Department of Pharmacognosy, King Saud University College of Pharmacy, PO Box 2457, Riyadh 11451, Saudi Arabia.
Virus Res. 2013 Dec 26;178(2):553-6. doi: 10.1016/j.virusres.2013.07.020. Epub 2013 Aug 23.
Hepatitis E Virus (HEV) ORF1 encodes the nonstructural polyprotein wherein a role of PCP-domain in ORF1 proteolysis and/or RNA replication still remains contested. A series of ORF1 mutants of HEV-SAR55 replicon were constructed and tested for viability in S10-3 cells. Six of PCP-'cysteine' (C457A, C459A, C471A, C472A, C481A and C483A) and three 'histidine' (H443L, H497L and H590L) mutants were lethal. Further, a highly conserved 'glycine-triad' (G815-G816-G817) in downstream X-domain, homologous to rubella virus protease-substrate (G1299-G1300-G1301) was identified where two of X-mutants (G816V and G817V) turned lethal. However, all ORF1 sequential nucleotide-mutants conserving the amino acids were viable, which clearly showed post-translational regulation of HEV replication by PCP- and X-domains. Moreover, while vector-expressed ORF1-fusion polyprotein yielded a ~191 kDa band in vitro, it produced ~78 and ~35 kDa fragments ex vivo. Collectively, the indispensability and functional effects of 'PCP-catalytic' and 'X-substrate' residues on HEV replication strongly supported a viral protease.
戊型肝炎病毒 (HEV) ORF1 编码非结构多蛋白,其中 PCP 结构域在 ORF1 蛋白水解和/或 RNA 复制中的作用仍存在争议。构建了一系列 HEV-SAR55 复制子的 ORF1 突变体,并在 S10-3 细胞中测试其生存能力。六个 PCP-“半胱氨酸”(C457A、C459A、C471A、C472A、C481A 和 C483A)和三个“组氨酸”(H443L、H497L 和 H590L)突变体是致命的。此外,在下游 X 结构域中鉴定到高度保守的“甘氨酸三联体”(G815-G816-G817),与风疹病毒蛋白酶-底物(G1299-G1300-G1301)同源,其中两个 X 突变体(G816V 和 G817V)变为致命。然而,所有保留氨基酸的 ORF1 连续核苷酸突变体都是可行的,这清楚地表明 PCP 和 X 结构域对 HEV 复制的翻译后调控。此外,虽然载体表达的 ORF1 融合多蛋白在体外产生约 191 kDa 的条带,但在体外产生约 78 和 35 kDa 的片段。总之,“PCP-催化”和“X-底物”残基对 HEV 复制的不可或缺性和功能影响强烈支持病毒蛋白酶。