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Human cytomegalovirus-encoded G protein-coupled receptor (GPCR) UL78 regulates viral reactivation | Journal of Virology
Cytomegalovirus (CMV) is a ubiquitous human herpesvirus, infecting the majority of the population worldwide. As with all herpesviruses, once an individual is infected with CMV, the virus remains in the person’s blood cells for life in a silenced state called latency, and this infection, for the most part, remains asymptomatic. When an infected individual’s immune system fails to function properly, however, CMV can become active (termed viral reactivation), which allows the virus to replicate and cause downstream disease. Our understanding of the cellular and viral factors that dictate this switch from silenced to activated remains incomplete. Here, we show a viral protein, UL78, is required for this switch. We find that UL78 helps to reshape cellular signaling, changing the cell environment from one that favors latency to one that supports reactivation. This highlights a new avenue for therapeutic intervention to prevent CMV reactivation and downstream disease.