Coronavirus Pandemic (COVID-19) (SARS-CoV-2) [2020]

Ah, I'd read about the apparent fall in proportion of new variant cases in London and the South East and the East of England which didn't make sense if it was a lot more infectious. In the comments on the Pipeline blog, there's a twitter thread in which somebody explains how the classification of what is a new variant case in this data is too narrow so probably misleading. Too much to hope for, I suppose. Regarding whether or not the new variant is more deadly, I wonder if they've taken into account the additional strain on hospital staff and resources in the current wave. It might be that fewer people are receiving potentially life-saving treatment due to lack of resources. However, if there is higher viral load with the new variant it would certainly make sense if it proved to be more deadly.
 
Ah, I'd read about the apparent fall in proportion of new variant cases in London and the South East and the East of England which didn't make sense if it was a lot more infectious. In the comments on the Pipeline blog, there's a twitter thread in which somebody explains how the classification of what is a new variant case in this data is too narrow so probably misleading. Too much to hope for, I suppose. Regarding whether or not the new variant is more deadly, I wonder if they've taken into account the additional strain on hospital staff and resources in the current wave. It might be that fewer people are receiving potentially life-saving treatment due to lack of resources. However, if there is higher viral load with the new variant it would certainly make sense if it proved to be more deadly.

It could be strain on hospitals leading to new deaths because of higher rate of new infections.

Or the virus itself is more deadly because if it infects cells more easily, it can infect more cells and replicate more virus, produce higher viral load on the infected patient and make it more difficult for the immune system to fight off the virus before it spreads all over the body.

Nobody is sure of all this yet.

None of it is good news. We can only hope it's not as bad or scary.
 
My brother passed yesterday. He seemed to be getting better but then took a turn on Saturday.
He was only 42 and my best friend.

People please be safe out there, wear a mask and sanitize your hands.
 
More good vaccine news and some bad variant news.

Good news first. The Novavax trials show efficacy of around 90% overall. This is from the UK trial and combines 95% efficacy against the older strains and 85% efficacy against the newer UK variant:

https://ir.novavax.com/news-release...-vaccine-demonstrates-893-efficacy-uk-phase-3

Slightly less good news is that the South African trial shows lower efficacy of around 60%. However, over 90% of the cases in that trial were the new SA variant which is definitely able to escape existing immunity. It is reported that a third of those enrolled had previously tested positive for Covid, presumably the older variant. Just how many of those were then infected with the new variant isn't clear from the report.

It would be kind of helpful to know if the reinfections with the SA escape variant were mild or not (same goes for similar mutations across in South America). No indication of this from any of the reports or studies I've read thus far. I suppose we're waiting for more data.

No surprise that the various vaccine producers are already working on new ones targeted at the SA variant, however. Looks like we'll probably be getting a vaccine this year then a booster next.
 
I'd like to be optimistic about reinfections with the ZA (South African) variant.

Presumably if you have generated some kind of immune response -- antibodies, T cells, B cells -- you might be in better position to fight off reinfection by this variant.

OTOH, if your lungs have been scarred up by your previous infections, not to mention tissue damage to other organs, you might be more vulnerable to a reinfection which reduces your blood oxygen levels. If your lungs have reduced capacity because of the scarring, maybe you're closer to a tipping point where a re-infection could do more damage more quickly.

It may be a race between your immune system responding to the new strain vs. whether you're fully recovered from the first infection. The hope is that people who've previously been infected have a head start of sorts.

But it's clear that on tests of plasma from recovered vs. vaccinated people, the latter fares much better vs. the new strains.

Checking plasma from 20 patients who recovered from the coronavirus earlier this year, the authors found that four of them had no loss of potency against either B.1.17 or B.1.351. 16 of the plasma samples showed a drop in potency against B.1.351, and 11 samples showed a drop against B.1.1.7. Those activity drops were 2.7 to 3.8 fold in the latter case, and 11 to 33-fold against the former (more on these numbers in just a moment). Most of that B.1.351 drop seems to be attributable to the E484K mutation. Here’s another preprint that’s just come out looking at convalescent plasma response to the B.1.351 variant and another closely related one, this time using live virus instead of pseudovirus constructs. They also find that the IC50 values are worse in the six patients they examined (more on this below!)

Now to the vaccinated-patient plasma samples, because that’s what a lot of people are really wondering about: how well does being vaccinated with the current agents provide you with protection against the new variants? The authors studied serum from 12 patients that had been given both doses of the Moderna vaccine and 10 patients who had had both doses of the Pfizer/BioNTech one. The activity drop against the B.1.1.7 variant was only about 2-fold in both groups, whereas the overall activity drop against the B.1.351 variant was 6.5-fold in Pfizer vaccinnees and 8.6-fold in Moderna ones.

OK, real-world time. First, those numbers tell us that being vaccinated provides a person with more protection than being infected with the coronavirus itself. That was already thought to be the case for the more common coronavirus forms out there, but it’s good to see that it carries over to these two new variants as well. You will get substantially better protection from being vaccinated, and you don’t have to take your chances with the unpredictable and potentially deadly course of an actual coronavirus infection, either.


https://blogs.sciencemag.org/pipeli...tion-against-the-new-variants-real-world-data
 
It appears that most of the vaccines are likely to provide perhaps 50 to 60% efficacy against the South African variant which is a good start. We just need to discover if serious cases amongst the vaccinated are reduced massively, even with this variant. It doesn't really matter if it is more infectious and you're more likely to catch it (or catch it again), if the worst the majority will have to deal with is a week or so in bed. A large proportion of people infected don't have any real respiratory problems, so you'd hope that they would encounter the same situation if reinfected with a new variant.

It would be very nice indeed if the vaccine programmes in place now could make a major difference to hospitalisations and deaths in the next month or so. That might give some hope that we can definitely get this thing under control this year with perhaps just a booster required for the most vulnerable (or anyone who wants it) every few years. All eyes on Israel over the next month or two.

Longer-term, we'll have to decide what to do about children. Will there be a vaccine which can be given to them safely? Do they need one if the vast, vast majority are (hopefully) likely to build up immunity from repeated mild infections?
 
Opinion: The coronavirus is mutating. Will our vaccines keep up?

Opinion by John M. Barry
Jan. 28, 2021 at 1:32 a.m. GMT+1

John M. Barry is the author of “The Great Influenza: The Story of the Deadliest Pandemic in History”, and Distinguished Scholar at the Tulane University School of Public Health and Tropical Medicine.


Making vaccines is hard. Making vaccines that keep up with mutations is even harder. The race is now on to keep up with the mutating coronavirus.

Mutations occur when the genetic code of an organism is not copied accurately during cell replication. This is true in humans and viruses, but viruses make orders of magnitude more copying mistakes than humans do. These mutations are random, and the vast majority have no impact on or damage the virus.

For example, influenza mutates so rapidly that approximately 99 percent of virus particles produced by an infected cell are defective — so defective that they cannot infect another cell and replicate. Unfortunately, the part of the influenza virus most easily recognized by our immune systems — which the influenza vaccine mimics to stimulate an immune response — can mutate without destroying the virus’s ability to infect. Vaccine makers are constantly playing catch-up.

That's why making a flu vaccine is so difficult. Each year scientists change the vaccine to try to match changes in the virus, but vaccine production and distribution takes months. By the time people get inoculated, a precise match is impossible.

Because of this, the best influenza vaccine ever produced was only 60 percent effective in preventing illness. In most flu seasons, the success rate is usually considerably less; and in the 2004-2005 season, the vaccine was only 10 percent effective.

By contrast, the measles virus also mutates rapidly, but the part of the virus that the immune system recognizes — and that the vaccine mimics — cannot change. That’s why, despite billions of measles vaccinations over a period of decades, the virus has been unable to escape the vaccine.

We have already seen mutations in the spike protein of SARS-Cov-2 that allows the virus to enter cells more easily. That advantage is causing one variant to spread more rapidly; within a few months, it has become the dominant virus in the United Kingdom, and it has already spread to other countries.

Countries with robust systems to identify those infected with the variant, isolate them and trace contacts may have a chance to prevent the variant from becoming dominant or slow its spread until their populations are vaccinated. Unfortunately, the United States never built that infrastructure and the Centers for Disease Control and Prevention has predicted this variant could become the dominant virus here by March.

Increased transmissibility is a serious problem, but the Moderna and Pfizer vaccines work well against the variant first identified in the United Kingdom. If nothing else changed and if people comply with social distancing and masking, a wide distribution of the vaccine would eventually contain it.

More worrisome are two new strains: one in South Africa and one in Brazil. Lab studies indicate that the antibodies generated by the Moderna and Pfizer vaccines are less effective against the South African strain than against the previously dominant strain. It remains unclear how much difference this will make in people because the studies indicate that antibodies still work well enough to provide significant protection, and also because antibodies comprise only one part of the immune response; the variant might still be just as vulnerable to T-cells, memory B cells and the rest of our bodies’ immune response.

But it’s still troubling, and scientists are now preparing a booster shot designed specifically for the mutated spike protein of this strain.

More troubling may be the strain which has surfaced in Manaus, a Brazilian city of 2.2 million where an estimated 76 percent of the population has been infected and therefore should have enough naturally acquired immunity to constrain, if not suffocate, the spread of covid-19. That was the case for a while. But a new strain similar to the one in South Africa emerged, and infections caused by it are surging again in Manaus. This strongly suggests the virus has acquired the ability to evade naturally acquired immunity.

Both the Brazilian and South African strains have spread to other countries. On Monday, the strain from Manaus was identified in Minnesota.

Even if these new strains remain highly susceptible to the vaccines we already have, their emergence suggests that SARS-Cov-2 has the ability to mutate enough that it could, over time, evade a vaccine.

That means several things. First, the virus is never going away. Even if it could be eliminated from the human population, it can infect other mammals, mutate in them and then jump back to humans.

Second, the more people infected, the more opportunity the virus has to mutate in a direction that creates problems. So, it is in the self-interest of wealthy countries to get vaccines distributed worldwide to limit those opportunities.

Third, covid-19 will become much like influenza, requiring year-round, worldwide, surveillance of new strains and regular updating and administration of vaccines. We may not need a new vaccine every year, but we will need new vaccines, nonetheless.

There is one other answer. Scientists must search for parts of the virus that remain stable amid mutations and still generate an immune response. With influenza, scientists have made progress toward this. For both viruses, that’s the vaccine we need. That is now the holy grail.


https://www.washingtonpost.com/opinions/2021/01/27/covid-vaccines-new-strains/
 
A unicorn.

https://www.theguardian.com/austral...owing-coronavirus-and-its-startling-discovery
In a high security laboratory in Sydney, where a select group of researchers go to extreme lengths to work with samples of blood and swabs containing Covid-19, virologist Stuart Turville found a unicorn.

“A beautiful, immunological unicorn,” Turville, an associate professor with the Kirby Institute at the University of New South Wales, said.

“We found him when we were analysing samples from the Red Cross blood bank from people who have had Covid. And he had the most amazing Covid response I’ve ever seen.”

The unicorn is a 50-year-old father of three named Damian living on the NSW Central Coast who developed symptoms of Covid-19 in March. His symptoms were severe enough to take him to the hospital emergency department, but after being given oxygen he was sent home the same day. Bizarrely, when he was tested for the virus with the gold-standard PCR nasal swab, the lab kept returning a negative result for Covid-19.

“When they initially diagnosed him they couldn’t find virus in his nasopharyngeal area [the upper part of the throat behind the nose],” Turville told Guardian Australia.
“So they kept on swabbing him and swabbing him, but they couldn’t find it. He kept on saying to them, ‘Look, I’m sick, my son’s got it, I have to have it’. And it was only when they looked at his blood, his serum, they said; ‘Oh, yeah, you’ve had it. And you’ve got the most amazing immune response’.”

Most people who have Covid-19 develop a decent immune response.

“But this guy’s response is 100 to 1,000-fold that,” Turville said.

“His response is that good. To put it in context, we are eight or nine months out since he was infected. And he still ranks in the top 1% of responders, so what that means is if we could ever bottle a vaccine that could mimic his response, you’d want to do it. I would say that we’re going to see him responding just as well probably a year out, and maybe after about two years we might start to see some response decay.”

Usually, patients who show a particularly robust immune response to Covid-19 end up in an intensive care ward. In many of these severely unwell patients, the immune system overreacts in what is called a “cytokine storm”. Cytokines are proteins that can trigger an inflammatory response so aggressive that not only are virus cells attacked but cells in the blood vessels, urinary tract, organs and blood vessels are also destroyed, leading to organ failure and sometimes death. For some reason Damian’s response, though strong, did not bring on such an aggressive storm.

“That’s something we’re trying to get our head around,” Turville said.
 
A unicorn.

https://www.theguardian.com/austral...owing-coronavirus-and-its-startling-discovery

“When they initially diagnosed him they couldn’t find virus in his nasopharyngeal area [the upper part of the throat behind the nose],” Turville told Guardian Australia.
“So they kept on swabbing him and swabbing him, but they couldn’t find it. He kept on saying to them, ‘Look, I’m sick, my son’s got it, I have to have it’. And it was only when they looked at his blood, his serum, they said; ‘Oh, yeah, you’ve had it. And you’ve got the most amazing immune response’.”

The fact that he had it but it wasn't picked up by tests really makes me wonder if I've had it.

In mid-September, I had the worst flu like illness I've ever had. Came on out of nowhere, went from sinuses to lungs, and left me with a lingering cough for a couple of weeks. It hit my lungs hard, and one morning I woke up struggling to breathe, which has never happened to me with any flu before.

I'm a champ, so I kept smoking weed throughout.

I work in a nursing home, and I wasn't allowed back to work until my test came back negative and my symptoms had cleared up. I had a test 1 week before getting ill, 1 taken in the car park during my illness, and 1 the week after I returned. All negative.

Mid-November, one of the residents tested positive for Covid. He already had dementia, and the covid made him delirious even by his usual standards. So, every shift, I was looking after him, changing his pad, cleaning his arse, trying to get him to have a drink. The entire time he was pawing at me and my PPE, coughing, spluttering, shouting, spitting out some of the juice he'd just taken. The air was thick with disease.

This lasted for about a month. I was the only one that saw to him, as my colleague was at risk. I picked up a bunch of extra shifts that month, and worked almost every day.

So, almost every day for a month, 4/5 times per shift, I was in a room with a man who was just seeping covid. I was wearing PPE, but I pretty quickly consigned myself to the, in my mind, fact that I was going to get it.

I was tested once or more per week. All came back negative. Not once did I come down with any symptoms.

I'd previously put it down to a combination of PPE and getting lucky. Now though, I'm wondering if I had it in September, only tested negative, and had an immunity by the time it was in my workplace.
 
Regarding the numbers in Manaus, the estimates of 70% infected in the first wave are almost certainly inaccurate so any article stating it as fact is probably based on a false premise. If nothing else, the Infection Fatality Rate was much too low back then to indicate such a large number of infections. Other cities in Brazil had a greatly higher IFR so they were hit much harder but didn't make the news in the same way. Terrible though the situation in Manaus undoubtedly was, it probably wasn't anywhere near a 70% infection rate.

It remains to be seen just now many reinfections we'll get from the South African and similar South American variants. We also need to know if reinfections are likely to be milder than the original which would be logical for most infections, but perhaps not for this novel virus.
 
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