Comparative sequence analysis identified mutations outside the NSP4 cytotoxic domain of tissue culture-adapted ATCC-Wa strain of human rotavirus and a novel inter-species variable domain in its C-terminus

Comparative sequence analysis identified mutations outside the NSP4 cytotoxic domain of tissue... Complete nucleotide sequence of the tissue culture-adapted ATCC*-Wa strain of human rotavirus NSP4 was determined. Sequence analysis detected two alternate forms of the gene with a nucleotide difference at position 331 (A or G) in the coding sequence (NSP4-A or NSP4-G) leading to a change from neutral glutamine 97 in NSP4-A to a positively charged arginine 97 in NSP4-G originating from the same ATCC-Wa preparation. In addition to this, both forms of ATCC-Wa NSP4 revealed three mutations at nucleotide positions 88 (T to C), 142 (C to T) and 572 (G to A), when compared to the previously reported NSP4 sequence from virulent Wa strain. The former two mutations were in the coding sequence and resulted in a leucine 16 to serine 16 and a proline 34 to leucine 34 change, while the third mutation was in the 3′ non-coding region of the gene. The two amino acid changes may contribute to the ‘tissue culture-adaptation’ of ATCC-Wa strain. The ATCC-Wa NSP4 sequence was found to differ from the previously reported NSP4 sequence of attenuated Wa strain by lacking a mutation at 133 (T to C), though the mutations at 88 and 142 were present in both strains. Furthermore, comparison of deduced amino acid sequence of NSP4 from human, bovine, porcine and simian rotavirus strains identified a seven-residue (positions 135–141) inter-species variable domain in its C-terminal region. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Comparative sequence analysis identified mutations outside the NSP4 cytotoxic domain of tissue culture-adapted ATCC-Wa strain of human rotavirus and a novel inter-species variable domain in its C-terminus

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Publisher
Springer-Verlag
Copyright
Copyright © Wien by 2000 Springer-Verlag/
Subject
Legacy
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s007050070056
Publisher site
See Article on Publisher Site

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