Abstract
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.
Highlights
Junín virus (JUNV), a member of Mammarenavirus genus within the Arenaviridae family, is the etiological agent of Argentine Haemorrhagic Fever (AHF), a potentially lethal, endemic-epidemic disease affecting the population of the most fertile farming land of Argentina[1]
Even though the precise role of autophagy during JUNV infection remains unclear to date, our results indicate that autophagy promotion has a proviral role toward JUNV replication, providing important knowledge to a previously unknown association in the field of host cell-arenavirus interactions[15]
Autophagy has a proviral role during JUNV, LASV and MOPV infection where the early structural autophagic protein Atg[5] becomes crucial
Summary
Junín virus (JUNV), a member of Mammarenavirus genus within the Arenaviridae family, is the etiological agent of Argentine Haemorrhagic Fever (AHF), a potentially lethal, endemic-epidemic disease affecting the population of the most fertile farming land of Argentina[1]. We showed that JUNV triggers the accumulation of autophagic vesicles in a Beclin-1 and Atg5-dependent manner in permissive human A549 cells from 2 h postinfection (p.i.), indicating the early activation of the autophagic pathway after viral infection. Perez Vidakovics et al showed, by western blot and fluorescence microscopy, an increased level of LC3-II lipidation (a well-established autophagosome indicator) after 24 h of cell exposure to UV-inactivated JUNV P3441 particles, suggesting that the autophagy activation was independent of viral replication.
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