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Mycobacterium tuberculosis PE_PGRS62 Protein Inhibits Type I Interferon Responses to Promote HIV-2 Replication by
Chaohu Pan1, Hui Xu1, Min Huang1
1National Clinical Research Center for Infectious Diseases, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.
None:
Coinfection with Mycobacterium tuberculosis (Mtb) and human immunodeficiency virus type 2 (HIV-2) increased the viral load of HIV-2. Type I interferons (IFNs) are essential for limiting HIV-2 progression. However, it is unclear whether and how Mtb affects HIV-2 coinfection by regulating type I IFNs. Here Mtb PE_PGRS62 protein was identified as an inhibitor of stimulator of interferon genes (STING)-mediated type I IFN expression. Ectopic expression of PE_PGRS62 impaired type I IFN expression stimulated by cytosolic DNA, while knockout of pe_pgrs62 potentiated Mtb-induced type I IFN expression. PE_PGRS62 interacts directly with IFN regulatory factor (IRF) 3 and inhibits the interaction of IRF3 with TANK-binding kinase 1 (TBK1) as well as the binding of IRF3 to the IFNβ promoter. Furthermore, reduced HIV viral load was observed in pe_pgrs62 knockout Mtb-infected macrophages compared with wild-type Mtb. These findings reveal an important mechanism by which Mtb infection promotes HIV-2 immune evasion.
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