Covid 19

You’d think it would be obvious to him…..

 

The Mu variant, also known as lineage B.1.621 or VUI-21JUL-1, is one of the variants of SARS-CoV-2, the virus that causes COVID-19. It was first detected in Colombia in January 2021 and was designated by the WHO as a variant of interest on August 30, 2021.[1] The WHO said the variant has mutations that indicate a risk of resistance to vaccines and stressed that further studies were needed to better understand it.[2] Outbreaks of the Mu variant were reported in South America and Europe.[3] The lineage B.1.621 has a sublineage, labeled B.1.621.1 under the PANGO nomenclature, which has already been detected in more than 20 countries worldwide.[4]

Under the simplified naming scheme proposed by the World Health Organization, B.1.621 was labeled "Mu variant", and was considered a variant of interest (VOI), but not yet a variant of concern.[1]

 

Okay, so again, you’re not including any context to this unsourced quote. It’s already stated that the Mu variant is a “variant of interest”, not a “variant of concern”, so is this just aggressive posting on your part, like a dump and run? What is your actual POINT, or don’t you have one?

 

It appears that you’re trying to state (without bothering to engage anyone in a discussion, which is pretty chicken!) that “variants will come up, and there’s nothing that can be done about it”, but you’re wrong.

 

You do realize that each one of those links is to a source right? There is literally 4 different sources linked there.

1. "Tracking SARS-CoV-2 variants". who.int. World Health Organization. Retrieved September 1, 2021.
2. ^ "WHO monitoring new coronavirus variant named 'Mu'". france24.com. September 1, 2021. Retrieved September 1, 2021.
3. ^ Jump up to:a b "Why Has WHO Designated 'Mu' A Variant Of Concern? Find Out All About It". ndtv.com. September 1, 2021. Retrieved September 1, 2021.
4. ^ "Lineage B.1.621.1". cov-lineages.org. Retrieved September 1, 2021.
5. ^ "Mu COVID variant: All you need to know about the new UK coronavirus strain". BBC Science Focus Magazine. Retrieved 2021-09-01.
6. ^ "Variants: distribution of cases data". gov.uk. Government Digital Service. Retrieved September 1, 2021.
7. ^ Jump up to:a b c "Mu Lineage Report". outbreak.info. Retrieved September 1, 2021.
8. ^ "Mu COVID variant: All you need to know about the new UK coronavirus strain". BBC Science Focus Magazine. Retrieved 2021-09-01.
9. ^ "SARS-CoV-2 variants - Stanford Coronavirus Antiviral & Resistance Database". covdb.stanford.edu. Stanford University Coronavirus Antiviral & Resistance Database. Retrieved September 1, 2021.
10. ^ "Japan confirms first cases of mu variant of COVID-19". thebharatexpressnews.com. September 2, 2021. Retrieved September 2, 2021.
11. ^ "B.1.621.1 Lineage Report". outbreak.info. Retrieved September 2, 2021.

This post was supposed to be about COVID related news, that is what the point of the post was. To post the most recent news about COVID. If you check the dates on the sources, they are all within the last 48 hours or so.

 

Interesting info about people that may be immune to COVID before the virus even existed.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7237901/

Importantly, we detected SARS-CoV-2-reactive CD4+ T cells in ∼40%–60% of unexposed individuals, suggesting cross-reactive T cell recognition between circulating “common cold” coronaviruses and SARS-CoV-2.

 

Since you haven’t bothered to contextualize your content in any way, it does not relate to any particular discussion. Based on the content of your prior posts, a reader can only DEDUCE what you are trying to say, so in other words, your post fails to convey or interpret any real meaning. It’s already been stated that the Mu variant is one of many variants out there that have evolved from the original virus. It’s interesting, for sure, but what are you trying to say? At this point, I think you’re actually AFRAID to contextualize your content.
(I couldn’t help but notice the sarcasm in your post, drawing my attention to the fact that your quotes contained “current information”.) All well and good, but without context, most readers would not understand if you are trying to initiate a discussion about variants, or just throwing out quotes for the sake of throwing out quotes.

 

Well, there’s some context here now, so that’s always helpful.

 

Jesse, I would love to discuss the particulars of this study with you. Where did you find it?

 

None of which was the ORIGINAL source for the quote though was it? Many unverified sources, such as Wikipedia, will supposedly link to other sources although the conclusions are not actually within those sources. Those links are often to other references within the same source. Given that Wikipedia can be edited by anyone the potential for quality data resides with the links to external sources.

If you check the footnotes, the data was RETRIEVED recently not that the data is that recent. There is a HUGE difference and one any researcher would avoid like the plague and only reference the real articles.

Variants of concern or under investigation: data up to 19 May 2021

 

Discussion
There is a critical need for foundational knowledge about T cell responses to SARS-CoV-2. Here, we report functional validation of predicted epitopes when arranged in epitope MPs, utilizing PBMCs derived from convalescing COVID-19 cases. The experiments also used protein-specific peptide pools to determine which SARS-CoV-2 proteins are the predominant targets of human SARS-CoV-2-specific CD4+ and CD8+ T cells generated during COVID-19 disease. Importantly, we utilized the exact same series of experimental techniques with blood samples from healthy control donors (PBMCs collected in the 2015–2018 time frame), and substantial cross-reactive coronavirus T cell memory was observed.

Our results demonstrate that the epitope MPs are reagents well suited to analyze and detect SARS-CoV-2-specific T cell responses with limited sample material. We also developed and tested peptide pools corresponding to each of the 25 proteins encoded in the SARS-CoV-2 genome. Data from both the epitope MPs and protein peptide pool experiments can be interpreted in the context of previously reported T cell response immunodominance patterns observed for other coronaviruses, particularly the SARS and MERS viruses, which have been studied in humans, HLA-transgenic mice, wild-type mice, and other species. In the case of CD4+ T cell responses, data for other coronaviruses found that spike accounted for nearly two-thirds of reported CD4+ T cell reactivity, with N and M accounting for limited reactivity, and no reactivity in one large study of human SARS-CoV-1 responses (Li et al., 2008). Our SARS-CoV-2 data reveal that the pattern of immunodominance in COVID-19 is different. In particular, M, spike, and N proteins were clearly co-dominant, each recognized by 100% of COVID-19 cases studied here. Significant CD4+ T cell responses were also directed against nsp3, nsp4, ORF3s, ORF7a, nsp12, and ORF8. These data suggest that a candidate COVID-19 vaccine consisting only of SARS-CoV-2 spike would be capable of eliciting SARS-CoV-2-specific CD4+ T cell responses of similar representation to that of natural COVID-19 disease, but the data also indicate that there are many potential CD4+ T cell targets in SARS-CoV-2, and inclusion of additional SARS-CoV-2 structural antigens such as M and N would better mimic the natural SARS-CoV-2-specific CD4+ T cell response observed in mild to moderate COVID-19 disease.

Regarding SARS-CoV-2 CD8+ T cell responses, the pattern of immunodominance found here differed from the literature for other coronaviruses. However, stringent comparisons are not possible, as some earlier studies were not similarly comprehensive and did not utilize the same experimental strategy. The spike protein was a target of human SARS-CoV-2 CD8+ T cell responses, but it is not dominant. SARS-CoV-2 M was just as strongly recognized, and significant reactivity was noted for other antigens, mostly nsp6, ORF3a, and N, which comprised nearly 50% of the total CD8+ T cell response, on average. Thus, these data indicate that candidate COVID-19 vaccines endeavoring to elicit CD8+ T cell responses against the spike protein will be eliciting a relatively narrow CD8+ T cell response compared to the natural CD8+ T cell response observed in mild to moderate COVID-19 disease. An optimal vaccine CD8+ T cell response to SARS-CoV-2 might benefit from additional class I epitopes, such as the ones derived from the M, nsp6, ORF3a, and/or N.

There have been concerns regarding vaccine enhancement of disease by certain candidate COVID-19 vaccine approaches, via antibody-dependent enhancement (ADE) or development of a TH2 responses (Peeples, 2020). Herein, we saw predominant TH1 responses in convalescing COVID-19 cases, with little to no TH2 cytokines. Clearly more studies are required, but the data here appear to predominantly represent a classic TH1 response to SARS-CoV-2.

While it was important to identify antigen-specific T cell responses in COVID-19 cases, it is also of great interest to understand whether cross-reactive immunity exists between coronaviruses to any degree. A key step in developing that understanding is to examine antigen-specific CD4+ and CD8+ T cells in COVID-19 cases and in unexposed healthy controls, utilizing the exact same antigens and series of experimental techniques. CD4+ T cell responses were detected in 40%–60% of unexposed individuals. This may be reflective of some degree of cross-reactive, preexisting immunity to SARS-CoV-2 in some, but not all, individuals. Whether this immunity is relevant in influencing clinical outcomes is unknown—and cannot be known without T cell measurements before and after SARS-CoV-2 infection of individuals—but it is tempting to speculate that the cross-reactive CD4+ T cells may be of value in protective immunity, based on SARS mouse models (Zhao et al., 2016). Clear identification of the cross-reactive peptides, and their sequence homology relation to other coronaviruses, requires deconvolution of the positive peptide pools, which is not feasible with the cell numbers presently available, and time frame of the present study.

Regarding the value of cross-reactive T cells, influenza (flu) immunology in relationship to pandemics may be instructive. In the context of the 2009 H1N1 influenza pandemic, preexisting T cell immunity existed in the adult population, which focused on the more conserved internal influenza viral proteins (Greenbaum et al., 2009). The presence of cross-reactive T cells was found to correlate with less severe disease (Sridhar et al., 2013, Wilkinson et al., 2012). The frequent availability of cross-reactive memory T cell responses might have been one factor contributing to the lesser severity of the H1N1 flu pandemic (Hancock et al., 2009). Cross-reactive immunity to influenza strains has been modeled to be a critical influencer of susceptibility to newly emerging, potentially pandemic, influenza strains (Gostic et al., 2016). Given the severity of the ongoing COVID-19 pandemic, it has been modeled that any degree of cross-protective coronavirus immunity in the population could have a very substantial impact on the overall course of the pandemic, and the dynamics of the epidemiology for years to come (Kissler et al., 2020).

Limitations and Future Directions
Caveats of this study include the sample size and the focus on non-hospitalized COVID-19 cases. Sample size was limited by expediency. The focus on non-hospitalized cases of COVID-19 is a strength, in that these donors had uncomplicated disease of moderate duration, and thus it was encouraging that substantial CD4+ T cell and antibody responses were detected in all cases, and CD8+ T cell responses in the majority of cases. Complementing these data with MP T cell data from acute patients and patients with complicated disease course will also be of clear value, as will studies on the longevity of SARS-CoV-2 immunological memory. Additionally, lack of detailed information on common cold history or matched blood samples pre-exposure to SARS-CoV-2 prevents conclusions regarding the abundance of cross-reactive coronavirus T cells before exposure to SARS-CoV-2 and any potential protective efficacy of such cells. Finally, full epitope mapping in the future will add important detailed resolution of the human coronavirus-specific T cell responses.

In sum, we measured SARS-CoV-2-specific CD4+ and CD8+ T cells responses in COVID-19 cases. Using multiple experimental approaches, SARS-CoV-2-specific CD4+ T cell and antibody responses were observed in all COVID-19 cases, and CD8+ T cell responses were observed in most. Importantly, pre-existing SARS-CoV-2-cross-reactive T cell responses were observed in healthy donors, indicating some potential for pre-existing immunity in the human population. ORF mapping of T cell specificities revealed valuable targets for incorporation in candidate vaccine development and revealed distinct specificity patterns between COVID-19 cases and unexposed healthy controls.

 

But not much impact outside of speculation at this point.

 

https://www.bbc.com/news/health-584...ADs756UH35rTH_WLiQ_q6xc_OOEJJ8KSQY9sEYR1QfErE

Coronavirus vaccines cut risk of long Covid, study finds

By Smitha Mundasad
Health reporter

Being fully vaccinated against Covid-19 not only cuts the risk of catching it, but also of an infection turning into long Covid, research led by King's College London suggests.

It shows that in the minority of people who get Covid despite two jabs, the odds of developing symptoms lasting longer than four weeks are cut by 50%.

This is compared with people who are not vaccinated.

So far, 78.9% of over-16s in the UK have had two doses of a Covid vaccine.

Many people who get Covid recover within four weeks but some have symptoms that continue or develop for weeks and months after the initial infection - sometimes known as long Covid. It can happen after people experience even mild coronavirus symptoms.

The researchers, whose work was published in The Lancet Infectious Diseases, say it is clear that vaccinations are saving lives and preventing serious illness, but the impact of vaccines on developing long-lasting illness has been less certain.

They analysed data gathered from the UK Zoe Covid Study app, which tracks people's self-reported symptoms and vaccines and tests.

That meant that between December 2020 and July, the health was tracked of more than 1.2 million adults who received one coronavirus jab and 971,504 who received two jabs in that time frame.

• Just 0.2% of double-jabbed people said they had had a Covid infection after vaccination (2,370 cases)
• Of the 592 fully vaccinated people with Covid who continued to provide data for more than a month, 31 (5%) went on to get long Covid (defined as illness lasting 28 days or more after a positive test)
• In the unvaccinated group this figure was about 11%

Researchers found some people were more at risk of so-called breakthrough infections (getting Covid after a vaccine) than others - including frail, older adults and people living in deprived areas. This was particularly the case for people who had only had one jab.

 

Now for some real world data. My wife had a doctor's appointment today. Her last to this specialist because the doctor is leaving the group. The reason for her leaving was that she has two small children who cannot be vaccinated and with this new surge she just cannot deal with the thought of threatening the health and lives of her children. She weathered the first and second surges, but now there is no reason she can see to stay in the medical field while stupidity reigns. During the visit today two groups came into the office without masks, although there are mask requirements in the county, the medical facility, and the office in particular with multiple signs pointing out these facts. The people finally relented and put on masks once they were told they would have to leave otherwise. The doctor pointed out this alone could have caused an infection that could be taken home to her children and that it happens multiple times a day. She may return to medical practice if there is a positive turn in the pandemic, but in her experience that is not likely given the attitude of those people refusing to follow the basic protocols. As a result, my wife has to find another specialist who will also be approached by others needing care that would have been provided by this doctor.

 

Well, I see that Jesse has not disclosed where he got that report from. I also notice that it was published on June 25, 2020, when little was known about the original SAR-CoV-2. The truncated quote that he has used “suggesting cross-reactive T-cell recognition between circulating “common cold” coronaviruses and SARS-CoV-2” is a quote that is taken completely out of context. This published report is not, in any way, equating SARS-CoV-2 to the “common cold”, as that quote may suggest when it is taken out of context, nor is it saying that a person’s immune system can act as a “preventative”, or even a “prophylactic” agent against Covid infection. The Abstract section of the report clearly states that the researchers are:

“Understanding adaptive immunity to SARS-CoV-2 (which) is important for vaccine development, interpreting Coronavirus disease 2019 (COVID-19) pathogenesis, and calibration of pandemic control measures.”

Also, because the virus was new to us last year, in terms of what the researchers knew at the time, and because there wasn’t enough supporting data, the researchers needed to use earlier data and research from a MERS and SARS outbreak in China which occurred in 2003. I imagine that this is just another report that found its way online, and was taken out of context to support an online, MONETIZED website. So, again, if you’re going to post material from a report that was taken out of context, at least READ THE ENTIRE REPORT to understand what it says. Here are pages from that June 2020 report that you posted that explains the reasons for the research which concerned aiding vaccine development:

 

https://www.msn.com/en-us/health/me...hrough-covid-cases/ar-AANZMnz?ocid=uxbndlbing



New study reveals rate of "breakthrough" COVID cases
Tucker Reals

London — A study conducted in the U.K. offers some of the first large-scale, real-world data on how well vaccination protects people against catching a "breakthrough" COVID-19 infection, and how well it protects breakthrough patients from becoming seriously ill. The results are encouraging.

The peer-reviewed study published Wednesday in The Lancet medical journal will help policy makers and epidemiologists fill in a significant gap in the understanding of the true efficacy of three of the major vaccines being used worldwide.

The U.S. Centers for Disease Control and Prevention, for instance, doesn't have good data on how many people catch COVID-19 after being vaccinated, as it decided in the spring to track only serious, symptomatic breakthrough cases. The British study, on the other hand, used mass-testing data to determine how many breakthrough cases there actually are and how sick those people get.

The vaccines were never intended to prevent infections completely, but to reduce the rates of infection within a population and, most importantly, to reduce the severity of illness in people who do catch it. The study found that people who contracted the coronavirus despite being fully vaccinated were almost twice as likely to have no symptoms at all, compared to the wider population.

Crucially, the odds of a fully-vaccinated person who does catch COIVD-19 ending up hospitalized with severe symptoms were reduced by more than two-thirds compared to an unvaccinated coronavirus patient. The survey also found that the risk of breakthrough patients suffering from long-COVID, with symptoms lasting more than a month, were cut in half by full vaccination.

It's the latest dataset to offer convincing evidence that the vaccines work as intended.

 

Woman gets arrested for fake vaccination card and misspells “Moderna” as “Maderna”.

 

“We wanted to help people
We were smart and driven
We loved science and physiology, humans and disease
So we made a commitment
We signed up
It was an honor

We read thousands of pages
Attended hundreds of lectures
Pulled all-nighters
Took more exams than we thought possible
Finals week felt insurmountable
But it didn’t break us
It made us stronger
We learned statistics and biochemistry
Immunology and pathophysiology
We mastered genetics, virology and pharmacology
We read scientific papers and learned how to dissect them
Papers, not videos
It was an honor

We came running when you needed us
Literally, running down the hallway
To the ICU, the trauma bay, labor and delivery
I need help, you said
We can help, we said
It was an honor

There were moments that we thought would break us
Moments that drove us to journaling, to therapy, to nightmares
Broken babies.
Paralyzed children.
Dead pregnant mothers with three kids at home.
The wail of a mother whose son just died.
We bent but we did not break
We returned because you needed us
And we could help
It was an honor

Then there was fear
Fear of walking into our place of work
Fear that we’d be killed by going to work
Fear that we’d kill a loved one because of our work
There were tears and sleepless nights and anti-anxiety medications
But you banged your pots and pans
You sent us pizzas and called us heroes
You needed us
We could help
So we wore our masks, and our gowns, and our gloves, and our goggles
We decontaminated ourselves before going home and isolated ourselves from our families
We almost broke
It was an honor

How quickly the joy turned to defeat
Elation to rage
You’ve learned to do your own research now
You know better than we do
Gaslighting is your language
Your selfishness is astounding
You don’t want our help when we ask you to stay healthy
Yet you arrive at our doors begging for help at the end
You stole our resources
You hobbled our ability to help those who did what they were supposed to do
You killed our patients by filling our beds and using up our ventilators
We can’t help any more
You broke us
There is no more honor”
- Anonymous