Nicotinic acid receptor GPR109A promotes antiviral innate immune response through autophagy.

Emerging evidence suggests that GPCRs play a pivotal role in virus infection. However, the mechanisms underlying GPCRs-mediated type I interferon responses to protect host from viral infection are not systematically explored. In order to screen key functioning GPCRs in interferoninduced expression process, we applied gene chips analysis, where the GPR109A, ranked as the uppermost regulated GPCR, functions as a powerful antiviral factor, implicating its potential role as an antivirus target.