Key result
HAV proteinase 3C suppressed viral IRES-dependent translation and cleaved the polypyrimidine tract-binding protein (PTB) in Huh-7 cells.
HAV proteinase 3C suppresses viral IRES-dependent translation and cleaves PTB, suggesting a mechanism for down-regulating viral translation to allow for genome replication.
No immediate clinical implications; leaves open whether 3C protease targeting could modulate HAV replication in vivo.
Hepatitis A virus (HAV) infection is still an important issue worldwide. A distinct set of viruses encode proteins that enhance viral cap-independent translation initiation driven by an internal ribosome entry site (IRES) and suppress cap-dependent host translation. Unlike cytolytic picornaviruses, replication of HAV does not cause host cell shut off, and it has been questioned whether HAV proteins interfere with its own and/or host translation. HAV proteins were coexpressed in Huh-7 cells with reporter genes whose translation was initiated by either cap-dependent or cap-independent mechanisms. Among the proteins tested, HAV proteinase 3C suppressed viral IRES-dependent translation. Furthermore, 3C cleaved the polypyrimidine tract-binding protein (PTB) whose interaction with the HAV IRES had been demonstrated previously. The combined results suggest that 3C-mediated cleavage of PTB might be involved in down-regulation of viral translation to give way to subsequent viral genome replication.
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Kanda et al. (2009) studied Hepatitis A virus (HAV) infection. HAV proteinase 3C was evaluated on Viral IRES-dependent translation and cleavage of PTB. HAV proteinase 3C suppressed viral IRES-dependent translation and cleaved the polypyrimidine tract-binding protein (PTB) in Huh-7 cells.
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