The molecular microenvironment of coronaviral replicase complexes provides functional and spatial links between conserved cellular processes and viral RNA synthesis, and highlights potential targets for the development of novel antivirals.
Type-I interferon enriched microenvironment generated by Mycobacterium tuberculosis induces the Siglec-1 receptor expression in human macrophages, including on tunneling nanotubes, and contributes to the exacerbation of cell-to-cell transfer of HIV-1.
Animal studies of fatty liver disease over-estimate the benefit of drugs due to publication bias and are confounded by off-target weight loss, illustrating the challenge of successful translational across species.
A subset of EC/VCs have CD4+T cells with resistance specific to R5-tropic HIV infection associated with transcriptional down-regulation of ccr5, a phenotype that appears to be heritable, across multiple generations.
Signal-peptide cleavage of HIV-1 envelope glycoprotein is delayed because of alpha-helical structure covering the cleavage site, effecting early cleavage alters the folding pathway and resulting in localized misfolding and reduced viral fitness.