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Table 1 Selective autophagy in virus infection

From: The role of autophagy in viral infections

Selective autophagy (SA)

Virus name

Targeted cargos

SA receptors

SA associated factors

Interaction with the autophagy machinery

Effects

Refs.

Virophagy

VSV

-

TLR7

Glycoprotein G of VSV is detected by TLR7, and activates autophagy via the nutrient-sensing phosphoinositide 3-kinase-Akt signalling pathway

Autophagy restricts VSV replication

[146]

RVFV

p62

TLR-7, TRAF6, MYD88

Drosophila TLR-7 recognizes RVFV, which activates antiviral autophagy through TRAF6 and MyD88

Autophagy restricts RVFV replication

[147]

Orsay virus

Pathogen proteins

Ubiquitin

Orsay virus upregulates and enriches functional domains associated with ubiquitin-mediated proteolysis, including the ubiquitin ligase adapter F-box and MATH domain genes; on this basis, knockdown of an autophagy gene increases the pathogen load

Activation of autophagy reduces the pathogen load of Orsay virus

[148]

SINV

SINV capsid protein

P62

p62 interacts with SINV capsid protein; knockdown of p62 blocks the targeting of viral capsid to autophagosomes

Autophagy protects against SINV infection and slows down virus-induced cell death

[149]

HBV

viral core proteins

P62

Galectin-9

Galectin-9 restricts HBV replication via p62 -mediated selective autophagy of viral core proteins

Autophagy restricts HBV replication

[150]

HSV-1

HSV-1 nucleocapsids and viral particles

FANCC

The nucleocapsid of HSV-1 is captured by autophagosomes during its transition through the cytoplasm, which is regulated by FANCC

FANCC mediated virophagy reduces the host’s susceptibility to HSV-1

[151]

IAV

ATG16L1

Activation of non‐canonical autophagy causes LAP to control the microbial infection in vivo, inhibiting the fusion of IAV envelope with endosomes and facilitating the presentation of antigens on MHC II molecules

Non-canonical autophagy limits lethal infection by IAV

[152, 153]

CCHFV

LC3

CCHFV causes a massive lipidation of LC3 in hepatocytes

The genetic alteration of autophagy does not affect CCHFV replication

[155]

Mitophagy

IAV

Mitochondria

Ripk2

Ripk2−/− cells (accumulation of damaged mitochondria in cells) infected with IAV exhibit activated NLRP3 and increased levels of IL-18 and IL-1β

NOD-RIPK2 mediated mitophagy protects the host against virally triggered immunopathology

[173]

IAV

Mitochondria

MAVs

M2 protein increases the formation of ROS-dependent MAVS aggregates, while antagonizing the autophagy to reduce the MAVS aggregates degradation

M2 protein inhibits mitophagy and promotes innate immunity

[174]

IAV

Mitochondria

PB1-F2

MAVs, TUMF

PB1-F2 protein acts as an autophagy receptor and mediates the induction of complete mitophagy by simultaneously interacting with LC3B and TUFM, thereby increasing MAVS degradation

PB1-F2 protein promotes mitophagy, and weakens the production of type I IFN

[165, 179]

IAV

Mitochondria

NBR1

RIG-I; MAVs

PB1 preferentially associates with NBR1 that recognizes ubiquitinated MAVS and delivers it to autophagosomes for degradation

PB1 facilitates H7N9 virus infection by inhibiting innate immune signalling

[180]

HIV

Mitochondria

P62

NLRP3

HIV infection causes mitochondrial accumulation, thereby reducing the negative regulation of NLRP3

Inhibition of mitophagy up-regulates inflammation

[162, 163]

Human herpesvirus 8 (HHV-8)

Mitochondria

NIX

HHV-8-encoded viral interferon regulatory factor 1 (vIRF-1) binds to NIX to activate mitophagy

Activation of mitophagy maintains mitochondrial homeostasis and promotes HHV-8 replication

[164]

EBV

Mitochondria

NDP52

PINK1, MAVs-STING;

EBV encoded BHRF1 disturbs mitochondrial dynamics and stimulates mitophagy

Mitophagy inhibits the type I interferon response

[167]

HPIV3

Mitochondria

TUFM

The M protein of HPIV3 translocates to mitochondria and interacts with TUFM to induce mitophagy

Mitophagy inhibits the type I interferon response

[168]

SARS-CoV-2

Mitochondria

RIG-I-MAVs

The M protein of SARS-COV2 translocates to mitochondria to induce mitophagy

Mitophagy inhibits RIG-MAVS-mediated IFN-β signalling

[170]

ER-phagy

DENV/ ZIKV

ER

FAM134B

DENV/ ZIKV NS3-mediated cleavage of FAM134B blocks the formation of ER and viral protein-enriched autophagosomes

Flavivirus inhibits ER-phagy to promote its replication

[182]

DENV/ ZIKV

ER

FAM134B

BPIFB3

Depletion of BPIFB3 enhances the FAM134B-mediated ER-phagy

ER-phagy facilitates Flavivirus replication

[184]

EBOV

ER

FAM134B

FAM134B-mediated ER-phagy contributes to the degradation of viral components accumulated in the ER

Replication of EBOV is limited by FAM134B-dependent ER-phagy

[183]

WNV/DENV/ ZIKV

ER

RTN3.1A

WNV encoded NS4A protein binds RTN3.1A to hijack ER membranes, generates a replication permissive niche to remodel the host membrane and stabilize the viral protein in the ER

Flaviviruses target RTN3.1A to avoid ER-phagy, thereby promoting viral replication

[186]

Lipophagy

DENV

Lipid droplets

Lipophagy is activated and reposited triglycerides are depleted, resulting in an increase in the release of β-oxidized fatty acids in mitochondria, which generates ATP

Lipophagy- generated ATP is required for virus replication and assembly

[191]

DENV/ ZIKV

Lipid droplets

AUP1

DENV-NS4A exploits the acyltransferase activity of AUP1 to trigger lipophagy and leads AUP1 to relocalize from LDs to autophagosomes upon infection

Flaviviruses exploit the AUP1 to trigger lipophagy and increase progeny virus production

[192]

Aggrephagy

MCMV

Aggregates

RIPK1, NEMO, TBC1D,

VPS26B 5

MCMV M45 protein requires IPAM to induce aggregation and degradation of RIPK1 and NEMO, then M45 recruits TBC1D5 and VPS26B to facilitate degradation of aggregates

MCMV induced-aggrephagy contributes to immune evasion of the virus and cell viability

[197]

Ferritinophagy

HCMV

Ferritin

NCOA4

pUL38 protein of HCMV antagonizes USP24 to reduce ferritinophagy

Reduced ferritinophagy increases cell viability and successful virus infection

[204]

HPIV2

Ferritin

NCOA4

FTH1

V-2 protein of HPIV2 weakens ferritinophagy by interfering with the interaction between FTH1 and NCOA4

Reduced ferritinophagy allows infected cells to avoid apoptotic cell death, leading to effective viral replication of HPIV2

[205]