Human immunodeficiency virus-associated vasculopathy in transgenic mice

Brad T. Tinkle, Lien Ngo, Paul A Luciw, Tom Maciag, Gilbert Jay

Research output: Contribution to journalArticle

37 Scopus citations

Abstract

There is substantial clinical evidence for the development of vascular disorders in human immunodeficiency virus (HIV)-infected individuals, particularly in the form of vasculitis. Transgenic mice carrying a replication-defective HIV-1 provirus with selective deletion of the gag, pol, and env genes developed extensive vasculopathy. Restricted expression of HIV nonstructural genes in smooth muscle cells was accompanied by the migration and proliferation of these cells in blood vessels of all sizes and at different body sites. The frequent infiltration observed in the hypertrophic vessel walls occurred predominantly in the adventitia and was composed of primarily T cells and occasionally plasma cells. The intimal thickening generated significant luminal narrowing in some vessels, and the restricted blood flow led to ischemia in the affected tissues. Interestingly, the endothelium did not appear to support HIV gene expression or be involved in the pathological process. This transgenic model provides an opportunity to dissect the mechanism underlying HIV-associated vasculopathy.

Original languageEnglish (US)
Pages (from-to)4809-4814
Number of pages6
JournalJournal of Virology
Volume71
Issue number6
StatePublished - Jun 1997

ASJC Scopus subject areas

  • Immunology

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    Tinkle, B. T., Ngo, L., Luciw, P. A., Maciag, T., & Jay, G. (1997). Human immunodeficiency virus-associated vasculopathy in transgenic mice. Journal of Virology, 71(6), 4809-4814.