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Table 1 Cellular proteins involved in the regulation of enterovirus A71 mRNA translation

From: Translation control of Enterovirus A71 gene expression

Host factors

The effects of host proteins on EV-A71 translation

Refs

hnRNP A1/A2

hnRNP A1 promotes IRES-mediated translation after EV-A71 infection and its function in translation can be replaced by hnRNP A2.

[31,32,33]

PTB1

Nuclear PTB1 is transferred to the cytoplasm and interacts with EV-A71 IRES domain VI to promote viral mRNA translation.

[34,35,36,37]

PCBP1/2

PCBP1/2 also function as ITAFs by interaction with domain IV of type 1 IRES to promote viral translation.

[48,49,50]

Sam68

Sam68 binds specifically to EV-A71 IRES domains IV and V and acts as an ITAF to upregulate viral translation.

[41]

DDX3

DDX3 may indirectly binds to the domain VI of EV-A71 IRES and then unwind the secondary structure to facilitate ribosome entry.

[42]

HuR

HuR binds to the domain II of EV-A71 IRES by viral small RNA and promotes viral IRES-mediated translation.

[43]

Ago2

Ago2 binds to the domain II of EV-A71 IRES by viral small RNA and promotes viral IRES-mediated translation.

[43]

FBP1

FBP1 binds to the EV-A71 5′ UTR linker region to promote IRES-mediated translation and virus production. FBP1 activates viral IRES activity by competing with FBP2.

[44]

FBP2

FBP2 binds to the IRES of EV-A71 and acts as a negative regulator of viral IRES-mediated translation.

[45]

AUF1

AUF1 binds to the domain II of EV-A71 IRES by viral small RNA and represses viral IRES-mediated translation.

[46, 47]

SRp20

SRp20 interacts with PCBP2 and functions to promote type 1 IRES-mediated translation.

[51, 52]

Hsp27

Hsp27 activates viral protease 2Apro to cleave host eIF4G protein, and thus inhibits host cap-dependent translation and enhances viral IRES-mediated translation.

[53]

Hsc 70

Hsc70 enhances viral 2Apro activity to cleave host eIF4G protein, and thus inhibits host cap-dependent translation and enhances viral IRES-mediated translation.

[54]

MINK

EV-A71 infection induces the phosphorylation of MINK and then stimulates the transfer of hnRNP A1 into the cytoplasm where it binds to the viral IRES and promotes viral IRES-mediated translation.

[55]