Infectious mutants of HTLV-III with changes in the 3′ region and markedly reduced cytopathic effects

Amanda G. Fisher, Lee Ratner, Hiroaki Mitsuya, Lisa M. Marselle, Mary E. Harper, Samuel Broder, Robert C. Gallo, Flossie Wong-Staal

Research output: Contribution to journalArticlepeer-review

156 Scopus citations

Abstract

A variant of human T-lymphotropic virus type III (HTLV-III) is described that replicates but does not kill normal human T cells in vitro. This variant, designated X10-1, was derived from the genome of a cytopathic HTLV-III clone (pHXB2D) by excision of a 200-base pair segment in the 3′ region of the virus, spanning the env and 3′-orf genes. Comparable variants with 55 to 109 base pairs deleted exclusively in 3′-orf produced, in contrast, virus that was extremely cytopathic. On the basis of these findings it is concluded that the 3′-orf gene is not required for cytopathogenicity or replication of HTLV-III. In addition, the results suggest that virus replication and cytotoxicity are not intrinsically coupled. Furthermore, since clone X10-1 retains the ability to trans-activate genes linked to the viral long terminal repeats, trans-activation per se is not responsible for T-cell killing by HTLV-III. These results also raise the possibility that the carboxyl terminus of the envelope gene of HTLV-III has a direct role in T-cell killing by this virus.

Original languageEnglish
Pages (from-to)655-659
Number of pages5
JournalScience
Volume233
Issue number4764
DOIs
StatePublished - 1986

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