The virus - Cardioderma cor coronavirus (CcCoV) KY43, or CcCoV-KY43 - can bind to a receptor cell found in the human lung, but testing in Kenya suggests it has not spilled over into the local human population.

  • dgdft@lemmy.world
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    8 days ago

    I was curious too and found this review article that covered the topic pretty well:

    https://pmc.ncbi.nlm.nih.gov/articles/PMC12230189/#mbt270190-sec-0020

    Selected immunity genes included a B‐cell chemokine, interleukins involved in immune system regulation and NF‐κB activation and genes involved in responses to pathogens. Gene losses comprised pro‐inflammatory interleukins that induce the canonical NF‐κB pathway and other pro‐inflammatory cytokines. Within gene gains, an expansion of the APOBEC gene family was most notable; these genes encode DNA‐ and RNA‐editing enzymes that are implicated in restricting viral infection and transposon activity. Interestingly, the smaller genome size of bats was related to a lower transposable element content. The authors concluded that bats had evolved immunomodulatory mechanisms that enabled a higher tolerance to pathogens than is typical among mammals.

    So translated: Rather than firing off huge waves of new antibody variants trying to find one that’ll latch onto the virus, and cranking up the body temp to flush viral pathogens out completely like most mammals would, they make proteins that limit the rate that the virus can propagate into fresh cells.