January 6, 2017
This week, a study examines how two precursor forms of vitamin D may help protect against HIV infection. Another study supports the idea of protease inhibitor monotherapy, specifically for individuals with high CD4 counts and who have had undetectable viral loads for years. Finally, people in New York City are being diagnosed earlier and starting treatment sooner than they were a decade ago. To beat HIV, you have to follow the science!
Two precursor forms of vitamin D may protect against HIV infection through three distinct mechanisms, a study published in Journal of Acquired Immune Deficiency Syndromes found.
Researchers used different concentrations of the two provitamins, cholecalciferol and calcidiol, to culture peripheral blood mononuclear cells (PBMCs) from 39 Colombian and Italian volunteers who are not living with HIV. These cells, along with untreated PBMCs serving as controls, were then infected with X4-tropic HIV and certain properties were measured.
Cholecalciferol lowered the percentage of cells infected with HIV and the concentration of p24 viral protein in the infected cells. The provitamin also affected the expression of immune activation markers in T cells and reduced HIV infection in CD4+ cells. Calcidiol, in turn, lowered productive HIV infection and affected mitochondrial RNA expression of the CCR5 co-receptor.
Study authors explained that these vitamin D precursors may protect against HIV by "inducing antiviral gene expression, reducing the viral coreceptor CCR5 and ... promoting an immunophenotype" that restricts HIV.
Taking only a ritonavir (Norvir)-boosted protease inhibitor (PI) may be a viable therapy option for people living with HIV whose viral load has been suppressed for years and who have a high CD4 cell count, according to results from the PIVOT trial reported in AIDS.
The viral loads of fewer than a third of the 290 study participants rebounded after starting PI monotherapy, and that rebound occurred mostly during the first nine months after the switch to the PI.
A return to a detectable viral load while taking only one HIV medication was more likely among people whose HIV had been suppressed for shorter periods before switching to the PI (hazard ratio 0.81 per additional year <50 copies/ml; P < 0.001), who had a lower CD4 cell count (hazard ratio 0.73 per additional 100 cells/μL for CD4+ nadir; P = 0.008), and who were people of color (hazard ratio 1.87 for people of color versus white, P = 0.025). Study authors suggested that the racial difference observed could be due to social factors, but did not rule out a biological cause.
By 2012, people living with HIV in New York City were diagnosed earlier and started antiretroviral therapy sooner than in 2006, an analysis published in The Journal of Infectious Diseases found.
The study drew on data from the city's population-based HIV Surveillance Registry and included HIV diagnoses between 2006 and 2012 among people who were at least 13 years old at the time of diagnosis. The conclusions are based on a trend over time of higher CD4 cell counts at diagnosis and treatment start among those with newly acquired HIV.
These counts increased from 325 cells/μL in 2006 to 379 cells/μL in 2012 for diagnosis, and from 178 cells/μL to 360 cells/μL during the same period for starting HIV treatment. However, people of color and those acquiring HIV through routes other than men who have sex with men (MSM) had lower CD4 cell counts than did their counterparts during the same period.
Warren Tong is the senior science editor for TheBody.com and TheBodyPRO.com. Follow Warren on Twitter: @WarrenAtTheBody.
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