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. 2022 Jan 3;11:786348. doi: 10.3389/fcimb.2021.786348

Table 1.

Autophagy-mediated antiviral immune responses.

Host Virus Viral protein(s) Host protein(s) Functions References
Animal SINV Capsid p62; LC3 p62 adaptor protein mediates autophagic viral protein clearance, thus promoting cell survival (Orvedahl et al., 2010)
SINV Capsid SMURF1 Acts as a mediator of virophagy (Orvedahl et al., 2011)
SINV Capsid FANCC Interacts with the capsid protein, facilitating virophagy (Sumpter et al., 2016)
HIV-1 Tat p62 Selective degradation of Tat in a ubiquitin-independent manner (Sagnier et al., 2015)
IAV containing avian PB2 PB2; vRNP p62; LC3 p62 targets vRNP to form an autophagosome through interaction with viral PB2 (Liu et al., 2021)
IBDV VP2 p62; LC3 p62 mediates the selective autophagic degradation of VP2, thus targeting IBDV replication (Li et al., 2020b)
HCV NS5A Scotin; LC3 Scotin recruits the NS5A protein to autophagosomes for degradation (Kim et al., 2016)
HIV-1 Capsid TRIM5α; ATG8s TRIM5α functions both as a regulator of autophagy and as an autophagic cargo receptor mediating HIV-1 restriction (Mandell et al., 2014a; Mandell et al., 2014b; Ribeiro et al., 2016)
Plant CLCuMuV βC1 ATG8f ATG8f targets βC1 for degradation (Haxim et al., 2017)
TLCYnV C1 ATG8h; XPO1 ATG8h interacts with C1, directing it for degradation in an XPO1-mediated, nuclear export pathway-dependent manner (Li et al., 2020a)
CaMV P4 and viral
particles
NBR1; ATG8a NBR1 targets P4 and viral particles, thus mediating their autophagy-dependent degradation (Hafren et al., 2017)
TuMV HCPro NBR1; ATG8a HCPro is selectively degraded by the autophagy pathway through binding with NBR1 (Hafren et al., 2018)
TuMV NIb Beclin1; ATG8a Beclin1 interacts with Nib, targeting it for selective degradation (Li et al., 2018)
RSV p3 P3IP; ATG8f P3IP directs the selective autophagic degradation of p3 through interaction with ATG8, thereby limiting virus infection (Jiang et al., 2021)
CMV 2b rgs-CaM; ATG8 rgs-CaM interacts with 2b for autophagy degradation (Nakahara et al., 2012)