Actual article title, though I disagree with the “high-dose” qualifier as it corresponds roughly to a vitamin D3 dose of ~7,000 IU daily, which is not really a pharmacological dose. While the authors were not brave enough to claim that vitamin D supplementation could be an effective prophylactic measure for HIV/AIDS they did demonstrate that lack of sunlight (in this case due to low UVB exposure of people in the winter) and the accompanying vitamin D deficiency result in both a suppressed immune system and a semi-anemic condition. Both of those effects of sunlight deficiency were reversed by supplementing vitamin D3 for 6 weeks, at a dose of 60,000 IU once weekly. Perhaps most importantly, the blood of people deficient in vitamin D was vulnerable to infection/replication with HIV, while the blood of supplemented subjects was highly resistant to the pathogen. Whether that means vitamin D supplementation alone can prevent (maybe treat?) HIV/AIDS is as of yet unanswered, but the authors seem confident-enough in their results to state that vitamin D can become a powerful tool in the fight against the disease, especially in low-income regions like Africa (where the study was conducted), and where only a cheap and widely available intervention such as vitamin D has a chance of being adopted.
“…To investigate the functional consequence of seasonal serum 25(OH)D levels on the immune system, we next investigated seasonal differences in full blood count (FBC) and the effect of vitamin D3 supplementation on FBC in Xhosa participants. Vitamin D3 supplementation in the winter increased WBC count (P = 0.0016) and in particular lymphocyte count (P = 0.023), and there was a winter trend for decreased monocytes (Fig. 2 A–C). In the winter, participant’s RBC parameters tended toward macrocytic anemia [evidenced by decreased RBC and RBC distribution width (RDW), increased mean corpuscular volume, and a trend toward decreased Hb], and this tendency was reversed by supplementation (P ≤ 0.0007) (Fig. 2 D–F and Fig. S4A).”
“…Infection of PBMCs in winter, compared with summer, resulted in greater productive HIV-1 infection on day 9, as measured by culture supernatant p24 antigen levels. This result was seen in PBMCs isolated from both Xhosa (P = 0.0003, Fig. 2 G–I) and Cape Mixed (P < 0.0001, Fig. S4 E and F) participants. This winter increase in HIV-1 infection was seen with both preparations of HIV-1, with ∼1-log higher p24 measured from cells infected with unpurified virus (Xhosa median 7,038 pg/mL unpurified vs. 738 pg/mL purified) (Fig. 2 H and I). After 6 wk of vitamin D3 supplementation in winter, the winter increase in HIV-1 p24 was attenuated, and Xhosa participants’ PBMCs showed a diminished capacity for productive HIV-1 infection: on day 9 p24 levels had dropped to the level as observed in summer (Fig. 2G). Again, this decrease occurred with infections using both purified and unpurified virus (Fig. 2 H and I), demonstrating the robustness of oral vitamin D3 supplementation in suppressing productive HIV-1 infection in peripheral blood cells ex vivo. Moreover there was a significant negative correlation between paired serum 25(OH)D and day 9 p24 concentrations from PBMCs infected with purified virus, across all time points (Spearman rs = −0.36; P < 0.0001), indicating a direct correlation between serum 25(OH)D levels and the ability of peripheral blood cells to limit productive HIV-1 infection.”