COVID-19 caused profound epigenetic changes in the lungs of patients who died from the disease. Such alterations particularly affected genes related to hyperinflammation and fibrosis. 1/
In a new study, researchers analysed an extensive collection of lung autopsy samples from patients who died from COVID-19 and compared them with healthy lungs from people who died from other unrelated diseases. 2/
Comparison of the DNA between both groups showed epigenetic differences in more than 2,000 regulation points of the genetic material. 3/
A detailed analysis revealed that they were genetic sequences mainly associated with promoting a state of hyperinflammation, such as the overproduction of interferons and chemokines, chemical signals used by the immune system to promote inflammation. 4/
This study first time pinpoint specific DNA methylation events that might result in long-term complications.
Remodelling this DNA methylation landscape by epigenetic agents could potentially be a strategy to mitigate the fibrotic environment seen in longCovid cases. 5/
Importantly, since DNA methylation inhibitors are used in hematological malignancies, these agents could be considered to treat the severe disorder, as currently assessed on the first clinical trial of this type. 6/
Epigenetics is the control layer a cell uses to finely tune whether a gene will be active or not, without modifying its genetic information. Alterations in the epigenetic program of a cell can make it behave way different than expected. 7/7
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The Omicron variant is the most successful lineage to date as demonstrated by its rapid spread & dominance across the world. Its success was explained by the accumulation of RBD mutations in the binding footprint of the virus’s main entry host receptor, hACE2 1/
A new study based on analysis of of over 13 million SARS-CoV-2 genomes, collected over 3 years, revealed that during the first year of the pandemic, the SARS2 genome was subject to strong conservation, with only 3.6% of sites under diversifying pressure in RBD of the Spike 2/
However, a sharp increase in diversification of the RBD was observed during 2021 (8.1% of sites under diversifying pressure), indicating selective pressures that promote the accumulation of mutations. This period coincided with broad viral infection & vaccination worldwide. 3/
Like most other envelop glycoproteins, SARS-CoV-2 Spike undergoes multiple post-translational modifications, in particular S-acylation, which attaches a medium chain fatty acid via a thioester bond to cysteine residues in its cytoplasmic tail. 1/
Acylation has been shown to influence the lipid composition of the virions and to drastically enhance the fusogenic capacity of the produced viruses. The efficiency of Spike S-acylation is therefore determinant for infectivity. 2/
A new study finds that SARS-CoV-2 infection triggers a change in the transcriptional start site of the zdhhc20 gene, both in cells & in an in vivo infection model. 3/
Is it some specific entity post-SARS-CoV-2 infection? Or a non-specific post-viral phenomenon seen after recovery following any viral infection? Or something that some doctors refer “all in your head.” 1/
Another lingering question is whether long COVID and ME/CFS are the same thing. What makes long COVID distinct from ME/CFS, even when the symptoms are the same, is the presence of a specific virus and the knowledge of when the infection occurred. 2/
“Historically, we didn’t have the ability to pinpoint what infectious agent had caused a person’s ME/CFS. We could maybe see what antibodies a person had against different viruses, but we never knew exactly when the infectious event happened”. 3/
LongCovid is frequently present with neuropathic symptoms including numbness, paresthesias, etc consistent with small fiber neuropathy (SFN). Evidence suggests SFN may be the key pathological finding in LongCovid. 1/
A new study provides preliminary evidence that small fiber neuropathy (SFN) is responsive to treatment with IVIG. The SFN is linked with neurovascular dysregulation and dysautonomia. 2/
Many patients with LongCovid also have overlapping symptomatology with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and/or Postural Orthostatic Tachycardia Syndrome (POTS). Prior to the pandemic, ME/CFS and POTS have been linked to SFN. 3/
Why certain populations or communities are more susceptible to Covid19 than others?
Which changes in human and virus proteins may make someone more likely to catch COVID-19? 1/
A group of researchers predicted that some human genetic factors could influence susceptibility. They analysed missense coding variants in several SARS-CoV-2 proteins and its human protein interactors that could enhance binding affinity to SARS-CoV-2. 2/
They studied 468 missense variants from human proteins and 212 variants from SARS-CoV-2 proteins and computationally predicted their impacts on binding affinities to SARS-CoV-2 proteins. 3/
Another study explores SARS-CoV-2 impact on the cognition. We still don’t know whether cognitive decline emerges with the onset of COVID-19 and whether it is more pronounced in patients with #LingCovid or severe COVID-19. 1/
A longitudinal cohort study compared the cognitive performance of 276 patients with COVID-19 to that of 217 controls across 4 neuroinflammation or vascular disease-sensitive domains of cognition using data collected both before and after the pandemic starting in 2015. 2/
Longitudinal models indicated a significant decline in cognitive throughput following COVID-19, after adjustment for pre-COVID-19 functioning, demographics, and medical factors 3/