Xiaobo Lei

TL;DR: It is shown that the SARS-CoV-2 spike protein is less stable than that of SARS -CoV, and limited cross-neutralization activities between SARS and COVID-19 patients’ sera showlimited cross- neutralization activities, suggesting that recovery from one infection might not protect against the other.

TL;DR: This study shows that Sars-CoV-2 perturbs host innate immune response via both its structural and nonstructural proteins, and thus provides insights into the pathogenesis of SARS-Cov-2.

TL;DR: It is shown that EV71 inhibits anti-viral type I interferon (IFN) responses by targeting the mitochondrial anti-Viral signaling (MAVS) protein—a unique adaptor molecule activated upon retinoic acid induced gene-I and melanoma differentiation associated gene (MDA-5) viral recognition receptor signaling—upstream of type Iinterferon production.

TL;DR: Results suggest that inhibition of RIG-I-mediated type I IFN responses by the 3C protein may contribute to the pathogenesis of EV71 infection.

TL;DR: It is reported that EV71 inhibits the induction of innate immunity by Toll-like receptor 3 (TLR3) via a distinct mechanism that downregulates a TRIF, TIR domain-containing adaptor inducing beta interferon (IFN-β) and induces TRIF cleavage in the presence of Z-VAD-FMK, a caspase inhibitor.