Introduction: HTV replication may be induced by immune activation due to acute infections and vaccinations. Objectives: We studied the effect of common acute infections (e.g. PCP, bacterial pneumonia, bacteremia and cellulitis) on HIV replication and the expression of markers of immune activation. Methods: We prospectively evaluated 32 HTV-infected adults (18 females and 14 males, median CD4 count 91 cells/ml) on stable or no antiretroviral therapy with documented acute infections. HIV RNA levels (RT-PCR) and serum markers of immune activation including TNF-α, soluble (s)TNF-R1, STNF-R2, IL-6, IL-10, IL-2, sIL-2R, sCD4, and sCD8 were assessed in available plasma at four time points: preillness, acute illness (within 48 hours), two week and four week convalescent visits. Results: HIV RNA levels (median copies/ml) were as follows: Visit Type (n) Day HIV RNA Comparison Δ for Paired Samples Pre-illness (19) -60 122,399 NA NA Acute (32) 0 429,393 Pre + 458,102 (p=0.001) Two-week (20) 15 267,759 Acute - 103,862 (p=0.01) Four-week (14) 30 177,123 Acute - 196,024 (p-0.025) Cross-sectional linear regression analysis revealed a significant correlation between viral load and SIL-2R. The increase in HIV RNA with illness was correlated with increases in TNF-R2, SIL-2R, and IL-10, while the decrease at 4 weeks was correlated with decreases in TNF-R2 and SIL-2R. TNF-α, IL-2, IL-6, sCD8, and sCD4 were not correlated with HTV RNA levels or changes. Conclusions: Some common acute infections are associated with transient increases in plasma HIV RNA levels (duration 2-4 weeks). Significant changes in viral load during acute illness may be the result of immune activation. Viral load measurements should be interpreted cautiously during periods of possible immune activation.
|Original language||English (US)|
|Number of pages||1|
|Journal||Clinical Infectious Diseases|
|Publication status||Published - 1997|
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