June 24, 2016
This week, a study examines the effects of antiretroviral therapy on arterial inflammation in people living with HIV. Another study finds that while a higher CD4 count at treatment initiation is strongly associated with a lower mortality rate, the association essentially vanishes after five years on treatment. To beat HIV, you have to follow the science!
Starting antiretroviral therapy (ART) is insufficient for stopping the progression of HIV-associated cardiovascular disease in the short term, according to a small study published in JAMA Cardiology.
The study measured coronary plaque and other cardiovascular markers before and six months after starting HIV treatment with elvitegravir/cobicistat/emtricitabine/tenofovir (Stribild) in 12 men living with HIV who had not previously taken antiretrovirals. It also assessed participants' systemic immune and metabolic factors and analyzed the same factors in a control group of 12 people who were not affected by HIV.
While almost all (11 of 12) study participants achieved viral suppression (below 20 copies/mL) six months after starting ART, one-third (4) experienced increased or new-onset coronary plaque.
Overall, HIV treatment did not reduce arterial inflammation as measured by aortic target-background ratio in the participants living with HIV. The study authors concluded that while HIV treatment dampens some immune activation indices, "[c]omplementary strategies to reduce arterial inflammation among ART-treated HIV-infected individuals may be needed."
The study was published online ahead of print in JAMA Cardiology.
A higher initial CD4 count is strongly associated with a lower mortality rate during the first year after starting combination antiretroviral therapy (ART), but that association essentially vanishes after five years on treatment, according to a study published in Clinical Infectious Diseases.
The study analyzed the records of 37,496 patients in Europe and North America who had started ART between 1996 and 2001. Overall mortality per 1,000 person years (mortality rate, MR) six months after starting treatment was 32.8, but dropped by almost half to 16.0 after 5-10 years on ART.
Study participants who began treatment at CD4 counts below 50 were more than twice as likely to die during the first six months of treatment (MR = 88), but had only a slightly higher MR (18.6) after 5-10 years on treatment. For those starting treatment with a CD4 count of at least 500, MR after six months was about one-quarter of the overall rate (8.5), but increased to 11.9 after 5-10 years on treatment.
This shows that "the burden of increased mortality associated with starting treatment late is alleviated for those who survive 5 years on ART," study authors concluded.
The study was published online in Clinical Infectious Diseases.
A Spanish study recently reported in AIDS proposed a clinical score for determining which elite or viremic HIV controllers are likely to progress to detectable viral loads. The 204 elite controllers in the study were defined as HIV-infected individuals who had never taken antiretrovirals, but whose viral load stayed below 50 copies/mL for at least one year, while the 271 viremic controllers had viral loads between 50 and 2,000 copies/mL for the same period.
Over the course of 2-10 years almost one-third of these 475 patients lost virologic control and nearly half of study participants' CD4 counts fell by more than 25%. Loss of controller status was more likely in those who were coinfected with hepatitis C, had a higher viral load, had a lower nadir CD4 count, had a sexual risk for HIV infection or had been followed for a shorter period.
The proposed clinical score would quantify such factors and be used as an "objective adjunct to clinical judgment" for determining the start of HIV treatment in elite and viremic controllers.
The study was published online in AIDS.
Barbara Jungwirth is a freelance writer and translator based in New York.
Follow Barbara on Twitter: @reliabletran.
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