Mutational analysis of the human immunodeficiency virus: The orf-B region down-regulates virus replication

Paul A Luciw, C. Cheng-Mayer, J. A. Levy

Research output: Contribution to journalArticle

214 Scopus citations

Abstract

Mutations were made by recombinant DNA techniques in an infectious molecular clone of the human immunodeficiency virus San Francisco isolate 2 (HIV(SF2)) [formerly the prototype isolates of the acquired immunodeficiency syndrome-asociated retrovirus (ARV-2)]. The effect of these changes on the replicative and cytopathologic properties of the virus was studied by transfecting modified virus clones into cultured human cells. Mutations in the gag, pol, env, and tat regions precluded virus replication and cytopathology in lymphoid cells. A mutation in orf-A dramatically reduced but did not abolish virus replication. Mutant viruses with deletions in the orf-B region were highly cytopathic and replicated to ~5-fold higher levels than wild-type virus. They also produced ~5-fold more viral DNA in infected lymphoid cells than did wild-type virus. Thus, the orf-B region may function to down-regulate virus replication. This mutational analysis of the HIV(SF2) genome is a means of assessing genes regulating viral replication and cytopathology.

Original languageEnglish (US)
Pages (from-to)1434-1438
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume84
Issue number5
StatePublished - 1987
Externally publishedYes

ASJC Scopus subject areas

  • General
  • Genetics

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