T. Dumenil

TMEM106B-mediated SARS-CoV-2 infection allows for robust ACE2-independent infection in vitro but not in vivo

This study identifies TMEM106B as a key mediator of ACE2-independent SARS-CoV-2 infection in vitro but shows no in vivo neuroinvasiveness or respiratory tract replication in mice.

Increased neurovirulence of omicron BA.5 and XBB variants over BA.1 in K18-hACE2 mice and human brain organoids

This study shows that omicron BA.5 and XBB variants are more neurovirulent than BA.1 in mice and human brain organoids, leading to increased brain infection and mortality.

ACE2-independent SARS-CoV-2 infection and mouse adaption emerge after passage in cells expressing human and mouse ACE2

The paper describes the generation of mouse-adapted SARS-CoV-2 variants through serial passaging in co-cultures of human and mouse ACE2-expressing cells, revealing ACE2-independent infection capabilities.

Microplastic consumption induces inflammatory signatures in the colon and prolongs a viral arthritis

This study shows that microplastic consumption in mice causes mild colon inflammation and prolongs viral arthritis by increasing Th1, NK cell, and neutrophil signatures.

An inconvenient association between granzyme A and Nicotinamide Nucleotide Transhydrogenase

The paper identifies an association between granzyme A and Nicotinamide Nucleotide Transhydrogenase in mice, showing that Nnt, not GzmA loss, affects disease outcomes and highlights inconsistencies in Nnt sequencing data.

ACE2-lentiviral transduction enables mouse SARS-CoV-2 infection and mapping of receptor interactions

This paper develops an ACE2-lentivirus system to enable SARS-CoV-2 infection in mice, showing it can model viral replication, inflammation, and vaccine testing.

Bromodomain and Extraterminal Inhibition Blocks Inflammation-Induced Cardiac Dysfunction and SARS-CoV-2 Infection (Pre-Clinical)

The paper identifies BET inhibitors as potential cardio-protective drugs that block inflammation-induced cardiac dysfunction and SARS-CoV-2 infection in pre-clinical models.

APC Mutation marks an aggressive subtype of BRAF mutant colorectal cancers

This study identifies APC mutations as a marker of aggressive BRAF mutant colorectal cancers, associated with poor prognosis and enhanced tumor growth in mouse models.