June 22, 2015
Vitamin D deficiency affected two thirds of two HIV-negative South African groups during winter, in a 100-person prospective study. High-dose supplementation reversed that deficiency and lowered HIV replication measured by p24 antigen levels in peripheral blood mononuclear cells (PBMCs), according to study results published in the journal PNAS.
Well known for its role in bone health, vitamin D can also affect the progression of infectious diseases, including HIV infection. Ultraviolet B (UVB) radiation varies seasonally in the high and low latitudes, including South Africa, and drives seasonal vitamin D variation. Native South Africans are dark-skinned and live in a country of high HIV prevalence.
To determine UVB levels in two Cape Town populations and their potential impact on HIV disease progression, researchers conducted this longitudinal study in 50 dark-skinned Xhosa Cape Town residents and 50 moderately dark-skinned Cape Mixed residents. They measured individual UVB exposure in summer and winter, estimated dietary vitamin D, drew blood samples, and genotyped participants for 10 single-nucleotide polymorphisms (SNPs) associated with vitamin D deficiency. Participants took 50,000 IU of vitamin D weekly (as cholecalciferol) for six weeks in winter, and 30 Xhosa people had serum 25-hydroxy vitamin D, abbreviated 25(OH)D, remeasured after supplementation. The researchers collected PBMCs, infected them with HIV-1, and estimated HIV-1 replication in PBMCs by measuring HIV-1 p24 antigen levels.
In winter, 18% of Xhosa people and 12% of Cape Mixed people had severe vitamin D deficiency (< 30 nmol/L), and overall deficiency rates (< 50 nmol/L) were 64% and 70%, respectively. Linear regression analysis determined that personal net UVB exposure was the principal determinant of 25(OH)D levels (P < .0001), with lesser contributions from the area of skin exposed and certain SNPs.
Among the 30 Xhosa people with follow-up after winter vitamin D supplementation, 23 (77%) gained optimal 25(OH)D levels (≥ 75 nmol/L). In winter, red blood cell measures tended toward macrocytic anemia, and vitamin D supplementation reversed this trend. Supplementation in the Xhosa group significantly increased white blood cell count (WBC) (P = .0016) and lymphocyte count (P = .023).
In both Xhosa and Cape Mixed people, productive HIV infection of freshly isolated PBMCs (measured by p24 antigen level) was approximately 10-fold greater in the winter (when 25(OH)D levels were low) than in the summer. In Xhosa people treated with high-dose vitamin D in the winter and followed for six weeks, supplementation attenuated the winter increase in p24 antigen, as p24 levels fell to those recorded in the summer. The investigators charted a significant negative correlation between 25(OH)D levels and p24 concentrations in PBMCs (P < .0001).
The researchers concluded that the reversal of vitamin D deficiency in dark-skinned people by vitamin D supplementation prevents anemia, raises WBC counts and decreases productive HIV infection in freshly isolated PBMCs. They proposed that vitamin D supplementation "may be a simple, cost-effective intervention, particularly in resource-poor settings, to prevent disease progression in persons infected with HIV-1 by suppressing viral replication."
The practical value of these findings remains uncertain, however, since the estimated 10-fold p24 reduction in isolated cells must be considered modest in a country that now recommends antiretroviral therapy for all pregnant and breastfeeding women regardless of CD4 count and for all other adolescents and adults with a CD4 count ≤ 500.
Mark Mascolini is a freelance writer focused on HIV infection.
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