Cellular membranes as contested territories in the virus-host conflict

Cellular membranes emerge as contested territories in the virus-host conflict. Many viruses depend on host membrane systems throughout their life cycle for entry, replication, assembly, and egress. At the same time, innate immune sensing and interferon (IFN) signaling are themselves organized around membrane-associated platforms. Cellular membranes therefore function both as essential substrates for viral replication and as central sites of antiviral defense. In this review, we examine how IFN-induced responses reshape membrane biology through coordinated changes in lipid metabolism, membrane biophysics, intracellular trafficking, and organelle organization. These membrane-centered defenses restrict viral entry, alter endomembrane permissiveness, interfere with virion release, and disrupt the formation and function of virus-induced replication organelles. We further discuss how positive-strand RNA viruses counteract these pressures by reprogramming lipid metabolism and actively remodeling intracellular membranes to preserve replication-competent niches. Together, these observations support a unifying framework in which viruses and host defenses compete for control over membrane identity, organization, and accessibility. This membrane-centered perspective connects innate immune signaling, membrane homeostasis, and viral replication, and highlights membrane-associated processes as promising targets for broad-spectrum antiviral strategies.