SETD3 Is Pivotal for Infection by Multiple Human Enteroviruses

An intriguing strategy for the development of novel antivirals is to target host cell factors essential for viral infection. This approach, termed “host-directed therapy” (HDT), is of potentially great value when vaccines or agents targeting viral proteins are not feasible due to high viral genetic diversity (1). In an exciting example of this concept, Diep et al. describe the use of a genome-scale CRISPR screen to show that the protein histidine methyltransferase SETD3 is crucial for the replication of multiple human enteroviruses (EV) (2). Interestingly, the methylation activity of the cytosolic SETD3 is dispensable for EV RNA replication. The authors detected an interaction between SETD3 and the viral 2A protease (2A) of various EVs, and found that disruption of the SETD3-2A interaction, but not of 2A catalytic activity, induced the replication defect. These findings were confirmed and extended in several mouse models of EV infection. In summary, this study identifies a host protein (SETD3) that plays a critical role in the replication of a broad range of clinically important EVs, and pinpoints the SETD3-2A interaction as a viable therapeutic target.

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References

1. Heaton, SM. Clin Transl Immunology. 2019 Jul 8;8(7):e1067.
2. Diep et al. Nat Microbiol. 2019 Sep 16.