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导致新生儿腹泻病的G3P2轮状病毒在VP4、VP7和NSP4序列上与导致新生儿无症状感染的G3P2毒株不同。

G3P2 rotaviruses causing diarrhoeal disease in neonates differ in VP4, VP7 and NSP4 sequence from G3P2 strains causing asymptomatic neonatal infection.

作者信息

Kirkwood C D, Coulson B S, Bishop R F

机构信息

Department of Gastroenterology, Royal Children's Hospital, Parkville, Victoria, Australia.

出版信息

Arch Virol. 1996;141(9):1661-76. doi: 10.1007/BF01718290.

Abstract

During longitudinal epidemiological studies of rotavirus infections in children in Melbourne, Australia human G3P2 rotavirus strains causing asymptomatic or symptomatic infections have been identified. Eleven strains (AS strains) associated with asymptomatic infection of newborn babies from 1974-1984, and five strains (S strains) associated with symptomatic infection of newborn babies (4) or a 22 week old infant (1) during 1980-1986 were studied. The entire nucleotide sequences of genes coding for VP4, VP7, NSP4 and VP6 were derived for representative AS and S strains. The nucleotide sequences of neutralization epitope regions present on the outer capsid proteins VP4 and VP7 (regions C and F) showed extensive conservation of nucleotide and deduced amino acid sequence in all strains. Minor variations were observed over the 12 year period in VP7 epitope regions A and B in some strains. Specific conserved amino acids differences between the asymptomatic and symptomatic strains were observed in the genes encoding VP4 at aa133 and 303 (asparagine or threonine) and 380 (serine or isoleucine), VP7 at aa27 (threonine or isoleucine), aa29 (isoleucine or threonine), aa42 (valine or alanine) and aa238 (asparagine or aspartic acid/serine) and NSP4 at aa135 (isoleucine or valine). No amino acid changes were identified in gene 6. The observed amino acid differences occurred in proteins that have been implicated in virulence, and correlate with differences in clinical symptoms of infants infected with these strains. These results permit speculation about the genetic basis for virulence of human strains.

摘要

在澳大利亚墨尔本对儿童轮状病毒感染进行的纵向流行病学研究中,已鉴定出导致无症状或有症状感染的人G3P2轮状病毒株。研究了1974年至1984年期间与新生儿无症状感染相关的11株病毒(AS株),以及1980年至1986年期间与新生儿(4例)或一名22周龄婴儿(1例)有症状感染相关的5株病毒(S株)。推导了代表性AS株和S株编码VP4、VP7、NSP4和VP6的基因的完整核苷酸序列。在外衣壳蛋白VP4和VP7上存在的中和表位区域(C和F区域)的核苷酸序列在所有毒株中显示出核苷酸和推导氨基酸序列的广泛保守性。在12年期间,一些毒株的VP7表位区域A和B出现了微小变异。在编码VP4的基因中,无症状和有症状毒株之间在氨基酸133、303(天冬酰胺或苏氨酸)和380(丝氨酸或异亮氨酸)处,VP7在氨基酸27(苏氨酸或异亮氨酸)、29(异亮氨酸或苏氨酸)、42(缬氨酸或丙氨酸)和238(天冬酰胺或天冬氨酸/丝氨酸)处,以及NSP4在氨基酸135(异亮氨酸或缬氨酸)处观察到特定的保守氨基酸差异。基因6中未发现氨基酸变化。观察到的氨基酸差异出现在与毒力有关的蛋白质中,并且与感染这些毒株的婴儿的临床症状差异相关。这些结果允许对人毒株毒力的遗传基础进行推测。

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