L. Baillon

Transcriptional reprogramming from innate immune functions to a pro-thrombotic signature upon SARS-CoV-2 sensing by monocytes in COVID-19

Mutations that adapt SARS-CoV-2 to mustelid hosts do not increase fitness in the human airway.

The paper identifies spike mutations that adapt SARS-CoV-2 to mustelid hosts and assesses their impact on human infectivity and antigenicity.

Increased transmission of SARS-CoV-2 lineage B.1.1.7 (VOC 2020212/01) is not accounted for by a replicative advantage in primary airway cells or antibody escape

This study shows that SARS-CoV-2 variant B.1.1.7 does not replicate better in airway cells or escape antibodies, suggesting its increased transmissibility is due to other factors.

Resistance of endothelial cells to SARS-CoV-2 infection in vitro

This study shows that endothelial cells are resistant to SARS-CoV-2 infection due to low ACE2 and TMPRSS2 expression, suggesting vascular dysfunction in COVID-19 arises from inflammatory factors rather than direct viral infection.

The furin cleavage site of SARS-CoV-2 spike protein is a key determinant for transmission due to enhanced replication in airway cells.

This study shows the furin cleavage site in SARS-CoV-2 spike protein enhances replication in airway cells, contributing to transmission efficiency.

A rare variant in ANP32B impairs influenza virus replication in human cells

This study identifies a rare variant in ANP32B that impairs influenza virus replication by disrupting FluPol dimer formation and function.

Ribosomal protein imbalance launches a C/EBP-based program to preserve tissue integrity

The paper identifies Xrp1 as a C/EBP that promotes elimination of cells with reduced ribosomal protein gene copy numbers through an autoregulatory loop.