It looks like you're using an Ad Blocker.
Please white-list or disable AboveTopSecret.com in your ad-blocking tool.
Thank you.
Some features of ATS will be disabled while you continue to use an ad-blocker.
originally posted by: puzzled2
So between Xmas and New year no-one will die without a positive result for a sars-cov-2 infection therefore they will claim Millions are dying and will be justified in forcing the jabs they already have the laws, goons and public opinion to do so.
“We didn’t see Delta coming. I think most scientists did not – upon whose advice and direction we have relied – didn’t see Delta coming,” Harris said.
“We didn’t see Omicron coming. And that’s the nature of what this awful virus has been, which as it turns out, has mutations and variants.”
House Committee Report Reveals Trump's Efforts To "Undermine" COVID Response
The success of a SARS-CoV-2 variant depends on many factors, but there are three elements that are particularly crucial: transmissibility, immune evasion, and virulence. Any mutation that productively impacts one of these three factors is a dangerous one. Any variant with higher transmissibility, a better capacity to evade our natural (innate) immunity, or heightened virulence is one to keep a vigilant eye on.
More often than not, however, this vigilant eye is reserved for what happens within the spike (S) protein of SARS-CoV-2. Understandable, since the S protein plays a major role in allowing the virus to enter and infect our cells, but perhaps slightly misguided.
A new report, led by researchers with the Oak Ridge National Laboratory, prompts us to shift our focus towards the entirety of the viral genome, rather than just the S protein. Applying tools from the field of human genetics, Garvin et al. suggest that mutations outside of SARS-CoV-2’s spike protein may be just as significant as those within. The reason for this? Epistasis.
Many traits are polygenic, meaning a variety of different genes all affect the way that trait is eventually expressed. When multiple genes affect the same trait, they can end up interacting with one another in different ways. Epistasis is a kind of polygenic interaction. At its simplest, it’s when the expression of one gene or genetic mutation is modified by the presence of another.
the interaction of genes that are not alleles, in particular the suppression of the effect of one such gene by another.
Epistasis refers to the behavioral effect of interaction among gene alleles at multiple locations. Epistasis is observable when phenotypic differences among individuals with the same genotype at one locus depend on their genotypes at another locus.
CD4+ T lymphocytes get their nickname of helper T cells because they assist another type of immune system cell, the B lymphocyte (B cell), to respond to surface proteins — antigens — on viruses such as SARS-CoV-2. Activated by the CD4+ T cells, immature B cells become either plasma cells that produce antibodies to mark infected cells for disposal from the body or memory cells that “remember” the antigen’s biochemical structure for a faster response to future infections. Therefore, a CD4+ T cell response can serve as a measure of how well the immune system responds to a vaccine and yields humoral immunity.
The researchers found that the monkeys were able to mount a good memory response against the virus regardless of T cell depletion. "We found we got really good memory responses regardless of whether we depleted T cells or not. Basically, we found very strong virus neutralizing antibodies, and they are the most important antibodies in controlling the infection. That was unexpected by most immunologists, virologists and vaccinologists," said Hasenkrug.
"The other thing that happens during a memory response is that antibodies mature, becoming, stronger and more potent at binding the viral pathogen. We saw indications of this through what’s called 'class switching.'" said Hasenkrug. "Class switching" was also unexpected in these monkeys with depleted T cells. "We don’t have a firm explanation as to why that happened, but we think it involves some sort of compensatory response, which you can see in our study. For example, when we depleted CD8+ T cells, we saw stronger CD4+ T cell or B cells responses in some animals. When the animals are missing something, they will try to make up for it by making more of something else."
Hasenkrug doesn’t know why the T cells didn’t turn out to be more important, but it is probably a good thing that they are not required, because then, people who fail to mount sufficient T cell responses still have opportunities to recover.
"This implies that the innate immune response is critical for initial control of the virus, rather than the adaptive immune responses we studied," said Hasenkrug.
The new study shows that while the immune system often mounts a strong response against a particular site on the virus's "spike" protein called the receptor binding domain, this region is actually not as good at inducing a strong response from CD4+ helper T cells.
Without a strong CD4+ T cell response, however, people may be slow to mount the kind of neutralizing immune response that quickly wipes out the virus. Luckily, the broad immune response comes in handy, and most people have immune cells that can recognize sites other than the receptor binding domain.
Among the many epitopes they uncovered, the researchers identified several additional epitopes on the SARS-CoV-2 spike protein. Grifoni says this is good news. By targeting many vulnerable sites on the spike protein, the immune system would still be able to fight infection, even if some sites on the virus change due to mutations.
"The immune response is broad enough to compensate for that," Grifoni says.
Since the announcement of the fast-spreading UK variant of SARS-CoV-2 (called SARS-CoV-2 VUI 202012/01), the researchers have compared the mutated sites on that virus to the epitopes they found. Sette notes that the mutations described in the UK variant for the spike protein affect only 8% of the epitopes recognized by CD4+ T cells in this study, while 92% of the responses is conserved.
CD4+ T lymphocytes get their nickname of helper T cells because they assist another type of immune system cell, the B lymphocyte (B cell), to respond to surface proteins -- antigens -- on viruses such as SARS-CoV-2. Activated by the CD4+ T cells, immature B cells become either plasma cells that produce antibodies to mark infected cells for disposal from the body or memory cells that "remember" the antigen's biochemical structure for a faster response to future infections. Therefore, a CD4+ T cell response can serve as a measure of how well the immune system responds to a vaccine and yields humoral immunity.
In their study, Blankson and colleagues found that the number of helper T cells recognizing SARS-CoV-2 spike proteins was extremely low prior to vaccination -- with a median of 2.7 spot-forming units (SFUs, the level of which is a measure of T cell frequency) per million peripheral blood mononuclear cells (PBMCs, identified as any blood cell with a round nucleus, including lymphocytes). Between 7 and 14 days after vaccination, the T cell frequency rose to a median of 237 SFUs per million PBMCs. At six months after vaccination, the level dropped slightly to a median of 122 SFUs per million PBMCs -- a T cell frequency still significantly higher than before vaccination.
The researchers also looked six months after vaccination at the ability of CD4+ T cells to recognize spike proteins atop the SARS-CoV-2 delta variant. They discovered the number of T cells recognizing the delta variant spike protein was not significantly different from that of T cells attuned to the original virus strain's protein.
Although the study was limited because of the small number of participants, Blankson feels it pinpoints areas that merit further research.
"The robust expansion of T cells in response to stimulation with spike proteins is certainly indicated, supporting the need for more study to show booster shots do successfully increase the frequency of SARS-CoV-2-specific T cells circulating in the blood," says Blankson. "The added bonus is finding that this response also is likely strong for the delta variant."
In lab studies working with live Omicron virus, the researchers showed that this variant still relies on the ACE2 receptor to infect human lung cells. That’s really good news. It means that the therapeutic tools already developed, including vaccines, should generally remain useful for combatting this new variant.
Once again, these data show that boosting the immune system after a pause produces enhanced immunity against new viral variants, even though the booster was designed from the original virus. Your immune system is awfully clever. You get both quantitative and qualitative benefits.
It’s also worth noting that the Omicron variant mostly doesn’t have mutations in portions of its genome that are the targets of other aspects of vaccine-induced immunity, including T cells. These cells are part of the body’s second line of defense and are generally harder for viruses to escape. While T cells can’t prevent infection, they help protect against more severe illness and death.
There is a growing concern that ongoing evolution of SARS-CoV-2 could lead to variants of concern (VOC) that are capable of avoiding some or all of the multi-faceted immune response generated by both prior infection or vaccination, with the recently described B.1.1.529 (Omicron) VOC being of particular interest. Peripheral blood mononuclear cell samples from PCR-confirmed, recovered COVID-19 convalescent patients (n=30) infected with SARS-CoV-2 in the United States collected in April and May 2020 who possessed at least one or more of six different HLA haplotypes were selected for examination of their anti-SARS-CoV-2 CD8+ T-cell responses using a multiplexed peptide-MHC tetramer staining approach. This analysis examined if the previously identified viral epitopes targeted by CD8+ T-cells in these individuals (n=52 distinct epitopes) are mutated in the newly described Omicron VOC (n=50 mutations). Within this population, only one low-prevalence epitope from the Spike protein restricted to two HLA alleles and found in 2/30 (7%) individuals contained a single amino acid change associated with the Omicron VOC. These data suggest that virtually all individuals with existing anti-SARS-CoV-2 CD8+ T-cell responses should recognize the Omicron VOC, and that SARS-CoV-2 has not evolved extensive T-cell escape mutations at this time.
Doctors in South Africa, where the variant was first detected, have said patients are reporting experiencing night sweats.