4th Conference on Retroviruses and Opportunistic Infections Washington, DC - January 22-26, 1997

Conf Retroviruses Opportunistic Infect 1997 Jan 22-26; 4th:147 (abstract no. 450)

Javan C, Shaunak S; Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.

Background: The switch of primary viral isolates from NSI to SI is a useful prognostic indicator in HIV-1+ patients. However, its relevance to the in-vivo pathogenesis of AIDS remains to be determined because autopsy studies in AIDS patients have shown that the predominant tissue viral genotype is NSI. The reason for this difference between studies performed during life and after death is not clear.

Methods: 67 HIV-1 positive patients were monitored prospectively for 2 years. Every 4 months, their viral phenotype was determined by co-culturing the patient's PBMN cells with MT2 cells and monitoring for syncytia for 21 days. At the same time, the patient's PBMN cells were also cultured with PHA-activated PBMN cells and maintained for 21 days. Culture supernatants were then harvested and tested for p24 (EIA, Coulter). Provided HIV-1 was isolated from the PBMN co-cultures, the result of the MT2 assay was recorded as showing an SI or an NSI phenotype.

Results: In 43 (64%) patients the viral phenotype remained NSI. In 10 (15%) patients the viral phenotype remained SI. In 5 (7%) patients the viral phenotype changed from NSI to SI. In 2 (3%) patients the viral phenotype showed a single switch from SI to NSI. In the remaining 7 (11%) patients, there was multiple switching between SI and NSI phenotypes. Multiple switching of the viral phenotype was only seen in patients with a CD4 count of less than or equal to 100/µL.

Conclusions: Frequent sampling over a period of 2 years showed that multiple switching of the viral phenotype is common in the peripheral blood of patients with low CD4 counts. These results suggest that NSI phenotypes of HIV-1, which probably originate from tissue macrophages, are making a significant contribution to the circulating pool of HIV-1 in the PBMN cells of patients with AIDS.

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