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A follow-up study of immune parameters in unvaccinated COVID-19 convalescents 10 weeks and 10 months after a first and mostly mild infection with the Wuhan-strain Hu-1 showed a long-term reduction of innate and adaptive immune cells, associated with a shift from Th1 to Th2 cytokine pattern.
This study identified a small peptide P3 in the S2 subunit of the SARS-CoV2 S protein with sequence homology to bacterial superantigens and the capacity to induce unexpected proliferation of T-cells.
These findings demonstrate that transfer of IgG from long COVID patients to mice replicates disease symptoms, underscoring a causative and heterogeneous role of IgG in the pathogenesis of long COVID.
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Immune modulation associated with exposure to Plasmodium falciparum may contribute to a reduced severity of SARS-CoV-2 infection among people living in malaria-endemic regions.
This study demonstrates diversity of intracellular microbes in immune cells of healthy individuals, SARS-CoV-2 positive patients, and COVID-19 recovered individuals.
Biological (immunological, virological and hormonal) features of long COVID syndrome more than one year after acute infection.
The findings suggest that higher levels of autoantibodies directed against specific chemokines are associated with favorable disease outcomes in COVID-19 convalescents.
Individuals with neuro-PASC had a distinct pattern of T cell activation and specific immune responses against the SARS-CoV-2 nucleocapsid (N) protein.
Unique monocyte signatures define subgroups of long COVID patients and confirm prolonged changes in innate immunity during COVID-19 convalescence. Given the heterogeneity of clinical presentations, it seems likely that distinct pathophysiological pathways cause different long COVID phenotypes
According to the authors, high levels of SARS-CoV-2 S protein genetic diversity in individuals with advanced poorly controlled HIV infection markedly increase the risk for the emergence of new VOCs in these individuals.
