Volume 52, Issue 1 pp. 31-34
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Phenotypic variations and switches in HIV isolated from the blood and the gastrointestinal tissues of patients with HIV-1 infection

W. Al-Mulla

W. Al-Mulla

Faculty of Medicine, Kuwait University, Kuwait

Departments of Medicine and Microbiology and Infectious Diseases, Faculty of Medicine, University of Calgary, Alberta, Canada

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D. Church

D. Church

Departments of Medicine and Microbiology and Infectious Diseases, Faculty of Medicine, University of Calgary, Alberta, Canada

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M. J. Gill

Corresponding Author

M. J. Gill

Departments of Medicine and Microbiology and Infectious Diseases, Faculty of Medicine, University of Calgary, Alberta, Canada

Department of Microbiology and Infectious Diseases, Faculty of Medicine, University of Calgary, 3330 Hospital Drive, N.W., Calgary, Alberta, T2N 4N1, Canada===Search for more papers by this author

Abstract

The objective of this study was to determine the initial and subsequent phenotypes of HIV-1 isolated from the blood, duodenal, and colonic biopsies of 51 HIV-1 positive patients followed prospectively over 2 years. Blood and tissues were cocultured with stimulated peripheral blood monocytes, and HIV was analyzed for phenotypic expression of syncytia-induction (SI). A total of 45/51 patients had HIV-1 isolated from the blood and 35/51 had HIV isolated from gastrointestinal tract. In 12/45 patients SI-HIV-1 was isolated from the blood. In 6/12 patients the blood phenotype reverted to the NSI phenotype. SI phenotypes were also isolated from the colon and duodenum of 8/35 patients and reversion from SI to NSI virus phenotype was again observed in gut tissue of 3/8 patients. These results show that gastrointestinal tissues can harbor SI HIV phenotype. Discordant phenotypes can be found in tissue and blood of late-stage patients. Reversion of phenotypic SI expression to NSI may occur in patients receiving monotherapy as antiretroviral treatment. These results suggest that gastrointestinal tissues may act as a separate and distinct site involved in HIV replication and its associated pathogenesis. J. Med. Virol. 52:31–34, 1997. © 1997 Wiley-Liss, Inc.

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