AIDSWEEKLY Plus, Monday, 17 March 1997
Daniel J. DeNoon, Senior Editor
Lymphoid tissues infected by AIDS-related opportunistic infections (OIs) are crawling with HIV.
In many of the cells tested for HIV by in situ hybridization, the viral signal was so bright that the cell could not be seen.
The findings came during studies designed to help answer one of the main puzzles of HIV disease: why does HIV viral load continue to increase even when CD4 T lymphocytes - thought to be the primary host cells for the virus - are virtually eliminated?
The answer appears to be that tissue macrophages are the primary host for HIV in the later stages of AIDS, according to J.M. Orenstein of George Washington University, Washington, D.C., and S.M. Wahl of the National Institutes of Health, Bethesda, Maryland. Orenstein reported their data at the Fourth Conference on Retroviruses and Opportunistic Infections, held January 22-26 in Washington, D.C.
"The dynamic relationship between opportunistic pathogens, macrophages, and high levels of viral replication suggest that co-infection is an impetus for HIV production, and that macrophages contribute to plasma viremia, particularly in late-stage HIV disease," Orenstein and Wahl wrote in their presentation abstract.
The researchers noted that bursts of increased viremia occur in people with HIV infection after vaccination or infection. To find out where the virus comes from in people with small numbers of CD4(+) T lymphocytes, they used in situ hybridization to explore AIDS patients' lymph-node tissues for co-expression of HIV and OI pathogens.
"Unprecedented levels of HIV production were evident in tissues with OIs," they reported. "For example, in disseminated Pneumocystis carinii, a heavily infected node exhibited striking concentrations of HIV-1 signal."
The few lymphocytes remaining in the lymph nodes had much less expression of viral RNA than macrophages.
Electron microscopy showed that the HIV/P. carinii co- infected cells had HIV particles within macrophage vacuoles, budding from plasma membranes, and co-localized with P. carinii.
"The viral explosion was not limited to P. carinii infection but was also evident in other OI-infected tissues," Orenstein and Wahl wrote. "Mycobacterium avium-infected mononuclear and especially Langerhans-type multinucleated cells were often totally obscured by [the] in situ hybridization viral signal."
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