Two novel spliced genes in human cytomegalovirus
1 MRC Virology Unit, Institute of Virology, Church Street, Glasgow G11 5JR, UK 2 Department of Virology, Royal Free and University College Medical School, Royal Free Campus, Rowland Hill Street, Hampstead, London NW3 2QG, UK 3 Section of Infection and Immunity, University of Wales College of Medicin...
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Veröffentlicht in: | Journal of general virology 2003-05, Vol.84 (5), p.1117-1122 |
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Zusammenfassung: | 1 MRC Virology Unit, Institute of Virology, Church Street, Glasgow G11 5JR, UK
2 Department of Virology, Royal Free and University College Medical School, Royal Free Campus, Rowland Hill Street, Hampstead, London NW3 2QG, UK
3 Section of Infection and Immunity, University of Wales College of Medicine, Tenovus Building, Heath Park, Cardiff CF14 4XX, UK
Correspondence Andrew Davison a.davison{at}vir.gla.ac.uk
Two novel spliced genes (UL131A and UL128) flanking UL130 were predicted from sequence comparisons between human cytomegalovirus (HCMV) and its closest known relative, chimpanzee cytomegalovirus (CCMV), and the splicing patterns were confirmed by mRNA mapping experiments. Both genes were transcribed with late kinetics and shared a polyadenylation site. Comparisons with wild-type HCMV in infected human tissues showed that three of five isolates passaged in cell culture contained disruptions of UL128, one was frameshifted in UL131A and one exhibited a deletion affecting UL131A and UL130. CCMV and the Colburn strain of simian cytomegalovirus, which have been passaged in cell culture, also exhibit disruptions of UL128. These observations indicate that expression of either one of UL128 and UL131A is deleterious to growth of primate cytomegaloviruses in cell culture. Although the functions of these genes are unknown, sequence comparisons suggest that UL128 encodes a -chemokine.
The GenBank accession numbers of the HCMV sequences reported in this paper are AY169795 AY169800 .
Published ahead of print on 20 February 2003 as DOI 10.1099/vir.0.18952-0 |
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ISSN: | 0022-1317 1465-2099 |
DOI: | 10.1099/vir.0.18952-0 |