Gammaherpesvirus infection unveils exaggerated germinal center responses in an SR-BI-deficient host

Lipid metabolism affects diverse acute viral infections. In contrast, less is known about the effect of lipid metabolism on chronic virus infection, including in the context of an intact host. Host lipid homeostasis is maintained via a combination of endogenous lipid synthesis that takes place in most cell types and cellular interaction with exogenous, circulating lipids. This study focuses on defining the interaction between SR-BI, a primary HDL receptor, and natural gammaherpesvirus infection. We found that SR-BI deficiency led to increased expression of lytic gammaherpesvirus genes during acute gammaherpesvirus replication in the lungs. Importantly, chronic gammaherpesvirus infection unveiled the physiological role of SR-BI as a negative regulator of the germinal center response, a B cell differentiation process that is critical for physiological B cell responses and that is manipulated by gammaherpesviruses to establish chronic infection.