October 27, 2017
Credit: BrianAJackson for iStock via Thinkstock
This week, we gain a new perspective on the relative risk of cardiovascular disease for people with HIV compared to people with diabetes. We also learn about a disagreement regarding the effect of HIV treatment on viral replication; find new insight into how neurocognitive issues affect medication adherence; and increase our understanding of Kaposi sarcoma risk in the modern HIV treatment era.
To beat HIV, you have to follow the science!
Among men, lifetime cardiovascular disease (CVD) risk is higher for people living with HIV (PLWH) than for the general population, a U.S. mathematical model published in Clinical Infectious Diseases showed. Among women, however, risk levels were found to be similar.
The researchers' simulations yielded a 65% lifetime CVD risk among men living with HIV; 59% among men who were HIV negative but deemed to be at high risk for HIV; and 55% among the general male U.S. population. By comparison, simulations found a 44% lifetime CVD risk among women living with HIV; 37% among women who were HIV negative but deemed to be at high risk for HIV; and 46% among the general female U.S. population.
Among both sexes, the relative CVD risk ratio was found to be 1.75 for HIV and 2.0-2.1 for diabetes. "Given that the projected CVD risk among PLWH was similar to those with diabetes, we believe that HIV should be considered a major risk factor for CVD and that PLWH could benefit from preventive strategies similar to persons with diabetes mellitus," study authors concluded.
Contrary to prior findings, HIV might not continue to replicate in lymph tissue after antiretroviral therapy is started, a re-analysis published in Open Forum Infectious Diseases asserts.
Scientists at Northwestern University had previously sequenced DNA samples from three people living with HIV before they started antiretrovirals, and over the first six months they were on treatment. According to that analysis, the virus continued to replicate in lymphoid tissue.
However, researchers from the National Cancer Institute dispute these findings. In the current study, they analyzed the same viral sequences as the first study, as well as DNA from four people who had been virally suppressed for at least seven years. The variation in viral sequences during the first half year on treatment may be due to shifting provirus populations, rather than viral replication, they observed. Furthermore, when a different analytical approach was used, the genetic distance between the viral DNA before and after treatment could not be detected in most samples.
"This finding shows that the appearance of evolution clearly depends on the choice of routing method," noted the authors, who concluded that the first study did not prove that HIV continues to replicate during antiretroviral therapy.
Medication adherence declined significantly among people with HIV-associated neurocognitive disorders (HAND) compared to neuropsychologically normal participants in a small Swiss pilot study published in Open Forum Infectious Diseases.
Fifty-nine people living with HIV were followed for three years. Slightly over one-third had no neurocognitive issues, 27% had HAND, and the remainder had other cognitive problems, mainly depression. Drug adherence was measured via digital pill bottle caps. During the study period, medication adherence in the HAND arm declined by half compared to the arm without neurocognitive impairments. People with HAND were also more likely to have a detectable viral load compared to the other arms.
The best way to treat HAND is to start antiretrovirals early and maintain the treatment; "Therefore, developing effective strategies to enhance medication adherence in these patients is crucial," study authors concluded. Their suggested interventions included inviting patients' partners to adherence support groups.
People living with HIV in South Africa and men who have sex with men in Europe and the Americas are at especially high risk of contracting Kaposi sarcoma (KS), even in the modern era of effective antiretroviral treatment, an analysis of data from global HIV cohorts published in Clinical Infectious Diseases found.
Researchers compared demographic characteristics, CD4+ cell counts and other information on more than 200,000 people from 57 countries who began to take antiretrovirals after 1995. KS incidence rates were much lower in the Asia-Pacific than in other areas of the world. Across the globe, low CD4+ cell count (< 50 cells/µL) increased the risk for contracting KS. However, CD4+ cell count played less of a role in reducing KS risk in South Africa than it did elsewhere.
Study authors hypothesize that regional differences may be related to the relative prevalence of human herpesvirus 8 (HHV-8) coinfection. "While a vaccine against HHV-8 remains unavailable, early ART initiation and maintenance of high CD4 cell counts are essential to reducing the incidence of KS in populations at high risk for HHV-8 coinfection," they concluded.
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