Heat shock induction of HIV production from chronically infected promonocytic and T cell lines

Sharilyn K. Stanley, Peter B. Bressler, Guido Poli, Anthony S. Fauci

Research output: Contribution to journalArticlepeer-review


HIV infection is associated with a long period of clinical latency before the development of symptoms and HIV-related disease. Two chronically HIV-infected cell lines, U1 (promonocytic) and ACH-2 (T-lymphocytic) have been developed as models for studying the mechanisms governing viral latency and the reactivation of virus expression. We have previously shown that a variety of physiologic stimuli, including cytokines and cell stress, can up-regulate HIV expression from these cell lines. In this study we demonstrate that heat shock can also up-regulate the production of virus from both ACH-2 and U1 cells. Heat induction of virus appears to be mediated at the transcriptional level as established in long terminal repeat-chloramphenicol acetyl transferase transient transfection experiments with the use of U937 cells. This inductive effect in part requires the NF-κB-binding region of the HIV-long terminal repeat. Furthermore, although physiologic levels of heat are not sufficient to directly induce virus production from these cells, these temperatures are able to synergistically enhance virus production in U1 cells stimulated with IL-6 and granulocyte macrophage-CSF. In contrast, the inductive effect of other cytokines (i.e., TNF-α) was not affected by heat stimulation. These in vitro observations suggest that the hyperthermia associated with opportunistic infections, particularly in conjunction with certain cytokines that are released during immune reactions, may play a role in the in vivo induction of HIV expression in infected cells.

Original languageEnglish
Pages (from-to)1120-1126
Number of pages7
JournalJournal of Immunology
Issue number4
Publication statusPublished - Aug 15 1990

ASJC Scopus subject areas

  • Immunology


Dive into the research topics of 'Heat shock induction of HIV production from chronically infected promonocytic and T cell lines'. Together they form a unique fingerprint.

Cite this