Translation of Capped Virus mRNA in Encephalomyocarditis Virus-infected Cells

Abstract

SUMMARYThe pattern of protein synthesis in HeLa cells simultaneously infected with encephalomyocarditis virus (EMCV) and Semliki Forest virus (SFV) has been analysed throughout the time course of the infection. The ratio of the picornavirus protein ? versus the togavirus late protein C increased when the m.o.i, of EMCV was raised, and the ratio of C/? increased with higher multiplicities of SFV. Under some conditions, the co-infected cells simultaneously synthesized the picornavirus and togavirus proteins, and the cells exclusively translated the capped 26S mRNA from SFV at the end of the co-infection experiment. The influence of the time of addition of the second virus on the relative translation of the capped and uncapped mRNAs was also studied. When HeLa cells were co-infected with 5 p.f.u

Translation Driven by Picornavirus IRES Is Hampered from Sindbis Virus Replicons: Rescue by Poliovirus 2A Protease

“…The inability of picornavirus IRES to be translated in SV-infected cells is not observed when cells are doubly infected with picornaviruses and alphaviruses. 41,42 In those cells, viral translation is coupled to transcription in each type of viral replicative foci. In the case of SV replicons containing IRES, translation is not coupled to transcription, probably due to the absence of one or more viral proteins necessary to enhance translation of IRES-containing mRNAs.…”

“…In fact, years ago, we found that togavirus-infected cells efficiently translate picornavirus mRNAs when cells are doubly infected with SFV and PV or EMCV. 41,42 Therefore, it was unexpected to find that sgmRNAs containing PV IRES were inefficiently translated when synthesized by the SV replication machinery. To investigate whether this phenomenon only occurs with PV IRES or whether this failure to direct translation also occurs in other viral IRESs, we constructed new SV replicons containing different classes of viral IRESs.…”

Insights from structural studies of the cardiovirus 2A protein

“…Besides its primary role in stimulating frameshifting, 2A causes a variety of pathological effects in the host cell. Perhaps most notably, it contributes to translational shut-off [ 86 , 87 ]. Many picornaviruses do this by proteolytically cleaving eukaryotic initiation factor 4G (eIF4G), which prevents assembly of the eukaryotic initiation factor 4F complex (eIF4F) and thereby inhibits cap-dependent initiation on host mRNAs (reviewed in [ 41 , 88 ]).…”