Autophagy Modulation in Mammarenavirus Infection

GALLO, GIOVANNA; ROLDÁN, JULIETA; DELGUI, LAURA

Journal of Immunological Sciences

Journal of Immunological Sciences

Año: 2020 vol. 4 p. 45 - 51

Mammarenavirus genus groups viruses causing human haemorrhagic diseases, including the New World (NW) Junín virus (JUNV), and the Old World (OW) viruses Lassa (LASV), among others. The high mortality and morbidity rates associated to pathogenic mammarenaviruses, the absence of vaccines and the constant threat of new emerging species, make these viruses a public health concern in endemic areas. Autophagy is a widely-known intracellular metabolic pathway involved in maintaining the cellular homeostasis in response to several stress conditions.In a previous work, we determined the role of autophagy in JUNV-infected cells. Our results indicate that JUNV, after being endocytosed and once the viral replication begins in the cytoplasm, induces an autophagic response in the infected cells and that a functional autophagy pathway is required for efficient virus replication. Recently, the interaction of OW LASV and the non- pathogenic one Mopeia (MOPV) with autophagic factors has been explored. The authors detected interaction with two well-known autophagic adaptors, NDP52 and TAX1BP1, and reported that, in Atg5 (an essential early autophagic protein) silenced permissive cells, less viral RNA and fewer infection particles were produced upon MOPV and LASV infection. Moreover, they observed that MOPV induced autophagy, which was required for efficient production of newly-formed infectious particles, suggesting a proviral role of autophagy. Here we discuss the implications of our findings in the context of others regarding mammarenavirus infection and the autophagy pathway.