Translation of Hepatitis A Virus IRES Is Upregulated by a Hepatic Cell-Specific Factor
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Translation of Hepatitis A Virus IRES Is Upregulated by a Hepatic Cell-Specific Factor. / Sadahiro, Akitoshi; Fukao, Akira; Kosaka, Mio; Funakami, Yoshinori; Takizawa, Naoki; Takeuchi, Osamu; Duncan, Kent E; Fujiwara, Toshinobu.
in: FRONT GENET, Jahrgang 9, 10.08.2018, S. 307.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Translation of Hepatitis A Virus IRES Is Upregulated by a Hepatic Cell-Specific Factor
AU - Sadahiro, Akitoshi
AU - Fukao, Akira
AU - Kosaka, Mio
AU - Funakami, Yoshinori
AU - Takizawa, Naoki
AU - Takeuchi, Osamu
AU - Duncan, Kent E
AU - Fujiwara, Toshinobu
PY - 2018/8/10
Y1 - 2018/8/10
N2 - Many viruses strongly prefer to infect certain cell types, a phenomenon known as "tropism." Understanding tropism's molecular basis is important for the design of vaccines and antiviral therapy. A common mechanism involves viral protein interactions with cell-specific surface receptors, but intracellular mechanisms involving translation have also been described. In this report, we focus on Hepatitis A Virus (HAV) tissue tropism from the standpoint of the translational machinery. HAV genomic RNA, like other positive stranded RNA viruses, is devoid of a cap structure and its translation is driven by highly structured RNA sequences termed internal ribosome entry site (IRES) in the 5' untranslated region (UTR). Unlike most viral IRESs, HAV IRES-mediated translation requires eIF4E and the 3' end of HAV RNA is polyadenylated. However, the molecular mechanism of HAV IRES-mediated translation initiation remains poorly understood. We analyzed HAV-IRES-mediated translation in a cell-free system derived from either non-hepatic cells (HeLa) or hepatoma cells (Huh-7) that enables investigation of the contribution of the cap and the poly(A) tail. This revealed that HAV IRES-mediated translation activity in hepatoma cell extracts is higher as compared to extracts derived from a non-hepatic line. Our data suggest that HAV IRES-mediated translation is upregulated by a hepatic cell-specific activator in a poly(A) tail-independent manner.
AB - Many viruses strongly prefer to infect certain cell types, a phenomenon known as "tropism." Understanding tropism's molecular basis is important for the design of vaccines and antiviral therapy. A common mechanism involves viral protein interactions with cell-specific surface receptors, but intracellular mechanisms involving translation have also been described. In this report, we focus on Hepatitis A Virus (HAV) tissue tropism from the standpoint of the translational machinery. HAV genomic RNA, like other positive stranded RNA viruses, is devoid of a cap structure and its translation is driven by highly structured RNA sequences termed internal ribosome entry site (IRES) in the 5' untranslated region (UTR). Unlike most viral IRESs, HAV IRES-mediated translation requires eIF4E and the 3' end of HAV RNA is polyadenylated. However, the molecular mechanism of HAV IRES-mediated translation initiation remains poorly understood. We analyzed HAV-IRES-mediated translation in a cell-free system derived from either non-hepatic cells (HeLa) or hepatoma cells (Huh-7) that enables investigation of the contribution of the cap and the poly(A) tail. This revealed that HAV IRES-mediated translation activity in hepatoma cell extracts is higher as compared to extracts derived from a non-hepatic line. Our data suggest that HAV IRES-mediated translation is upregulated by a hepatic cell-specific activator in a poly(A) tail-independent manner.
KW - Journal Article
U2 - 10.3389/fgene.2018.00307
DO - 10.3389/fgene.2018.00307
M3 - SCORING: Journal article
C2 - 30147706
VL - 9
SP - 307
JO - FRONT GENET
JF - FRONT GENET
SN - 1664-8021
ER -
