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9th Conference on Retroviruses and Opportunistic InfectionsSeattle, Washington - February 24 -February 28, 2002 |
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Conf Retroviruses Opportunistic Infect 2002 Feb 24-28;9:abstract no. 21
Gottlieb GS, Sow P, Hawes S, Ndoye I, Redman M, Coll-Seck AM, Faye M, Diop A, Kuypers JM, Critchlow CW, Respess R, Mullins J, Kiviat N; Univ. of Washington, Seattle
BACKGROUND: In comparison to HIV-1, HIV-2 infection is characterized by slower disease progression and lower rates of transmission. Gaining insights into the relationship between plasma HIV RNA viral load, PBMC HIV DNA levels, and the rate of CD4+ cell decline associated with HIV-2 as compared to HIV-1 infection is essential to understanding the very different natural histories of infection with these closely related viruses.
METHODS: In this study, we examine the relationship between plasma HIV RNA viral load, PBMC HIV DNA levels, and CD4+ T-cell decline associated with HIV-1 as compared to HIV-2 infection among 472 HIV-1- and 114 HIV-2-infected individuals prospectively followed in Senegal, since October 1994.
RESULTS: HIV-1 plasma RNA levels were significantly greater than those of HIV-2, even when adjusted for CD4+ T-cell count (unadjusted mean log10 plasma HIV RNA copies/mL: 4.92 ± 1.24 vs 2.18 ± 1.86, HIV-1 and HIV-2 respectively, p<0.0001). Mean HIV-1 and HIV-2 PBMC DNA viral levels did not significantly differ (mean log10 1.42 ± 0.76 copies HIV-1 vs 1.54 ± 0.92 copies HIV-2 /µg PBMC DNA, p = 0.17). CD4 counts were strongly correlated with PBMC HIV DNA levels in both HIV-1 and HIV-2, although this relationship appears to be stronger in HIV-2 compared to HIV-1 (p=0.01). In multivariate analysis, PBMC HIV DNA viral load levels were positively associated with HIV plasma RNA viral load levels, irrespective of CD4 count or HIV type. In 169 individuals with baseline CD4+ T cells > 200/µl followed longitudinally, the annual rate of CD4+ T-cell count decline in the HIV-2 cohort was approximately one-fourth that of the HIV-1 cohort (4.1%/year [95% CI: -0.5-9.2] vs 15.9%/year (95% CI: 11.1-20.3), and was linear over time. However, when stratified for plasma RNA viral load, the rate of CD4 decline per year for the HIV-1 and HIV-2 cohorts were similar (increasing approximately 4.1% and 3.3% per year, respectively, for each log10 increase in viral load).
CONCLUSIONS: Marked differences in plasma viral loads between HIV-1- and HIV-2-infected individuals do not appear to be due to differences in the levels of infected PBMC target cells. However, HIV plasma RNA viral loads are highly correlated with PBMC viral load levels. Other mechanisms for maintaining elevated HIV-1 viral loads may be occurring: possibly including elevated virus production per infected PBMC, other reservoirs of elevated HIV-1 production compared to HIV-2, or less aggressive immune responses to HIV-1. Plasma viral load is predictive of rate of CD4+ T-cell decline over time, and the viral load/rate correlation appears to be similar in all HIV infected individuals, irrespective of whether they harbor HIV-1 or HIV-2.
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Copyright © 2002 - Foundation for Retrovirology and Human Health. Reproduction of this abstract (other than one copy for personal reference) must be cleared through the Foundation for Retrovirology and Human Health. Licensed (AIDSLINE) from National Library of Medicine.
