Archives of Virology

, Volume 141, Issue 3, pp 439–447

Heat shock induces HIV-1 replication in chronically infected promyelocyte cell line OM10.1

Authors

  • K. Hashimoto
    • Department of MicrobiologyFukushima Medical College
  • M. Baba
    • Division of Human Retroviruses, Center for Chronic Viral Diseases, Faculty of MedicineKagoshima University
  • K. Gohnai
    • Roku-chome Clinic
  • M. Sato
    • Department of MicrobiologyFukushima Medical College
  • S. Shigeta
    • Department of MicrobiologyFukushima Medical College
Original Papers

DOI: 10.1007/BF01718308

Cite this article as:
Hashimoto, K., Baba, M., Gohnai, K. et al. Archives of Virology (1996) 141: 439. doi:10.1007/BF01718308

Summary

A long period of clinical latency before development of symptoms is characteristic of human immunodeficiency virus type 1 (HIV-1) infection. OM10.1, a promyelocyte cell line latently infected with HIV-1, has been developed as a model for studying the mechanism of viral latency and the activation of virus expression. We found that this latently infected cell line with heat shock at 42°C for 2 h resulted in a high level of HIV-1 production without addition of any cytokines. The mechanism of activation was analyzed by using anti-TNF-α antibody and various inhibitors. Although the TNF-α level in culture supernatants was below the sensitivity of an ELISA assay system, addition of anti-TNF-α antibody in culture medium could partially suppress the heat shock induced HIV-1 production. Staurosporine (PKC inhibitor), pentoxifylline (NF-ϰB inhibitor), and Ro5-3335 (HIV-1 Tat inhibitor) also inhibited significantly the heat shock induced virus activation. In particular, staurosporine achieved approximately 90% inhibition of the HIV-1 antigen expression in heat shock-treated OM10.1 at a non-toxic concentration. Although the mechanism of HIV-1 activation with heat shock has not been fully elucidated yet, it is presumed PKC plays an important role in HIV-1 activation. Thus, the present observations will provide a further insight into the pathogenesis of HIV-1 infections.

Copyright information

© Springer-Verlag 1996