2) We posted a first study few weeks ago about how inflammation can trigger lasting phenotypes in immune and non-immune cells.
This article of NIH proposes a short but clear summary. covid19.nih.gov/news-and-stori…
3) "Researchers found that severe COVID-19 could cause lasting changes in stem cell gene expression that made the immune system produce more white blood cells"
Reference of this first study :
4) Then there was another study about the efficiency of the vaccination. cell.com/immunity/fullt…
5) Except for the subject of vaccination, there was a very jnteresting passage in this study:
"The deterioration of CD8+ T cell function is seen in patients with active viral infections that had been either eliminated, in the case of HCV or greatly reduced (HIV)...
6) This dysfunction persists for a year or more after the active phase of infection, suggesting lasting damage, despite the absence or near absence of the relevant virus. In this context, it may be that these attenuated CD8+ T cell responses contribute to long COVID ...
7) ... perhaps rendering patients unable to respond robustly to subsequent infections by SARS-CoV-2 variants or other pathogens."
While many of you know that the virus damages the immune system, there is still much to do, to convince the majority of people to protect themselves.
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What means "Epigenetic reprogramming of monocytes" and its consequences for long COVID ? (layman terms) frontiersin.org/articles/10.33…
2) SARS-CoV-2 infection can induce significant changes in the epigenetic landscape of monocytes. These changes can impact the expression of genes involved in immune responses, inflammation, and antiviral defense mechanisms.
Epigenetic modifications can alter the accessibility...
3) of genes involved in interferon signaling, resulting in impaired antiviral responses in monocytes.
Additionally, SARS-CoV-2 infection can lead to the activation of inflammatory pathways in monocytes, contributing to the cytokine storm observed in severe COVID-19 cases.
COVID-19 and the ACCUMULATION of so-called SENESCENTS cells ("ZOMBIE" cells) 😨
2 recent studies shed interesting light on this subject.
Fig. Immunosenescence and inflammaging : partners in the COVID-19 crime
2) In humans, viral replication and pathology increase with age.
“We found Covid-19 accelerates the presence of ‘zombie’ or senescent cells, which accumulate naturally and gradually in the brain as we get older,” found researchers.
3) 1st STUDY :
"Removal of senescent cells reduces the viral load and attenuates pulmonary and systemic inflammation in SARS-CoV-2-infected, aged hamsters" nature.com/articles/s4358…
3) The study :
"FcγR-mediated SARS-CoV-2 infection of monocytes activates inflammation"
First a short explanation on pyroptosis (for layman) :
Pyroptosis is a highly inflammatory form of cell death that leads to the release of pro-inflammatory cytokines nature.com/articles/s4158…
This mega-thread is an attempt to respond to the request of certain followers.
It was difficult to find interesting studies, due to the abandonment of testing policies, with the sole aim of covering up the pandemic.
2) One of the most interesting study :
"Testing at scale during the COVID-19 pandemic"
"Even the most extensive testing schemes have been found to miss many infectious individuals and to provide only partial population coverage." nature.com/articles/s4157…
3) "The rapid infectious course of SARS-CoV-2 and the possibility of its transmission by presymptomatic or asymptomatic individuals blunts the impact of population-scale testing, as many infectious individuals escape detection"
SARS-CoV-2 viral PERSISTENCE in lung alveolar MACROPHAGES is controlled by IFN-γ and NK cells
"Our findings reveal an interplay between NK cells and macrophages that regulated SARS-CoV-2 persistence in macrophages and was mediated by IFN-γ" nature.com/articles/s4159…
2) Fig. 2: SARS-CoV-2 is expressed in BALF Mac (Bronchioalveolar lavage Macrophages) from WTM and OM at more than 221 d p.i.
3) Fig. 3: SARS-CoV-2 replication in Mac in vitro alters Mac transcriptomic profile.