Knockout of TMEM41B strongly inhibited viral infection and delayed the progression of coronavirus disease in a mouse model, identifying it as a critical host factor for viral replication.
TMEM41B is a critical host factor for coronavirus replication, making it a potential target for broad-spectrum anti-viral therapeutics.
Emerging coronaviruses (CoVs) pose a severe threat to human and animal health worldwide. To identify host factors required for CoV infection, we used α-CoV transmissible gastroenteritis virus (TGEV) as a model for genome-scale CRISPR knockout (KO) screening. Transmembrane protein 41B (TMEM41B) was found to be a bona fide host factor involved in infection by CoV and three additional virus families. We found that TMEM41B is critical for the internalization and early-stage replication of TGEV. Notably, our results also showed that cells lacking TMEM41B are unable to form the double-membrane vesicles necessary for TGEV replication, indicating that TMEM41B contributes to the formation of CoV replication organelles. Lastly, our data from a mouse infection model showed that the KO of this factor can strongly inhibit viral infection and delay the progression of a CoV disease. Our study revealed that targeting TMEM41B is a highly promising approach for the development of broad-spectrum anti-viral therapeutics.
Sun et al. (Mon,) conducted a other in Coronavirus infection. TMEM41B knockout vs. Wild-type/control was evaluated on Viral infection and progression of CoV disease. Knockout of TMEM41B strongly inhibited viral infection and delayed the progression of coronavirus disease in a mouse model, identifying it as a critical host factor for viral replication.