From: PDX (and now) London, UK
This looks very interesting. A very clear breakdown of how immunity works, how vaccines can be developed to take advantage of weak points in a virus, and how we shouldn't worry that we won't have immunity if we've recently had this particular disease.
That antibodies decrease once an infection recedes isn’t a sign that they are failing: It’s a normal step in the usual course of an immune response.
Nor does a waning antibody count mean waning immunity: The memory B cells that first produced those antibodies are still around, and standing ready to churn out new batches of antibodies on demand.
I had reported on the B cells earlier but this adds new information. Thank you.
The damn virus has a bad habit of mutating frequently. I haven't seen any research on whether antibodies are still effective on all the variants. Since it would be unethical to give someone all the virus variants, we would have to do a huge amount of research on large pools of people who have had the virus. That won't likely happen soon - too many more urgent things for scientists to look at right now. Not trying to be a killjoy on our hopes, but we need to temper our expectations and not assume that those who have had it can go about with no precautions.
It is actually showing to mutate much less quickly than other viruses. In the article it mentions how it's not HIV, which does have such quick mutations it's impossible to create a vaccine.
The variants that exist now don't differ enough in ways that would inhibit current vaccines in trials from working. In fact vaccines are being made for virtually all areas and methods of fighting the virus, and there are many parts that can be used. Only very minor mutations are happening with Coronavirus and in areas that would not change either natural or vaccine immunity as scientists now see it, from what I've read.
You are talking vaccines, I was talking antibodies, which might target a different part of the virus. There are at least seven different versions of the virus.
Actually I am talking both. There are different versions, but read about them. It's changed remarkably little between variants, and the dominant form now appears to simply be just enough more contagious (with a variation on the spike protein connector) to have begun to dominate all other variants.
Being more contagious makes it more dangerous, but also would actually make it easier to get immunity to currently since this variant is beginning to dominate the worldwide outbreak.
The SARS-CoV-2 virus has a low mutation rate overall (much lower than the viruses that cause influenza and HIV-AIDS). The D614G variant appears as part of a set of four linked mutations that appear to have arisen once and then moved together around the world as a consistent set of variations.
"It's remarkable to me," commented Will Fischer of Los Alamos, an author on the study, "both that this increase in infectivity was detected by careful observation of sequence data alone, and that our experimental colleagues could confirm it with live virus in such a short time."
Fortunately, "the clinical data in this paper from Sheffield showed that even though patients with the new G virus carried more copies of the virus than patients infected with D, there wasn't a corresponding increase in the severity of illness," said Saphire, who leads the Gates Foundation-supported Coronavirus Immunotherapy Consortium (CoVIC).
This is interesting.
The attention lavished on G614 may obscure a bigger question, however: With the virus having spread to at least 11 million people worldwide, why aren’t more mutations that affect its behavior emerging?
Perhaps there’s just little selection pressure on the virus as it races through millions of immunologically naïve people, scientists say. That could change with the advent of vaccines or new therapies, forcing the virus to evolve. But it could also indicate that the virus has been with people longer than we know, and was spreading before the first known cases in Wuhan, China, in December 2019. “The evolution of this virus to become a human pathogen may have already happened and we missed it,” Rasmussen says.
Wang thinks a version of the virus may have circulated earlier in humans in southern Asia, perhaps flying under the radar because it didn’t cause severe disease. “If it happens in a small or remote village, even with some people dying, nobody is going to know there’s a spillover,” Wang says. The virus could then have infected an animal that was brought to Wuhan and started the pandemic.
At Dutch mink farms, after all, the virus jumped not just from humans to animals, but also back from animals to humans, Wang says. “If that can happen in the Netherlands, surely it can happen in a village in Thailand, or in Yunnan province in southern China.”
< Message edited by obvert -- 8/2/2020 9:27:31 AM >
"Success is the ability to go from one failure to another with no loss of enthusiasm." - Winston Churchill