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Table 2 host factors involved in NPEV infection cycle

From: Recent advances on the role of host factors during non-poliovirus enteroviral infections

Human host factor: Viral Protein interaction

Role during viral infection cycle

Reference

EV-A71 3Cpro Cleaves Ubc6e at Q219G, Q260S and Q273G

Inhibits ERAD pathway to promote viral replication

[84]

EV-A71 2Apro Inhibits synthesis of Herp and VIMP ER proteins at translational level

EV-A71 3A facilitates interaction with ACBD3 and PI4PIIIβ at replication site for formation of replication complexes

Formation of membranous structures for viral replication

[93, 94]

Picornaviral 3CD protein induces PI4P and PIP2 and phosphatidylcholine synthesis during picornaviral infections

hnRNP A1 relocates to cytoplasm from nucleus and binds to the stem loop II of the EV-A71 IRES

Viral protein translation: Enhanced IRES dependent viral RNA production

[99,100,101,102,103, 109, 110]

EV-A71 induces proteasome, autophagy and caspase activity cleavage of FBP2 into a positive ITAF

Sam68 translocates into the cytoplasm and binds to viral IRES

[111, 112, 114, 117]

CV-B3, rhinovirus viral 3C protease cleaves AUF1 upon translocation to the cytoplasm

MINK binds to IRES acting as an ITAF

EV-A71 viral 3D RNA dependent RNA polymerase disrupts cell cycle division at S phase thus blocking entry into G2/M phase

Cell cycle arrest for efficient replication by accessing the host factors cell division machinery.

[148,149,150]

EV-D68 mediates synchronization of cell division at G0/G1

CV-A6 viral protein 3D and 3C disrupts cell division cycle at G0/G1

PV, CV-B, CV-B3 virus induced autophagy through 3A and 2 BC viral proteins

Formation of replication complexes for viral replication.

[151,152,153,154,155,156, 159]

CV-B3 induces autophagosome formation without lysosome degradation in fibroblasts and BALB/C mice

CV-B3 induces DRP1 initiated mitochondrial fragmentation

Virus egress through the autophagosome-bound-mitochondrion-virus complex

[161]

EV-A71-VP1 and 2C proteins induce autophagy through localization with LC3 and MPR

Enhanced EV-A71 replication through formation of amphisome

[163, 164]

EV-A71 2 BC protein interacts with SNARE, STX17, SNAP29 and LC3B proteins leading to formation of autolysosome in RD cells

Enhanced viral replication

[165]

EV-D68 can disrupt autophagy process downstream

Promotes viral replication and egress from infected cells; promoting viral infection within the cells

[166]

CV-B3 viral protein 3C targets cleavage of SNARE and PLEKHM1 proteins

Impairs establishment of SNARE complexes thus providing conducive environment for viral replication

[170]

CV-B3 viral 2A protease cleaves SQSTM1/p62 a known intermediary of selective autophagy degradation of ubiquitinated proteins

Impairs NF-kB signaling and disrupts selective autophagy in infected cells to establish an efficient viral replication/infection

[173]

CV-B3 interacts with CALCOCO2 and SQSTM1

Targets autophagy receptors; targets mitochondrial antiviral signaling protein for degradation thus blocking establishment of antiviral state in the infected cells

[177]