September 3, 2015
This week we look at some promising early results from researchers who were able to modify human CD4+ cells to potentially make them immune to HIV. Another study examines how three different treatment regimens change artery wall thickness. In addition, researchers estimate what it would actually take to achieve universal treatment for all.
To beat HIV, you have to follow the science!
Researchers have been able to modify CD4+ cells using a gene-editing system known as CRISPR/Cas9, according to a report from the University of California, San Francisco. Using this technique, the scientists disabled the CXCR4 receptor of CD4+ cells, which could block certain types of HIV. These are just early laboratory results, but they show a lot of potential.
A study published in the journal AIDS followed 328 treatment-naive patients, with no history of cardiovascular disease, over three years to see how different antiretroviral therapy regimens affected carotid artery intima-media thickness (IMT), or artery wall thickness. The participants were started on tenofovir/emtricitabine (Truvada) together with either atazanavir (Reyataz) boosted with ritonavir (Norvir), darunavir (Prezista) boosted with ritonavir (Norvir) or raltegravir (Isentress). The researchers found that carotid artery IMT progressed slower in the atazanavir group versus the darunavir group, but saw immediate changes associated with raltegravir. They noted that hyperbilirubinemia may play a part in these changes.
An editorial published in The Lancet HIV explored what needs to be done to achieve immediate antiretroviral therapy for all people living with HIV. Perhaps the most startling figure mentioned is the number of people who are undiagnosed, which could be up to 50% of people living with HIV worldwide, according to the editorial. A recent study reported that of HIV-positive individuals entering the hospital worldwide, 30% were diagnosed at the time of admission, with a major cause of admission being AIDS-related illness. Therefore, one of the key steps in universal treatment is ensuring universal diagnosis.
A new study examined why the contraceptive depot medroxyprogesterone acetate (Depo-Provera or DMPA) is associated with a higher risk of HIV infection. After following 823 female participants, the researchers found that women taking oral contraceptives or receiving DMPA were more at risk for changes in the immune system that could increase their vulnerability to HIV than women who were not taking a hormonal contraceptive. Furthermore, DMPA use specifically was associated with an increase in these immune system changes, and certain vaginal infections also increased the risk.
A study following 1548 HIV-positive youth found that they had a substantially lower rate of viral suppression than older patients, according to report by Aidsmap. Looking at the HIV cascade of care numbers for all study participants, 54% were linked to care, 31% were retained in care and 31% started treatment, but only 7% achieved an undetectable viral load. For those who were not linked to care, the main reasons were: repeated failure to attend appointments (34%), inability to locate the participant (32%), refusal of care (11%) and absence from the service jurisdiction (11%).
Researchers in the United Kingdom estimated what it would take to reduce HIV incidence among MSM (men who have sex with men) to below one per 1000 person-years (or below 535 new infections a year) by 2030. Using a simulation model, the researchers found that the percentage of HIV-positive MSM who achieve an undetectable viral load would have to increase from below 60% currently to 90%, assuming no increase in condomless sex. To reach this, they suggest rapidly scaling up HIV testing to raise the percent of MSM diagnosed within one year of infection from 36% currently to 90%, with treatment started at diagnosis.
Is there a development this week in HIV research that you think we missed? Send us a tip!
Warren Tong is the senior science editor for TheBody.com and TheBodyPRO.com.
Follow Warren on Twitter: @WarrenAtTheBody.
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