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Open AccessArticle

Epstein–Barr Virus BALF0 and BALF1 Modulate Autophagy

Sorbonne Université, INSERM, Centre de Recherche Saint-Antoine, F-75012 Paris, France
Author to whom correspondence should be addressed.
Viruses 2019, 11(12), 1099;
Received: 22 September 2019 / Revised: 17 November 2019 / Accepted: 26 November 2019 / Published: 27 November 2019
(This article belongs to the Section Animal Viruses)
Autophagy is an essential catabolic process that degrades cytoplasmic components within the lysosome, therefore ensuring cell survival and homeostasis. A growing number of viruses, including members of the Herpesviridae family, have been shown to manipulate autophagy to facilitate their persistence or optimize their replication. Previous works showed that the Epstein–Barr virus (EBV), a human transforming gammaherpesvirus, hijacked autophagy during the lytic phase of its cycle, possibly to favor the formation of viral particles. However, the viral proteins that are responsible for an EBV-mediated subversion of the autophagy pathways remain to be characterized. Here we provide the first evidence that the BALF0/1 open reading frame encodes for two conserved proteins of the Bcl-2 family, BALF0 and BALF1, that are expressed during the early phase of the lytic cycle and can modulate autophagy. A putative LC3-interacting region (LIR) has been identified that is required both for BALF1 colocalization with autophagosomes and for its ability to stimulate autophagy. View Full-Text
Keywords: Epstein–Barr virus; BALF0/1; BALF1; BALF0; autophagy; vBcl-2 Epstein–Barr virus; BALF0/1; BALF1; BALF0; autophagy; vBcl-2
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Shao, Z.; Borde, C.; Quignon, F.; Escargueil, A.; Maréchal, V. Epstein–Barr Virus BALF0 and BALF1 Modulate Autophagy. Viruses 2019, 11, 1099.

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