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.
Compared with the approach isolating COVID-19 patients for a fixed period, the approach using repeated PCR testing mitigates unnecessarily lengthy isolation of patients while minimizing the risk of further transmission.
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.
Network propagation connects TWIST1 with epigenetic regulators CHD7, CHD8, and WHSC1, which collectively promote the bias toward neural crest while suppressing neural stem cell programmes, and subsequently enhance ectomesenchyme potential.
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.
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.