G3P2 ROTAVIRUSES CAUSING DIARRHEAL DISEASE IN NEONATES DIFFER IN VP4,VP7 AND NSP4 SEQUENCE FROM G3P2 STRAINS CAUSING ASYMPTOMATIC NEONATALINFECTION

Citation
Cd. Kirkwood et al., G3P2 ROTAVIRUSES CAUSING DIARRHEAL DISEASE IN NEONATES DIFFER IN VP4,VP7 AND NSP4 SEQUENCE FROM G3P2 STRAINS CAUSING ASYMPTOMATIC NEONATALINFECTION, Archives of virology, 141(9), 1996, pp. 1661-1676
Citations number
52
Categorie Soggetti
Virology
Journal title
ISSN journal
03048608
Volume
141
Issue
9
Year of publication
1996
Pages
1661 - 1676
Database
ISI
SICI code
0304-8608(1996)141:9<1661:GRCDDI>2.0.ZU;2-0
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 s trains (AS strains) associated with asymptomatic infection of newborn babies from 1974-1984, and five strains (S strains) associated with sy mptomatic infection of newborn babies (4) or a 22 week old infant (1) during 1980-1986 were studied. The entire nucleotide sequences of gene s coding for VP4, VP7, NSP4 and VP6 were derived for representative AS and S strains. The nucleotide sequences of neutralization epitope reg ions present on the outer capsid proteins VP4 and VP7 (regions C and F ) showed extensive conservation of nucleotide and deduced amino acid s equence in all strains. Minor variations were observed over the 12 yea r period in VP7 epitope regions A and B in some strains. Specific cons erved amino acids differences between the asymptomatic and symptomatic strains were observed in the genes encoding VP4 at aa133 and 303 (asp aragine or threonine) and 380 (serine or isoleucine), VP7 at aa27 (thr eonine or isoleucine), aa29 (isoleucine or threonine), aa42 (valine or alanine) and aa238 (asparagine or aspartic acid/serine) and NSP4 at a a135 (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 c linical symptoms of infants infected with these strains. These results permit speculation about the genetic basis for virulence of human str ains.