2) This study revealed the genetic adaptation of avian influenza A(H7N9) virus during human infections through deep sequencing of virus samples from infected patients and their surrounding poultry/environment.
It It addressed the key role of the gene PB2 also present in H5N1.
3) It found differing patterns of substitutions at the PB2-627 position between patient and poultry/environment samples, indicating dynamic host adaptation ("genetic tuning") of H7N9 occurring in humans during infection.
4) Patient samples showed mixed ratios of mammalian (Lys) and avian (Glu) signatures at PB2-627, while poultry/environment samples were dominated by the avian signature.
Longitudinal samples from one patient demonstrated gradual replacement of avian Glu by mammalian Lys ...
5) ... at PB2-627 over the course of infection.
Rapid adaptation of PB2-627 Lys in deceased patients correlated with disease severity and outcome, suggesting a link between viral pathogenesis and host adaptation.
6) A dominant PB2-627 Val emergence in viruses from seven patients in Shenzhen also correlated with disease severity indicators.
PB2-701 substitutions differed between human/poultry, with avian Asp dominant in all specimens and no dominant emergence of mammalian Asn.
7) The findings demonstrate dynamic in vivo genetic tuning of H7N9 during human infection and its association with viral pathogenesis.
This dynamic adaptation process may impact influenza virus evolution and virulence.
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WHY is it IMPOSSIBLE to COMPLETELY ELIMINATE the SARS-CoV-2 virus?
What causes the virus or its remnants to linger in our bodies even after a mild or asymptomatic infection?
(1st part : "The persistence")
This discussion will address these questions through multiple threads...
2) ...drawing from a wealth of published research due to the intricacy of the topic.
To start, weโll present a concise overview of five key studies that demonstrate the virus's persistence for weeks or even months following infection.
"Now this is not the end. It is not even the beginning of the end" (Winston Churchill)
This study shows that the Sarbecoviruses have the capacity to generate new variants rapidly, with RBD of two novel viral groups exhibiting high similarity to SARS-CoV-2 biorxiv.org/content/10.110โฆ
2) Over 3 years, researchers sampled 1,462 bats in Cambodia Steung Treng province, identifying extensive and diverse coronaviruses co-circulation. Using metatranscriptomic and amplicon sequencing, they generated 33 complete sarbecovirus genomes.
4) This study suggests that the viral family of Sarbecoviruses can reserve some unpleasant surprises, and quite rapidly:
โถ๏ธ They emphasize the "significant pandemic threat" posed by the genetic diversity and evolutionary dynamics of circulating bat coronaviruses.
Doctor, I'm confused ๐ค
I have a high level of antibodies, yet I'm still experiencing long COVID. Why is that?
"The ANTIBODIES PARADOX in LONG COVID Condition: Unraveling the Disconnect Between Humoral Immunity and Chronic Illness" nature.com/articles/s4146โฆ
2) The finding in this study of persistently higher anti-N antibody levels in people with Post-Covid Condition (PCC) compared to those with acute infection only, does seem paradoxical at first glance.
3) A few points on this:
โถ๏ธ The study suggests this may indicate "altered immune activation or viral persistence" in people with PCC, rather than just a stronger antibody response per se.
2) T-cells are like the superheroes of our immune system - they work hard to protect us from germs and viruses.
When a virus like SARS-COV-2 gets into our body, the T cells spring into action. There are different types of T cells, each with a special job to do.
3) - Some T cells are like the fighters, killing off the virus-infected cells.
- Other T cells are the coordinators, telling the other immune cells what to do.
- There are also T cells that act like the police, making sure the immune response doesn't go overboard.
2) The most important immune components in the nasal tissue for fighting COVID-19 are:
โถ๏ธ Monocytes and neutrophils
- These immune cells moved into the area under the nose lining during active COVID-19 infection and helped protect the underlying lymphoid tissue.
3)โถ๏ธ Macrophages
- As people recovered from COVID-19, macrophages started to help repair the nasal tissue.
โถ๏ธ Germinal centers and B cells
- The specialized germinal center structures in the nose contained active B cells that were producing antibodies against the COVID-19 virus
How SARS-COV-2 spreads (Re) and why there are differences between countries ?
An explanation for kids based on the astonishing new study of @firefoxx66 @richardneher and colleagues pubmed.ncbi.nlm.nih.gov/40233303/
2) With a really fast-spreading virus going around, like the one that causes COVID-19, when someone gets sick, they can pass the virus to other people. But some sick people end up spreading it to a lot more people than others.
2) The scientists in this study wanted to figure out how the virus is spreading and how much it's spreading from person to person. To do this, they looked at the genetic code, or the "DNA", of the virus.
Whenever the virus infects someone new, it can change a little bit.