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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]