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RNA m6A level is dually regulated during RV infection and development, METTL3 deficiency in IECs results in increased resistance to rotaviral infection through reduced m6A modificaitons on Irf7.

Statistical analysis and LASSO regression modeling provide insights into pathogen-specific host response patterns in cerebrospinal fluid from different disease etiologies to support future classification of pathogen type based on host response patterns in meningitis.

A picorna-like virus promotes the accumulation of caspase-cleaved drosophila inhibitor of apoptosis 1 by inducing the degradation of NTAN1, a key N-end rule degradation pathway component, leading to apoptosis inhibition and viral replication enhancement.

When antiviral compounds target oligomeric assemblages, the formation of chimeric oligomers within cells can negate selection for naturally occurring drug-resistant variants.

Comprehensive analyses of how mutations in a picornavirus capsid affect viral fitness provide novel insights into viral biology, evolution, and host interactions.

Genetic and biochemical analyses identify a pathway important for infection by many picornaviruses.

Quasi-enveloped hepatitis A virions undergo clathrin-mediated endocytosis, followed by ALIX-dependent trafficking to lysosomes where the quasi-envelope is degraded, triggering uncoating of the RNA genome in association with lysosomal membrane rupture.

Characterisation of within-host diversity of SARS-CoV-2 provides insights into the mutational and selective mechanisms driving its evolution and has important implications for using within-host variation to inform transmission inference efforts.

RNA virus replication is attenuated by an intrinsic restriction mechanism after introducing CpG/UpA dinucleotides into both non-translated and coding regions of viral genomes, which may be exploited in the design of attenuated virus vaccines.

Evolution-guided functional analyses identify an activating adaptor of the dynein intracellular transportation machinery, NINL, as a novel component of the antiviral immune response and reveal a mechanism by which viruses antagonize NINL function in a species-specific manner.