Type I interferon deficiency redirects antiviral immunity into NF-κB–driven inflammatory pathways, representing a maladaptive compensation that likely underlies the most common forms of virus-induced #immunopathology.
Type I interferon deficiency redirects antiviral immunity into NF-κB–driven inflammatory pathways, representing a maladaptive compensation that likely underlies the most common forms of virus-induced #immunopathology.
Source: Cell Reports, https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01251-8?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124724012518%3Fshowall%3Dtrue
Summary
The coronavirus disease 2019 (COVID-19) pandemic has reminded us of human infections with the H7N9 virus and has raised questions related to the clinical and molecular pathophysiological diversity between the two diseases. Here, we performed a proteomic approach on sera samples from patients with H7N9-virus or SARS-CoV-2-virus infection and healthy controls. Compared to SARS-CoV-2, H7N9-virus infection caused elevated neutrophil concentrations, T cell exhaustion, and increased cytokine/interleukin secretion. Cell-type deconvolution and temporal analysis revealed that T cells and neutrophils could regulate the core immunological trajectory and influence the prognosis of patients with severe H7N9-virus infection. Elevated tissue-enhanced proteins combined with alterations of clinical biochemical indexes suggested that H7N9 infection induced more severe inflammatory organ injury and dysfunction in the liver and intestine. Further mechanical analysis revealed that the high concentration of neutrophils might impact the intestinal enterocyte cells through cytokine-receptor interaction, leading to intestinal damage in patients with H7N9-virus infection.
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#aH7n9 #abstract #AVIANINFLUENZA #covid #COVID19 #health #immunopathology #research #sarsCov2 #vaccine
Influenza A viruses remain a global threat to human health, with continued pandemic potential. In this Review, we discuss our current understanding of the optimal immune responses that drive recovery from influenza virus infection, highlighting the fine balance between protective immune mechanisms a …
TANK-binding kinase-1 (TBK1) and its homologue IκB kinase-ε (IKKε) are critical in the induction of the interferon response and the response to infection by pathogens. Here the authors show that pharmacological targeting of TBK1 AND IKKε reduces the immunopathology seen in a murine model of SARS-COV-2 infection.
The immune responses to SARS CoV-2 infection in children are less well understood than in adults. Here the authors characterise immune responses to newer omicron lineages and relate these to previous infection with earlier lineages of SARS-CoV-2, implicating a reduced immunogenicity from omicron variants and imprinting from previous virus strains.
Nice little study this, using SNPs in CCL19 & CCL21 linked with higher levels of these chemokines associated with greater #COVID19 infection and mortality.
Wonder if there's a mechanism. Greater #Neutrophil chemotaxis 👉 tissue pathology?
#IDMastodon #MedMastodon #immunopathology #immunology
CCL19 (rs3136658) and CCL21 (rs2812377) variants are associated with susceptibility and related mortality of SARS-CoV-2 infection: a population-based correlation analysis
https://academic.oup.com/jid/advance-article/doi/10.1093/infdis/jiad032/7022103
Nisha Nayak, Abhijit Pati, Y Pavani, Sourav Sahu, Sudhanshu Ranjan, Aditya K Panda; CCL19 (rs3136658) and CCL21 (rs2812377) variants are associated with suscept
Infection with SARS-CoV-2 has been linked with substantive inflammation, lung pathology and development of COVID-19. Here the authors spatially associate CCL18 and CCL21 in distinct tissue niches with lung pathology of severe COVID-19.
Didn't make the title, but higher IL-6 concentration associated with higher risk of hospitalisation.
(cause or effect 🤔)
#IDMastodon #MedMastodon #immunology #immunopathology #virology #virus #RSV