Suppression of human immunodeficiency virus type 1 replication by a soluble factor produced by CD8 + lymphocytes from HIV-2-infected baboons

Christopher P. Locher*, David J. Blackbourn, Jay A. Levy

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)


Human immunodeficiency virus type 2 (HIV-2)-infected baboons (Papio cynocephalus) provide a valuable animal model for the study of acquired immunodeficiency syndrome (AIDS) pathogenesis since many features of disease progression resemble HIV-1-infection of humans. In some HIV-2-infected baboons that are clinically healthy, a CD8 + cell antiviral response, that is partly mediated by a soluble factor, controls vital replication in vitro. In the present study, we demonstrate that CD8 + cells derived from HIV-2- infected baboon peripheral blood, lymph nodes, adenoids and tonsils had antiviral activity in co-cultures of CD8 + and CD4 + cells that inversely correlates with vital load. A soluble factor was found to be active against the chemokine-resistant, syncytium-inducing HIV-1(SF2) and HIV-1(SF33) isolates and was relatively heat stable at 100°C for 10 min. Moreover, inhibition of the transcription from the long terminal repeat of HIV-1 was observed in IG5 cells after activation with phorbol 12-myristate 13-acetate. Therefore, the soluble suppressing activity of CD8 + cells in HIV-2-infected baboons may be analogous to the CD8 + cell antiviral factor described in human HIV-infected asymptomatic people.

Original languageEnglish
Pages (from-to)151-157
Number of pages7
JournalImmunology Letters
Issue number1-3
Publication statusPublished - 1 Mar 1999

Bibliographical note

Funding Information:
The authors would like to thank Karen Rice, Michelle Leland, Kathleen Brasky, Kenneth D. Carey, Thomas Butler, and Krishna Murthy of the Southwest Foundation for Biomedical Research, San Antonio, Texas for their excellent veterinary care of the baboons, Bineetha Ramachandran and Eric Collisson for technical assistance, Christine Beglinger and Ann Murai for secretarial assistance. This work was financially supported by NIH grants AI-34704 and AI-27763. C.P. Locher was the recipient of a postdoctoral training grant provided by the George Williams Hooper Foundation, University of California, San Francisco. D.J. Blackbourn received a scholar award from the University of California, Universitywide AIDS Research Program (F94-SF-008).


  • AIDS
  • Animal model
  • Baboon
  • CD8+ cell antiviral factor (CAF)
  • Human immunodeficiency virus type-2


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