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Vipin M. Vashishtha Profile picture
@vipintukur
Jul 25 • 6 tweets • 2 min read Twitter logo Read on Twitter
The evolution of SARS-CoV-2 has stunned the virologists & evolutionary biologists all over the world. It has even surpassed the hyper-mutability of the influenza’s H3N2 strain too!

In a new preprint, the evolution of the SARS2 Spike between Dec’23 & Feb’23 is analysed... 1/
To summarize the major lineages of SARS-CoV-2 & their Spike evolution during this period, a phylogenetic tree & median-joining network were reconstructed.

By the end of 2022, new variants such as BQ.1.1.10, BA.4.6.3, XBB, & CH.1.1, emerged with higher fitness than BA.5.
2/ Image
The phylogenetic tree of the spike DNA sequences revealed that the majority of variants belonged to three major lineages: BA.2 (BA.1.1.529.2), BA.5 (BA.1.1.529.5), and XBB. The median network showed that these lineages had at least six major diversifying centers. 3/ Image
The spike DNA sequences of these diversifying centers had the representative accession IDs (EPI_ISL_) of 16040256 (BN.1.2), 15970311 (BA.5), 16028739 (BA.5.11), 16028774 (BQ.1), 16027638 (BQ.1.1.23), and 16044705 (XBB.1.5). 4/
Selection analyses revealed 26 amino-acid sites under positive selection.

These sites included L5, V83, W152, G181, N185, V213, H245, Y248, D253, S255, S256, G257, R346, R408, K444, V445, G446, N450, L452, N460, F486, Q613, Q675, T883, P1162, and V1264. 5/
Continued surveillance and research are necessary to monitor the evolution and potential impact of these variants on public health. 6/

biorxiv.org/content/10.110…

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More from @vipintukur

Vipin M. Vashishtha Profile picture
Jul 24
Cortical thickness is altered in the brain structure of #LongCOVID patients with cognitive impairment!

A new study from Germany analyzed differences in cortical thickness between clinical subgroups based on 3T-MRI scans & signature inflammatory markers in n=120 participants 1/ Image
They studied 4 groups comprising healthy never-infected controls, healthy COVID survivors, & subgroups of long-COVID patients with and without cognitive impairment

Whole-brain comparison of cortical thickness between the 4 groups was conducted by surface-based morphometry. 2/
They identified distinct cortical areas w/ a progressive increase in thickness across diff groups, starting from healthy who had never been infected w/ COVID, followed by healthy COVID survivors, long-COVID patients w/out cognitive deficits & long-COVID w/ cognitive deficits. 3/ Image
Read 10 tweets
Vipin M. Vashishtha Profile picture
Jul 20
A recent study from Brazil shows that SARS-CoV-2 can infect liver cells i.e. hepatocytes, stimulating glucose production & leading to hyperglycemia in hospitalized patients, even if their blood sugar level was normal before they were admitted to hospital. 1/
The viral entry into liver cells is partially mediated by cooperation between the proteins GRP78 & ACE2. The latter, known to permit cell invasion by the virus throughout the body, is present on the surface of human liver cells in a LMW isoform instead of the regular one. 2/ Image
This is one of the researchers' novel findings. Previous studies suggested liver cells did not express ACE2. Hyperglycemia is a prevalent complication in hospitalized COVID patients that occurs regardless of their diabetes history & is associated with a worse clinical outcome 3/
Read 6 tweets
Vipin M. Vashishtha Profile picture
Jul 17
What’s going on in the brains of COVID-19 patients?

There is a long list of issues : cognitive decline, changes in brain size & structure, depression, suicidal thinking, tremors, seizures, memory loss, & new dementia have all been linked to previous SARS2 infections. 1/
In some cases, these long-term problems occur even in patients w/ relatively mild COVID-19

But, the key issue that’s still unresolved is whether the SARS-CoV-2 was entering the brain & causing damage directly, or triggering an immune response that led to brain changes? 2/
Early in the pandemic, researchers didn’t find the SARS-CoV-2 virus in the brains—but they did find significant damage to their blood vessels, which were coated with antibodies. 3/
Read 8 tweets
Vipin M. Vashishtha Profile picture
Jul 13
The precise mechanisms involved in severe COVID-19 pneumonia are unknown. A new study showed that interleukin-10 (IL-10) induced the expression of ACE2 in normal alveolar macrophages, causing them to become vectors for SARS-CoV-2. 1/
The inhibition of this system in hamster models attenuated SARS-CoV-2 pathogenicity.

They identified a IFNAR2-IL10RB readthrough transcript, COVID-19 infectivity-enhancing dual receptor (CiDRE), which was highly expressed in patients w/ COVID risk variants at IFNAR2 locus 2/ Image
CiDRE exerted synergistic effects via the IL-10-ACE2 axis in alveolar macrophages and functioned as a decoy receptor for type I interferons. 3/
Read 5 tweets
Vipin M. Vashishtha Profile picture
Jul 11
A new study demonstrates the host response to COVID-19 infection in the nasopharynx, highlighting that severe COVID-19 is a double-defect disease, requiring first a defective early control of the virus mainly through the two mechanisms…….1/
1) IFN-I depletion via aberrant STAT1 signaling, retinol metabolism, NRF2 antioxidant system, and dysregulated glucocorticoid and RAAS signaling 2/
2) an impaired ability to control proinflammatory responses by hyperactivating the host innate immunological pathways through neutrophil activation and degranulation, interleukin production and platelet aggregation. 3/
Read 5 tweets
Vipin M. Vashishtha Profile picture
Jul 10
The gastrointestinal tract can be heavily infected by SARS-CoV-2. Being an auto-immunogenic virus, SARS2 represents an environmental factor that might play a role in gut-associated autoimmune diseases (ADs). 1/
However, molecular mimicry between the virus and the intestinal epitopes is under-investigated. 2/
A new study elucidated sequence similarity between viral antigens & human enteric sequences, based on known cross-reactivity. SARS2 epitopes that cross-react w/ human gut antigens were explored & sequence alignment was performed against self-antigens implicated in enteric ADs 3/
Read 8 tweets

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