May 20, 2016
This week, a large HIV vaccine trial will test whether a promising regimen can increase the 31% efficacy found in a landmark 2009 vaccine study. Another study identifies mutations that may bolster HIV replication in the brain. To beat HIV, you have to follow the science!
The National Institutes of Health (NIH) announced a new HIV vaccine study, called HVTN 702, that will test an experimental vaccine regimen that has shown similar immune responses to the ones seen in RV144, the landmark 2009 Thai trial that found a final efficacy of 31% for the study's vaccine candidate in preventing HIV transmission.
Looking more closely at RV144, the vaccine regimen appears to have been up to 60% effective at preventing HIV within one year of vaccination. Therefore, HVTN 702's vaccine candidate is based off of the one tested in RV144, but the composition and schedule of the vaccine regimen has been adjusted in an effort to increase the potency and duration of immune responses.
HVTN 702 will follow approximately 5,400 men and women (at least 40% of each sex), between the ages of 18 and 35, across 15 sites in South Africa beginning in November 2016, with results expected in late 2020.
A protein known as BST-2 was found to limit the replication of simian immunodeficiency virus (SIV) in the central nervous system (CNS) of primates, according to a study published in The Journal of Clinical Investigation.
This discovery might help to develop better therapies for HIV-associated neurocognitive problems, according to the study press release.
The study authors noted that while BST-2 had been previously studied in vitro, the protein's effect on virus replication in vivo had not been studied before. They explained that for ethical reasons such studies cannot be performed on human participants; hence, rhesus macaques and SIV (the primate version of HIV) were used instead.
A non-neurovirulent simian virus was passed sequentially through these animals, causing that virus to mutate and eventually resulting in a neurovirulent version of the virus. More passes of the virus resulted in more mutations, which in turn increased the likelihood that the macaque had a neurological disorder.
The study then identified four specific mutations in that neurovirulent strain which appear to heighten the BST-2 antagonism of the virus. These mutations might be "the result of the viral adaptations to the CNS microenvironment to counteract BST-2 restriction more efficiently," study authors speculated.
Warren Tong is the senior science editor for TheBody.com and TheBodyPRO.com. Follow Warren on Twitter: @WarrenAtTheBody.
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