Rabbit Anti-Human CCR5 monoclonal antibody, clone 3I25M20

The long noncoding RNA (lncRNA), which could bind to target DNA, RNA, or protein, plays a vital role in the pathogenesis of viral replication and disease progression. Exploring how lncRNA regulates HIV infection is crucial for studying the pathogenesis, disease progression, and effective treatment of AIDS. Recently, Kulkarniet al.convincingly provided a molecular basis for association between CCR5AS lncRNA and outcome of HIV infection. Such results open a new avenue for the treatment and prevention of viral infections. In this study, we retell this story for a broad audience about how a new lncRNA enhances HIV-1 infection in easy-to-understand and jargon-free language.

Single-cell analysis of COVID-19 patient samples identifies activated immune pathways that correlate with severe disease. To investigate the immune response and mechanisms associated with severe coronavirus disease 2019 (COVID-19), we performed single-cell RNA sequencing on nasopharyngeal and bronchial samples from 19 clinically well-characterized patients with moderate or critical disease and from five healthy controls. We identified airway epithelial cell types and states vulnerable to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In patients with COVID-19, epithelial cells showed an average three-fold increase in expression of the SARS-CoV-2 entry receptorACE2, which correlated with interferon signals by immune cells. Compared to moderate cases, critical cases exhibited stronger interactions between epithelial and immune cells, as indicated by ligand-receptor expression profiles, and activated immune cells, including inflammatory macrophages expressingCCL2,CCL3,CCL20,CXCL1,CXCL3,CXCL10,IL8,IL1BandTNF. The transcriptional differences in critical cases compared to moderate cases likely contribute to clinical observations of heightened inflammatory tissue damage, lung injury and respiratory failure. Our data suggest that pharmacologic inhibition of the CCR1 and/or CCR5 pathways might suppress immune hyperactivation in critical COVID-19.