Which arm is crucial for viral clearance & protection against #SARSCoV2? 1/
Early on in the #pandemic questions arose regarding how #SARSCoV2 is cleared during acute/primary infection & what aspects of the #adaptive immune were necessary and sufficient for protection from repeat infection 2/
Using mouse models of SARSCoV2,@BenIsraelow Rt al demonstrate that both humoral and cellular adaptive immunity contributes to viral clearance in the setting of primary infection 3/
Either convalescent mice, or mice that receive #mRNA vaccination are protected from both homologous infection & infection with a VOC, B.1.351 4/
Additionally, they conclude that protection is largely mediated by antibody response and not cellular immunity, and highlight the in vivo protective capacity of antibodies generated to both vaccine & natural infection @VirusesImmunity@SaadOmer3 5/
Another study on Rhesus #Macaques finds that T cells play a role in the recovery from acute #SARSCoV2 infections, their depletion does not induce severe disease, & T cells do not account for the natural resistance of rhesus macaques to severe #COVID19@fitterhappierAJ 6/
Neither primed CD4+ or CD8+ T cells appeared critical for immunoglobulin class switching, the development of immunological memory or protection from a second infection 7/
CD4, CD8, & CD4/8 depletion in Macaques prior and during infection did not affect disease course and only mildy attenuated viral clearance! 8/
The debate continues.....Difficult to write-off the importance of T-cells. This virus is weird. Need more studies before we dump cellular arm. What we know, a harmony between the two is needed for a successful immune response! 9/
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A NEW study found that the SARS-CoV-2 nonstructural protein 15 (nsp15) helps the virus hide from the immune system in human lung and nasal cells. The nsp15 endoribonuclease is important in promoting virus replication and influencing disease severity. 1/
SARS2 variants lacking this activity exhibit impaired replication & cause milder disease, highlighting nsp15 as a key virulence factor. This underscores the importance of nsp15’s endoribonuclease activity in both promoting virus replication & influencing disease severity. 2/
The viral variants lacking nsp15 endoribonuclease activity elicited higher innate immune responses and exhibited reduced replication in human stem cell–derived lung alveolar type II epithelial cells, as well as in the lungs of infected hamsters. 3/
Researchers developed a 23-amino acid peptide that mimics ACE2 and effectively binds the SARS-CoV-2 spike protein, preventing viral entry. 1/
The peptide demonstrated potent antiviral activity against both the original and Omicron strains, with a therapeutic index greater than 20, indicating strong potential for therapeutic use. 2/
Moreover, future viruses from this family of coronaviruses may likely use ACE2 as their host cell receptor, as recently demonstrated in the MERS Virus of bats and, therefore, the ACE2 decoy therapeutic may have future applications as well. 3/
A NEW preprint found that submaximal exercise in people with #LongCOVID caused large microclots to fragment into smaller microclots and this then triggered increases in inflammatory and vascular injury markers. 1/
The breakdown of large microclots, rather than clearing them from circulation, was linked to reduced oxygen uptake and heightened inflammation. 2/
The data suggest that while the immune system tries to control inflammation caused by microclot fragmentation after physical exertion, its compensatory mechanisms are inadequate or failing. 3/
Globally, NB.1.8.1 is now the dominant variant. The WHO has issued a warning about rising COVID-19 activity in the Western Pacific, Southeast Asia, and Eastern Mediterranean, driven by NB.1.8.1 this week.
H/T: @RajlabN
Classified as a "variant under monitoring" by the WHO & “ Nimbus” by @TRyanGregory, NB.1.8.1 has triggered a seventh consecutive week of surges in Southeast Asia. Taiwan has seen ER visits double again this week. 2/
Researchers found that people with LongCOVID fatigue have damaged gut barriers & signs of immune activation.
Preexisting gastrointestinal symptoms before COVID infection predisposed people to developing LongCOVID fatigue. 1/
LongCOVID patients were found to have an increased LBP/sCD14 ratio & lower IL-33 levels, which indicates altered immune activation & a reduced intestinal barrier. In addition, there were increased IL-6 levels, which are considered a marker for systemic inflammation. 2/
LBP/sCD14 is the ratio of lipopolysaccharide binding protein to soluble CD14.
This study emphasizes the impact of SARS-CoV-2 infection on the gut, which might be associated with the onset of Fatigue seen in LongCovid patients. 3/
A new study from Germany found that intravenous administration of the SARS-CoV-2 spike protein in mice led to neuroinflammation and accumulation of alpha-synuclein in brain regions associated with Parkinson’s disease. 1/
Authors also discovered “sex-dependent alterations in astrocyte reactivity and parvalbumin-positive interneurons.” 2/
These findings suggest that exposure to the spike protein alone, without full viral infection, may contribute to neurodegenerative processes linked to Parkinson's, thus highlighting potential long-term neurological risks following COVID infection. 3/