Description
With annual epidemics occurring in all parts of the world and the risk of global outbreaks, IAV infections remain a major threat to public health. Infected host cells detect viral components and mount an interferon (IFN)-mediated response to restrict virus propagation and spread of infection. The contribution of endosomal cholesterol levels, especially in the context of the IFN-induced antiviral response, has remained controversial so far. Here we report that the elevation of endosomal cholesterol accumulation is part of the IFN response and plays a pivotal role in the early antiviral defense. We demonstrate that inducing endosomal cholesterol accumulation is antiviral in non-IFN primed cells, restricting incoming IAV particles, impairing mixing of IAV/endosomal membrane lipids, and inhibiting IAV endosomal escape. Our results establish a protective function of LE/L cholesterol accumulation and suggest endosomal cholesterol balance as a possible antiviral target.
| Choose primary session | Innate Immunity |
|---|---|
| Choose secondary Session | Virus host cell interaction |
