Chorioamnionitis, premature rupture of fetal membranes (FM), and subsequent preterm birth are associated with local infection and inflammation, particularly interleukin 1 beta (IL-1β) production. While bacterial infections are commonly identified, other microorganisms may play a role in the pathogenesis. Since viral pandemics, such as influenza, Ebola and Zika are becoming more common, and pregnant women are at increased risk of associated complications, this study evaluated the impact viral infection had on human FM innate immune responses. This study shows that a herpes viral infection of FMs sensitizes the tissue to low levels of bacterial lipopolysaccharide (LPS), giving rise to an exaggerated IL-1β response. Using an ex vivo human FM explant system and an in vivo mouse model of pregnancy, we report that the mechanism by which this aggravated inflammation arises is through the inhibition of the TAM receptor, MERTK, and activation of the inflammasome. The TAM receptor ligand, growth arrest specific 6 (GAS6), re-establishes the normal FM response to LPS by restoring and augmenting TAM receptor and ligand expression, and by preventing the exacerbated IL-1β processing and secretion. These findings indicate a novel mechanism by which viruses alter normal FM immune responses to bacteria, potentially giving rise to adverse pregnancy outcomes.