Participates in antiviral signaling. Acts as a negative regulator of MAVS-mediated antiviral responses, through the inhibition of the virus-induced RLH (RIG-like helicase)-MAVS interaction (PubMed:18200010). Instead, promotes autophagy by interacting with TUFM and subsequently recruiting the autophagy-related proteins ATG5 and ATG12 (PubMed:22749352). Also regulates MAVS-dependent NLRP3 inflammasome activation to attenuate apoptosis (PubMed:27393910). Has no inhibitory function on NF-kappa-B signaling pathway, but enhances NF-kappa-B and JUN N-terminal kinase dependent signaling through the production of reactive oxygen species (PubMed:18219313). Regulates viral mediated-inflammation and energy metabolism in a sex-dependent manner (By similarity). In females, prevents uncontrolled inflammation and energy metabolism and thus, may contribute to the sex differences observed in infectious and inflammatory diseases (By similarity). {ECO:0000250|UniProtKB:Q3TL44, ECO:0000269|PubMed:18200010, ECO:0000269|PubMed:18219313, ECO:0000269|PubMed:22749352, ECO:0000269|PubMed:27393910}. This is the function of NLRX1 (NLR family member X1, ENSG00000160703).