B. Hernaez, M. Cabezas, R. Munoz-Moreno, I. Galindo, M. A. Cuesta-Geijo and C. Alonso Pages 305 - 316 ( 12 )
Autophagy is a relevant cellular defense mechanism that directly eliminates intracellular pathogens and has a crucial role for innate and adaptive immune responses. Some viruses have developed tools to counteract this cellular response. A179L, the viral Bcl2 homolog of African swine fever virus, interacts with proapoptotic Bcl2 family proteins to inhibit apoptosis. Here we report that this gene manipulates autophagy by interacting with Beclin 1 through its BH3 homology domain. At subcellular level, A179L colocalized with Beclin 1 at mitochondria and the endoplasmic reticulum. Virus infection inhibited autophagosome formation in cells; however, when autophagy was induced prior to or at the time of infection the number of infected cells was severely decreased.
African swine fever virus, ASFV, autophagy, Beclin 1, BH3-only proteins, ER stress, viral Bcl2, viral Bcl2 homolog, autophagosomes, stress, starvation, homeostasis, hemorrhagic disease, pathogenesis, lymphoid hyperplasia.
Department of Biotecnologia, Instituto Nacional de Investigacion y Tecnologia Agraria y Alimentaria, INIA, Ctra. De la Coruna, Km 7.5, 28040 Madrid, Spain.