom line: You should do your best to avoid COVID reinfection and bolster your defenses against the virus. At this stage of the pandemic’s progression, it’s not realistic to suggest you can avoid any exposure to the virus, given that societal protections against its spread have been rolled back. But what you should do is take some common-sense precautions, which can help you avoid any contagious respiratory virus. (A cold or the flu may not pose as many potential health risks as COVID, but being sick is still not fun!)

It’s a good idea to wear a mask when you’re in a crowded environment (especially indoors), choose well-ventilated or outdoor spaces for group hangouts, and test for COVID if you have cold or flu-like symptoms, Dr. Al-Aly says. If you do get infected, talk to your doctor about whether your personal risk of a severe case is enough to qualify for a Paxlovid prescription (which you need to take within the first five days of symptoms for it to be effective).

The other important thing you should do is get the updated COVID vaccine (the 2024-2025 formula was recently approved and released). Unlike getting reinfected, the vaccine triggers “a very targeted immune response…because it’s [made with] a specific tiny part of the virus,” Dr. Melamed says. Meaning, you get the immune benefit of a little exposure without the potential of your whole system going haywire. Getting the current shot also ensures you restore any protection that has waned since you received a prior jab and that you have an effective shield against the dominant circulating strains. Plus, research shows that being vaccinated doesn’t just lower your chances of catching the virus; it also reduces your risk of having a severe case or winding up with long COVID if you do get it.

So, too, can the deceivingly simple act of keeping up with healthy habits—like exercising regularly, eating nutritious foods, and clocking quality sleep. Maintaining this kind of lifestyle can help you stave off other health issues that could increase your risk of harm from COVID, Harlan Krumholz, PhD, a cardiologist at Yale University and founder of the Yale Center for Outcomes Research and Evaluation (CORE), tells SELF. “Given that we will be repetitively exposed to the virus, the best investments we can make are in our baseline health,” he says.

Doing any (or all!) of the above is a big act of compassion for yourself, the people you love, and your greater community. “For the average person, it’s like, ‘Oh, COVID is gone,’ but they’re just not seeing the impact,” Dr. Al-Aly says, noting the invisibility of long COVID symptoms like disorienting brain fog and crushing fatigue. The truth is, in plenty of people, just one more infection could be the difference between living their best life and facing a devastating chronic condition.

[xtruss]

We're Having A COVID Summer Surge. Should You Get The Updated Vaccines Now?

The FDA Just Approved an Updated Vaccines, and Officials Say Paxlovid is Still Effective in Preventing Severe Cases.

— By Sanjay Mishra | August 22, 2024

A Colorized Ccanning Electron Micrograph of a Cell (Blue) Infected with the Omicron Strain of the SARS-CoV-2 virus (Yellow). Micrograph By National Institute of Allergy and Infectious Diseases (NIAID)/National Institutes Of Health/Science Photo Library

The summer of 2024—the fifth since the COVID-19 pandemic began—is projected to be the biggest summer wave of COVID infections to date.

Since early May, COVID infections have steadily increased in the United States, Europe, Singapore, New Zealand, and Australia. The U.S. Centers for Disease Control and Prevention estimates that COVID-19 infections are currently increasing in 25 states based on data from emergency department visits. However, hospitalizations and deaths from COVID remain at their lowest levels.

Now, the U.S. Food and Drug Administration has approved updated vaccines to protect against current variants of the virus.

This recent surge has been driven mainly by a new group of closely related Covid subvariants, known collectively as "FLiRT."

As the summer winds down, students across the U.S. will return to school. Traditionally, this also coincides with the season of respiratory viruses, such as flu, RSV, and increasingly COVID.

"Not sure what will happen this fall and winter," says Kei Sato, a virologist at the University of Tokyo. While the FLiRT variants are likely to keep evolving after summer, entirely new subvariants cannot be ruled out. "An Omicron-like event” seems to have occurred every year in the fall since 2021, says Sato.

Here's what you need to know about the new variants and the new vaccines.

What Are FLiRT Variants?

The "FLiRT" variant family includes the majority of currently circulating variants, identified with the letters KP, JN, and the variant LB.1.

The unofficial name "FLiRT" is an acronym for a set of mutations on the spike protein of SARS-CoV-2, the virus that causes COVID-19. The virus uses spike protein to bind with ACE2 receptors in our nose and lung cells to cause infection.

All proteins are made up of amino acids that string together like beads. Mutations can change one amino acid to another, thereby altering the behavior of the protein and making the virus more or less infectious, or able to dodge immunity.

The FLiRT subvariant family members are descended from the JN.1 variant that was dominant in the U.S. in early 2024. JN.1 itself was highly unusual because it acquired 41 mutations that differentiated it from Omicron XBB.1.5, which is the variant upon which the current bivalent COVID booster is based.

Should You Get The New Vaccines?

The two updated mRNA vaccines, manufactured by Pfizer-BioNTech and Moderna, target a FLiRT variant called KP.2. Anyone over the age of 12 can get the new shots, as long as they haven't received a booster in the last two months.

“Vaccination continues to be the cornerstone of COVID-19 prevention,” Peter Marks, director of the FDA’s Center for Biologics Evaluation and Research said in a statement.

Another vaccine targeting the variant JN.1 and manufactured by Novovax is also under review and could be approved soon.

Previous research also showed that older vaccines based on XBB.1.5, an earlier subvariant of Omicron, were still effective in preventing severe COVID-19. While this vaccine produces antibodies that still target the FLiRT variants, the efficiency is notably reduced. A recent infection from the JN.1 variant also seems to provide strong protection against all the FLiRT variants.

That said, the CDC recommends that everyone six months and older get a COVID vaccine. Those at high risk for serious COVID-19 should get vaccinated with the most recent versions available.

How Alarming Are FLiRT Variants?

Coronaviruses, such as SARS-CoV-2, frequently mutate to avoid recognition by antibodies. The two FLiRT mutations remove the sites on the virus where antibodies bind the SARS-CoV-2 virus.

Additional mutations on the FLiRT variants can either help the virus bind more efficiently to ACE2 receptors making it more infectious, help it evade previous immunity, or both, says Adrian Esterman, an epidemiologist at the University of South Australia, Allied Health & Human Performance in Adelaide, Australia

Early studies show that all existing FLiRT subvariants are very good at dodging previous immunity acquired through multiple COVID vaccinations—including the most recent COVID bivalent booster—or a breakthrough infection from a previous strain of Omicron.

But the good news is that by escaping the antibodies, the FLiRT variants have also seem to lost some ability to infect their target because the virus needed the original antibody-binding sites to bind the ACE2 receptor and enter cells.

"These variants are not yet particularly concerning, even with the new mutations that affect certain aspects of the virus's biology," says Shan-Lu Liu, a virologist at the Ohio State University.

It is common for viruses to acquire mutations that help them dodge immunity, which can affect their ability to infect cells, says Liu. "The viruses can quickly evolve new mutations to restore their infectivity."

But in the meantime, Sato thinks that waning immunity from previous vaccinations and infections, coupled with the FLiRT variant's ability to dodge remaining immunity, are probably the main reason for the recent surge in infections.

Liu also agrees that the currently rising numbers of COVID infections are mostly due to low booster uptake and increased summer travel.

Are COVID Medicines Still Effective?

Emergency department visits, hospitalizations, and deaths have all spiked during this summer but are still much lower compared to earlier waves of the pandemic.

There is no indication that these new FLiRT variants are more dangerous than other Omicron strains.

A study shows that Paxlovid is still effective against FLiRT variants. Other antiviral drugs such as molnupiravir and remdesivir are also expected to work since their mechanism of action is not affected by mutations in the spike protein.

[darkmaga-retard]

Peter Halligan

Aug 19, 2024

Dr. Raszek discusses a recent Dr. Bosschec paper that literally goes to the nth degree to explain the evolution of variants from the original through WIV, JN and especially BA2.8.6.

He explains how the S1 (mushroom head of the spike protein) and the S2 (arms and legs of the spike protein) work to bind to receptors like ACE2 and all about the role of the different types of sugars involved in processes.

Here is a link to the 88-minute video:

Drs. Bossche vs Raszek 2-0 (youtube.com)

“We do another super deep dive into the latest evolution of the virus to inquire if Dr. Bossche theory of the pandemic evolution becoming more deadly is supported by the latest emerging information or not! What we cover: *Why is SARS-CoV-2 evolution so insane *What is protein glycosylation *Detailed look at the evolutionary tree of coronaviruses *What are the unusual results of the latest sugar attachments to spike protein *How is the virus evolving in unusual ways to find new ways to infect us *What does this mean for potential virus pathogencity.”

Here is a link to the paper being discussed:

[pandemic-info]

I teach patho to nursing students. Every semester since spring of 2020, I have taught about Covid. And every semester to have to change my lecture to keep up with new data. I was teaching Covid this semester and I told them that if nothing else, understand the science.

I explained how Covid attaches to ACE2 receptors in the nose, throat, heart, kidneys, and gut first. That’s why you see a runny nose, sore throat, myocarditis and acute kidney failure first. There aren’t as many ACE 2 receptors in the lungs, so Covid hits the lungs later.

That’s why you see lag time between initial infection and respiratory symptoms. More importantly, I explained that Covid is not just a lung disease, it is a massive systemic inflammatory response to the virus. Covid also upregulates a protein called bradykinin, causing clots.

If nothing else, I told them to think of Covid as huge inflammatory process that causes injury, scarring and clots to form everywhere. That’s why we are seeing so many strokes, MIs, weird liver failure in peds, bowel ischemia, and long Covid. It all points to chronic inflammation. There is no immunity as the variants keep changing, kind of like the flu, which is why we get flu shots every year. We’ve just let this run rampant, so a slew of Covid variants keep popping up, rendering treatments less effective.

The worst part of this was when one student said that their parents had gotten Covid and asked how to keep them safe from the complications. Another student piped in and said she had Covid 3 times and was she at risk too? It was my moment of reckoning. I realized that there wasn’t much I could say except to protect themselves with masks, vaccinations, and to try not to get Covid again. I told them that if they had Covid, they were at higher risk of long Covid and lantern complications. There was nothing to be done.

Except to protect themselves going forward. After that there was silence. One of my students then said how disappointed in government and public health leaders he was. Another told me she was disappointed in her professors and her school for not being more vigilant.

I told them that as long as they understood the patho of the disease, they could guard against misinformation. I told them to educate their families and patients about the science, not the rumors. This left me feeling so sad. What have we done?

If I can teach this to first semester nursing students, why couldn’t we have taught this to everyone? People do not understand the disease and no one bothers to explain it. Perhaps that’s why we have failed so miserably.

We need to backtrack and explain the disease before we start talking about immunity debt (a non issue) and endemicity. My students are so young. It’s heartbreaking.

via Kali

[bpod-bpod]

Virus Trap

As SARS-CoV-2 began spreading across the globe, scientists raced to understand the virus’s biology and behaviour. They quickly discovered that entry into cells occurred via the ACE2 receptor, abundant in the lungs. But questions remained over why some people die from COVID-19 while others have mild symptoms or none at all. Differences in immune responses may be partly to blame, but researchers have also investigated other host factors influencing severity. A recent screen for human proteins that interact with SARS-CoV-2 led to the discovery of LRRC15 (stained green in this section of postmortem lung from a COVID-19 patient). LRRC15 binds tightly to the virus but, unlike ACE2, this stickiness prevents its entry into cells. Preliminary evidence indicates COVID-19 patients with high amounts of LRRC15 fair better than those with low levels, which if confirmed suggests drugs designed to boost or mimic the protein might help speed recovery.

Written by Ruth Williams

Image from work by Lipin Loo and Matthew A. Waller, and colleagues

Charles Perkins Centre, Dr. John and Anne Chong Lab for Functional Genomics, Centenary Institute, and School of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia

Image copyright held by the original authors

Research published in PLOS Biology, February 2023

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[longhaulerbear]

Gastrointestinal symptoms are common in Coronavirus Disease 2019 (COVID-19), related to infection of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) of intestinal cells through the angiotensin converting enzyme 2 (ACE2) receptor in the brush border. Also, patients are treated with multiple antibiotics. Therefore, an increase in gut dysbiosis and in the prevalence of Clostridium difficile infection (CDI) is expected in patients with COVID-19.

In COVID-19 there is bacterial and fungal dysbiosis that correlates with systemic and pulmonary inflammation, and illness severity. Further investigations are warranted to determine the efficacy of bacteriotherapy and FMT for modulating gut dysbiosis in COVID-19.

[cubojorbr]

Molécula sintetizada na USP age como escudo molecular e impede o vírus da COVID-19 de infectar a célula

Peptídeo foi inspirado na proteína ACE2, à qual o vírus SARS-CoV-2 se conecta para viabilizar a infecção; resultados indicam caminho para o desenvolvimento de novos antivirais

Julia Moióli | Agência FAPESP – Pesquisadores da Universidade de São Paulo (USP) sintetizaram um peptídeo inspirado no receptor natural do vírus SARS-CoV-2 nas células humanas, a proteína ACE2. A molécula se mostrou capaz de proteger células pulmonares humanas da infecção nos testes in vitro. Além disso, tratou a inflamação causada pelo vírus em camundongos suscetíveis à COVID-19. Esses…

[willowreader]

Many people have lost their teeth because of Covid. Here is why. Click View on Twitter to read the thread. The sources listed at the end of the thread are comprehensive. Here is what David wrote.

A community member (@dbdugger) brought to my attention after yesterday‘s post that bone damage occurs when macrophages are damaged by COVID-19. I thought it was worth covering this damage. Thank you Daniel!

This post explores how SARS-CoV-2 when infecting macrophages, can potentially lead to bone damage through hyperactive osteoclasts and brain damage via perivascular macrophages.

SARS-CoV-2 Infection of Macrophages

Macrophages are a diverse group of immune cells found in various tissues, where they perform functions such as pathogen recognition, inflammation regulation, and tissue repair. In the context of COVID-19, macrophages can become infected by SARS-CoV-2, leading to significant immune responses and tissue damage.

Mechanism of Infection

SARS-CoV-2 infects macrophages through receptors such as CD16 and ACE2. Once inside the macrophages, the virus activates inflammasomes, leading to the release of pro-inflammatory cytokines like IL-1 and IL-18, and a form of cell death called pyroptosis. This hyperinflammatory response contributes to severe lung inflammation and other COVID-19 complications[1][4].

This is the beginning of the explanation. Click on the link above for more.

[miraridoctor]

SARS-CoV-2, the virus that causes COVID-19, has infected millions of people worldwide since first emerging in 2019. A key feature of SARS-CoV-2 that enables its easy spread is its ability to evade and dysregulate immune responses. Understanding how t... #Mirari #MirariDoctor #MirariColdPlasma #ColdPlasma

[covid-safer-hotties]

Brigham and Women’s study: Drug-free nasal spray could protect against COVID, flu - Published Sept 25, 2024

The problem with such drugs is that they do not and cannot work in the throat and lung, other notable infection sites of both these viruses. Masking remains the best way to protect yourself from airborne pathogens, but this is an interesting development for prophylaxis. Studies have shown that neuro-covid symptoms are worst for people whose ACE2 receptors in the sinuses were infected. This could help combat that. The idea that it could also offer drug-free protection from allergens is also interesting. Further study is needed.

By Grace Zokovitch

A new study found a new drug-free nasal spray may protect against respiratory infections like COVID and the flu, according to Brigham and Women’s Hospital.

“The COVID pandemic showed us what respiratory pathogens can do to humanity in a very short time,” said Jeffrey Karp, co-senior author of the study and chair in Anesthesiology at Brigham and Women’s Hospital. “That threat hasn’t gone away.

“We need new, additional ways to protect ourselves and reduce the transmission of the disease,” Karp added.

The preclinical studies show the nasal spray called Pathogen Capture and Neutralizing Spray or PCANS may be able to block respiratory illnesses, the hospital announced. The study was done out of Brigham and Women’s Hospital and published in the journal Advanced Materials.

The hospital stated that protection methods like vaccines and masks can be beneficial but aren’t perfect, noting that “influenza and COVID-19 infections cause thousands of deaths and hundreds of thousands of cases of severe disease every year.”

Most viruses enter through human’s noses, the release stated, spreading when infected people breathe out tiny droplets of fluid. Healthy people inhale the droplets, the hospital said, infecting “cells that line the nasal passageways.”

Researchers formulated the nasal spray to stop the infection in the nose using ingredients that the FDA has approved for use in other nasal sprays or determined safe. The spray was tested in a laboratory setting using replicas of human noses and mice and has not been tested on humans.

“We developed a drug-free formulation using these compounds to block germs in three ways — PCANS forms a gel-like matrix that traps respiratory droplets, immobilizes the germs, and effectively neutralizes them, preventing infection,” said co-senior author Nitin Joshi, an Assistant Professor of Anesthesiology.

When sprayed in a nasal cavity replica, the release stated, “PCANS captured twice as many droplets as mucus alone.” Mice treated with the spray showed it block the influenza virus at 25 times the lethal dose, giving them “complete protection,” researchers said.

“PCANS forms a gel, increasing its mechanical strength by a hundred times, forming a solid barrier,” said primary author John Joseph, a former postdoctoral fellow at Brigham and Women’s Hospital.

“It blocked and neutralized almost 100% of all viruses and bacteria we tested, including Influenza, SARS-CoV-2, RSV, adenovirus, K Pneumonia and more.”

Researchers added that the inflammatory cells and cytokines in the lungs of animals treated with the spray were “normal.”

The hospital stated that the study “provides a strong foundation for future research” into PCANS and researchers are already exploring whether the spray may block allergens.

[screenshots123]

📆 29 Feb 2024 📰 Navigating the Omicron Maze: The Race to Outsmart XBB.1.5 with Next-Generation Vaccines 🗞️ Medriva

As the twilight of 2021 gave way to the dawn of a new year, a formidable adversary emerged on the horizon of our ongoing battle against COVID-19: Omicron's XBB.1.5 variant. With a tapestry of over 30 mutations adorning its spike protein, this variant not only challenged the efficacy of our vaccines but also altered the virus's playbook in interacting with mammalian ACE2 receptors. In this intricate dance of evolution, XBB.1.5 emerged as a dominant strain in the U.S. by late 2022, flaunting its prowess in evading antibodies while still being recognized by our immune system's memory.

[darkmaga-retard]

[The following is an excerpt from Lori Weintz’s book, Mechanisms of Harm: Medicine in the Time of Covid-19.]

If you think about a virus, what’s the purpose? What’s the virus trying to do? It’s trying to stay alive…And if the virus kills someone, if it kills the host, it dies with the host. So it totally defeats the purpose.  Because the goal of a virus is to survive, replicate, and spread, it tends to evolve toward being more infectious and less deadly. There are exceptions and other factors, but in general…that’s what virologists expect to see occur with SARS-CoV-2, the coronavirus that causes COVID-19. –Northeastern (University) Global News, December 13, 2021

In natural Covid infection, the virus enters the body through the nose and mouth. The spike protein of the virus binds with the ACE2 receptor in the nose and the virus replicates for a few days. The immune system either takes care of it there, or the virus continues into the lungs and a person becomes symptomatic while continuing to fight the infection.

For many people Covid has not been much more than a cold. Some have been completely asymptomatic. Others have had body aches and chills, fever, nasal stuffiness, nausea, cough, loss of taste and smell, exhaustion, and weakness, among other symptoms. Covid-19 can be a nasty disease, but from the beginning it had a 99.98% recovery rate, which means most people recover from Covid infection. The pattern for viruses is for them to become more transmissible, and less lethal. SARS-CoV-2 was no exception in this regard. With the advent of the Omicron variant, Covid became much milder than the original Wuhan and the Delta variants had been. 

[salvisalvatorevicidomini]

MERS Coronaviruses (with FCS and with affinity for ACE/2) are the key for the origin of SARS-CoV/2 during pre-pandemic, via transformation-recombination .... and these MERS CoVs are located in hosts of Europe and/or Africa - Middle East ...

The model is verified??

https://www.researchgate.net/publication/358443761

Identification of ACE2 as the Entry Receptor for Two Novel European Bat Merbecoviruses.

BioRxiv preprint, vers. Oct.2/2023.

DOI:10.1101/2023.10.02.560486.

[bpod-bpod]

SARS-CoV-2’s Favoured Fat

Obesity, in addition to advanced age, male gender and diabetes, is a significant risk factor for severe COVID, and new findings might explain why. This image shows fat cells (fat droplets coloured red) covered with the cell-surface receptor for SARS-CoV-2, ACE2 (green). Studies have shown that visceral fat – the type that surrounds major organs and is linked to cardiovascular and metabolic issues – has increased production of ACE2 compared with subcutaneous fat, and is consequently especially susceptible to infection. Moreover, such infection prompts these cells to produce large amounts of inflammatory cytokines, which would likely contribute to the dysregulated inflammation seen in the very worst cases of COVID. Interestingly, while visceral fat was particularly susceptible to the original virus strain it was less so to a more recently isolated strain – a finding which may explain why some strains are more life-threatening than others, particularly with respect to obese individuals.

Written by Ruth Williams

Image by Amanda Passos & Flávio Protasio Veras

Department of Biochemistry and Tissue Biology, Institute of Biology, University of Campinas, Campinas, SP, Brazil

Image copyright held by the original authors

Research published in Nature Communications, September 2022

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