Significance of premature stop codons in env of simian immunodeficiency virus

T. Kodama, D. P. Wooley, Y. M. Naidu, H. W. Kestler, M. D. Daniel, Y. Li, Ronald Charles Desrosiers

Research output: Contribution to journalArticle

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Abstract

The location of the translational termination codon for the transmembrane protein (TMP) varies in three infectious molecular clones of simian immunodeficiency virus from macaques (SIV(mac)). The SIV(mac)251 and SIV(mac)142 infectious clones have premature stop signals that differ in location by one codon; transfection of these DNAs into human HUT-78 cells yielded virus with a truncuted TMP (28 to 30 kilodaltons [kDa]). The SIV(mac)239 infectious clone does not have a premature stop codon in its TMP-coding region. Transfection of HUT-78 cells with this clone initially yielded virus with a full-length TMP (41 kDa). At 20 to 30 days posttransfection, SIV(mac)239 virus with a 41-kDa TMP gradually disappeared coincident with the emergence of a virus with a 28-kDa TMP. Virus production dramatically increased in parallel with the emergence of a virus with a 28-kDa TMP. Sequence analysis of viral DNAs from these cultures showed that premature stop codons arising by point mutation were responsible for the change in size of the TMP with time. A similar selective pressure for truncated forms of TMP was observed when the SIV(mac)239 clone was transfected into human peripheral blood lymphocytes (PBL). In contrast, no such selective pressure was observed in macaque PBL. When the SIV(mac)239 clone was transfected into macaque PBL and the resultant virus was serially passaged in macaque PBL, the virus replicated very well and maintained a 41-kDa TMP for 80 days in culture. Macaque monkeys were infected with SIV(mac)239 having a 28-kDa TMP; virus subsequently recovered from T4-enriched lymphocytges of peripheral blood showed only the 41-kDa form of TMP. These results indicate that the natural form of TMP in SIV(mac) is the full-length 41-kDa TMP, just as in human immunodeficiency virus type 1. Viruses with truncated forms of TMP appear to result from mutation and selection during propagation in unnatural human cells.

Original languageEnglish (US)
Pages (from-to)4709-4714
Number of pages6
JournalJournal of Virology
Volume63
Issue number11
StatePublished - 1989
Externally publishedYes

Fingerprint

Simian immunodeficiency virus
Simian Immunodeficiency Virus
transmembrane proteins
stop codon
Nonsense Codon
Macaca
Viruses
viruses
Proteins
Clone Cells
clones
Lymphocytes
lymphocytes
blood
transfection
Transfection
Terminator Codon
Viral DNA
Point Mutation
Codon

ASJC Scopus subject areas

  • Immunology

Cite this

Kodama, T., Wooley, D. P., Naidu, Y. M., Kestler, H. W., Daniel, M. D., Li, Y., & Desrosiers, R. C. (1989). Significance of premature stop codons in env of simian immunodeficiency virus. Journal of Virology, 63(11), 4709-4714.

Significance of premature stop codons in env of simian immunodeficiency virus. / Kodama, T.; Wooley, D. P.; Naidu, Y. M.; Kestler, H. W.; Daniel, M. D.; Li, Y.; Desrosiers, Ronald Charles.

In: Journal of Virology, Vol. 63, No. 11, 1989, p. 4709-4714.

Research output: Contribution to journalArticle

Kodama, T, Wooley, DP, Naidu, YM, Kestler, HW, Daniel, MD, Li, Y & Desrosiers, RC 1989, 'Significance of premature stop codons in env of simian immunodeficiency virus', Journal of Virology, vol. 63, no. 11, pp. 4709-4714.
Kodama T, Wooley DP, Naidu YM, Kestler HW, Daniel MD, Li Y et al. Significance of premature stop codons in env of simian immunodeficiency virus. Journal of Virology. 1989;63(11):4709-4714.
Kodama, T. ; Wooley, D. P. ; Naidu, Y. M. ; Kestler, H. W. ; Daniel, M. D. ; Li, Y. ; Desrosiers, Ronald Charles. / Significance of premature stop codons in env of simian immunodeficiency virus. In: Journal of Virology. 1989 ; Vol. 63, No. 11. pp. 4709-4714.
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AU - Desrosiers, Ronald Charles

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