Table 1.

Roles of autophagy (or autophagy-related genes) during viral infection in vivo

Virus	Host	Autophagy-related genes	Host-virus interplay	Ref.
RNA viruses
Togaviridae  Sindbis virus	Mouse	beclin 1	Ectopic Beclin 1 expression in Sindbis virus-infected neurons suppresses viral replication in the brain and reduces mouse mortality	[30]
	Mouse	Atg5	Depletion or disruption of Atg5 impairs CNS clearance of Sindbis virus capsid and increases the mortality of infected mice	[14]
Chikungunya virus	Mouse	Atg16L1	Chikungunya virus induces higher levels of apoptosis and increased lethality in Atg16L1 hypomorphic (Atg16L1HM) mice	[31]
Caliciviridae  MNV	Mouse	Atg16L1	MNV infection in Atg16L1HM mice induces Crohn's disease-like pathological features in the intestine	[41]
Dicistroviridae  Drosophila C virus	Drosophila	Atg18	Atg18 knockdown does not alter Drosophila C virus replication or the survival rate of DCV-infected flies	[10]
Orthomyxoviridae  Influenza A virus	Mouse	Atg5	Atg5 knockdown in the lung reduces influenza virus H5N1-induced inflammation, acute lung injury and mouse mortality	[51]
Picornaviridae  Coxsackievirus B3	Mouse	Atg5	Pancreatic acinar cell-specific disruption of Atg5 reduces Coxsackievirus B3 replication in the pancreas and pancreatic dysfunction	[80]
Rhabdoviridae  VSV	Drosophila	Atg7, Atg12, Atg18	Silencing these autophagy genes increases VSV replication in vivo and fly mortality after VSV infection	[10]
Sigma virus	Drosophila	p62/Ref(2)P	Permissive Ref(2)P alleles increase sigma virus infectivity in flies, whereas restrictive or non-functional alleles decrease sigma virus infectivity	[90]
Virgaviridae  TMV	Arabidopsis	ATG3, BECLIN 1, ATG7, VPS34	Silencing these autophagy genes increases TMV local replication and the spread of hypersensitive-related programmed cell death to uninfected tissues in plants	[29]
DNA viruses Hepadnaviridae  HBV	Mouse	Atg5	Liver-specific knockout of Atg5 impairs HBV replication in vivo	[81]
Herpesviridae  HSV-1	Mouse	beclin 1	An HSV-1 mutant lacking the ability to inhibit Beclin 1 (HSV-1 ICP34.5Δ68-87) is attenuated in a intracerabral infection model	[25]
	Mouse	beclin 1	HSV-1 ICP34.5?68-87 is attenuated in a corneal infection model in wild-type mice, but not in Rag1 −/− mice lacking B and T cells	[28]
	Mouse	Atg5	CD4+ T cell priming after HSV-1 mucosal infection is impaired in lethally irradiated wild-type mice reconstituted with Atg5–/– hematopoietic cells	[19]
	Mouse	beclin 1, Atg5	HSV-1 ICP34.5Δ68-87 is attenuated in an intravaginal infection model likely due to the antiviral role of autophagy in dorsal root ganglion neurons	[26]
HSV-2	Mouse	Atg5	Dendritic cell-conditional deletion of Atg5 impairs CD4+ T cell priming and increases mouse susceptibility to HS-2	[19]
γ-Herpesvirus 68 (γHV68)	Mouse	beclin 1	γHV68 carrying a vBcl2 variant unable to suppress autophagy fails to efficiently maintain latent infection in the spleen	[27]