HIV-1 infection stimulates T cell invasiveness and synthesis of the 92-kDa type IV collagenase.

Published

Journal Article

Tissue-specific localization of HIV-1-infected lymphoid cells may contribute to clinical manifestations of AIDS. Therefore we investigated the effect of HIV-1 infection on mechanisms of T lymphocyte invasion, a process required for movement of cells into and out of the circulation. In the present study, we demonstrate that HIV-1-infected human lymphocytes secrete increased amounts of the human 92-kDa type IV collagenase when compared to uninfected lymphocytes. Furthermore, HIV-1-infected lymphocytes degrade the extracellular matrix proteins collagen IV and fibronectin, and they are more invasive through a reconstituted basement membrane when compared to uninfected cells. The addition of either antibody to the 92-kDa collagenase or TIMP-2, a type IV collagenase inhibitor, abolishes invasive activity. These data suggest that HIV-1-infected lymphocytes express phenotypic characteristics that are consistent with an enhanced ability to leave the circulation and to localize in target tissues. Local viral infection or the release of viral proteins, cytokines, or proteolytic enzymes in tissues may contribute to pathogenesis.

Full Text

Duke Authors

Cited Authors

  • Weeks, BS; Klotman, ME; Holloway, E; Stetler-Stevenson, WG; Kleinman, HK; Klotman, PE

Published Date

  • June 1, 1993

Published In

Volume / Issue

  • 9 / 6

Start / End Page

  • 513 - 518

PubMed ID

  • 8347396

Pubmed Central ID

  • 8347396

Electronic International Standard Serial Number (EISSN)

  • 1931-8405

International Standard Serial Number (ISSN)

  • 0889-2229

Digital Object Identifier (DOI)

  • 10.1089/aid.1993.9.513

Language

  • eng