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Updated: Aug 9, 2026

Oral Combinational Antiretroviral Treatment in HIV-1 Infected Humanized Mice
Published on: October 6, 2022
Vitamins C and E in adolescents and young adults with HIV infection
Charles B Stephensen1, Grace S Marquis, Robert A Jacob
1US Department of Agriculture Agricultural Research Service, Western Human Nutrition Research Center at the University of California-Davis, Davis, CA 95616, USA. cstephen@whnrc.usda.gov
Background:
Oxidative stress during HIV infection may impair immune function, cause more rapid disease progression, and increase requirements for dietary antioxidants such as vitamins C and E.
Objectives:
The study had 2 principal objectives. The first was to ascertain whether HIV infection and immune activation were associated with lower plasma concentrations of ascorbate, urate, and alpha- and gamma-tocopherols and with total antioxidant status (TAS). The second objective was to ascertain whether these antioxidants were associated with protection against oxidative damage.
Design:
This was a cross-sectional study involving 241 HIV-positive and 115 HIV-negative subjects aged 14-23 y. Subjects were primarily female (76%) and African American (70%), and 21% were Hispanic.
Results:
Plasma ascorbate was significantly lower, but gamma-tocopherol and TAS were significantly higher in subjects with HIV infection when the analysis was adjusted for dietary intake and sex. Plasma alpha-tocopherol did not differ significantly by HIV status. Plasma gamma-tocopherol also was higher in subjects with oxidative damage than in those without such damage. More than 90% of subjects had adequate plasma concentrations for both ascorbate and alpha-tocopherol, although alpha-tocopherol concentrations were lower than expected on the basis of third National Health and Nutrition Examination Survey data.
Conclusions:
Low plasma ascorbate concentrations in HIV-positive subjects suggest that vitamin C requirements are significantly higher in those with HIV infection. Plasma tocopherol concentrations were not depressed by HIV infection and may be maintained by compensatory mechanisms such as the activity of alpha-tocopherol transfer protein.
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