Background:  Vitamin E has a complex role in maintaining immune function, and variable roles have been ascribed to it in HIV-1 infection. Low serum vitamin E has been found in advanced HIV-1 infection, and a small number of studies have suggested that vitamin E supplementation may slow HIV-1 disease progression. We hypothesized that vitamin E levels prior to HIV-1 seroconversion might influence HIV-1 RNA set point viral load and survival after HIV-1 infection.

Methods:  Vitamin E status was assessed for 67 female sex workers from Mombasa, Kenya, for whom the date of HIV-1 infection could be reliably estimated. Vitamin E levels were measured in stored samples from the last pre-seroconversion, RNA-negative visit, at a median of 30 days prior to HIV-1 acquisition. HIV-1 RNA set point was measured in the first sample collected 4 to 24 months after the estimated date of infection. Linear regression was used to estimate associations between vitamin E and HIV-1 RNA set point. Cox proportional hazards regression models were used to look for an association with survival. Analyses were adjusted for age, parity, education, use of hormonal contraception, presence of a genital ulcer, and year of infection.

Results:  Median pre-seroconversion vitamin E levels were 7.5 mg/L (IQR, 5.2 to 9.5 mg/L). After adjustment for potential confounding factors, each 1 mg/L increase in the vitamin E level was associated with a 0.12 log₁₀ copies/mL (95% CI 0.03 to 0.21 log₁₀ copies/mL) increase in HIV-1 RNA viral load set point (p = 0.01). Pre-seroconversion vitamin E levels were associated with increased mortality, with a hazard ratio of 2.2 (95% CI 1.4 to 3.6, p = 0.001) per 1 mg/L increase in vitamin E.  After adjustment for viral load set point, increased mortality persisted (HR = 2.1, 95% CI 1.3 to 3.4, p = .003).

Conclusions:  Higher pre-seroconversion vitamin E levels were associated with both higher HIV-1 RNA viral set point and mortality. The association between vitamin E level and mortality remained significant after adjustment for HIV-1 RNA viral set point, suggesting an effect independent of set point viral load. The mechanism by which vitamin E affects disease progression is unknown, but vitamin E can increase CCR5 expression and thereby influence HIV-1 susceptibility. Although vitamin E has been considered beneficial in HIV disease, our findings indicate that higher vitamin E levels prior to HIV-1 acquisition may be associated with increased viral replication and mortality.