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Fine needle aspiration can be a noninvasive method of sampling immune cells and of assessing the amount of virus in palpable lymph nodes of HIV patients. A comparison between samples of biopsied lymph node cells (LNC) and peripheral blood mononuclear cells (PBMC) taken from 17 HIV-infected patients showed a difference in HIV RNA content and viral load. Both the viral load and RNA counts were higher in lymphoid tissue than in the blood cell samples.

The prototypic macrophage-tropic HIV-1 isolate, HIV-1BaL, cannot replicate in the monocytoid cell line THP-1. After induction of differentiation by a phorbol diester, a fraction of THP-1 cells became permissive to HIV-1BaL. In contrast, this treatment decreased permissiveness for the lymphotropic isolate HIV-1LAI. Viral DNA was not synthesized in unstimulated THP-1 cells, as determined with PCR, suggesting that the block to HIV-1BaLreplication in these cells occurred at an early step of the virus replicative cycle prior to or at the level of reverse transcription. Virus binding studies showed that differences in cell permissiveness for HIV-1BaLwere not due to altered virus binding. Substantial amounts of HIV-1BaLbound to both undifferentiated and differentiated THP-1 cells, and this binding could not be prevented by blocking with the anti-CD4 antibody Leu3a, which did prevent the binding of HIV-1LAIto CEM T lymphoid cells. While Leu3a was very effective st preventing the infection by HIV-1LAIin CEM cells, it was less effective in preventing HIV-1BaLinfection of differentiated THP-1 cells or primary macrophages. Although it is likely that molecules other than CD4 on monocytic cells can mediate binding of macrophage-tropic HIV, the binding of HIV-1BaLto THP-1 cells was not sufficient for infection, because binding was the same in nonpermissive undifferentiated cells as in permissive differentiated cells. Thus, the restriction of viral replication in this model cell system occurs at some step after virion binding. Comparison of differentiated THP-1 cells with their undifferentiated counterparts may provide an approach to defining cellular determinants of HIV host range other than CD4 expression and to characterizing the incompletely defined steps of vital entry.