Abstract

Host cells exhibit a wide array of responses upon infection to limit pathogen replication efficiency. Nukui et al. (e00033-20) found that posttranslationally modifying key viral proteins via S-nitrosylation limits human cytomegalovirus (HCMV) replication efficiency. The viral protein pp71 inhibits the potent STING antiviral pathway, thereby reducing subsequent innate responses. However, protein S-nitrosylation of pp71 limits the capacity of this viral protein to undermine the host STING pathway, providing an additional level of antiviral response to infection.

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