HIV-1 infection with multiple founder variants points to poorer clinical outcomes than infection with a single variant, according to a paper published today in Nature Medicine. In the study researchers analyzed large sample sets from two important HIV vaccine efficacy trials -- the Step HIV vaccine clinical trial (HVTN 502) and RV144, the landmark vaccine clinical trial conducted in Thailand -- to evaluate whether genetic characteristics of the founder viral populations could influence markers of clinical outcomes.
01 September 2015 | Eurekalert Inf Dis
Inflammation is the generic term for the body’s response to injury. During injury, the immune system—our body’s defense system—activates a complicated network of cells and chemical signals. Acute inflammation, immune activation that’s rapid and self-limited, is essential for healing. But chronic inflammation, immune activation that continues even after the initial injury is gone, is problematic. Chronic inflammation is like a volume control knob on a stereo being stuck—with the volume turned all the way up.
24 August 2015 | BETA blog
A research team at the IRCM, led by molecular virologist Éric A. Cohen, PhD, made a significant discovery on how HIV escapes the body’s antiviral responses. The team uncovered how an HIV viral protein known as Vpu tricks the immune system by using its own regulatory process to evade the host’s first line of defence. The findings, published yesterday in the scientific journal PLOS Pathogens, pave the way for future HIV prevention or cure strategies.
16 July 2015 | Institut de Recherches Cliniques de Montreal
A research team led by Weill Cornell Medical College scientists has discovered a way to limit replication of the most common form of HIV at a key moment when the infection is just starting to develop. The study, published June 25 in Nature Communications, has shed light on a potential new element of human immunity against HIV-1 and could provide a powerful new strategy — perhaps as part of an HIV vaccine — to limit the severity of the disease.
26 June 2015 | Weill Cornell Medical College
After finding out that I was an elite controller, I felt a lot of confusion. I knew what an elite controller was, but that didn’t translate to knowing what it actually meant to be one. I wasn’t new to the HIV world—I had previously been involved in HIV research—but I felt like I knew nothing about what was going on in my own body.
24 June 2015 | BETA blog
In a finding that furthers the understanding of human immunodeficiency virus (HIV), researchers from Children's Hospital Los Angeles discovered two locations where a single difference in HIV's genetic code altered the way the virus infected the cell, thereby influencing the progression of the disease.
18 June 2015 | Eurekalert Inf Dis
Investigators from Massachusetts General Hospital and the Ragon Institute of MGH, MIT and Harvard have added another piece to the puzzle of how a small group of individuals known as elite controllers are able to control HIV infection without drug treatment. The research team reports finding that dendritic cells of elite controllers are better able to detect the presence of HIV, which enables them to stimulate the generation of T cells specifically targeting the virus.
12 June 2015 | Eurekalert Inf Dis
HIV can genetically evolve and independently replicate in patients' brains early in the illness process, an analysis of cerebral spinal fluid has found. Prompt diagnosis and treatment with antiretroviral therapy should reduce the risk that the virus could find refuge and cause damage in the brain, where some medications are less effective -- potentially enabling it to re-emerge, even after it is suppressed in the periphery, say researchers.
27 March 2015 | Eurekalert Inf Dis
Biomarkers of inflammation increase during acute HIV infection and remain elevated despite early suppressive antiretroviral therapy, according to a study presented at CROI 2015, in Seattle, Washington.
27 February 2015 | The Body Pro
The results confirmed the team's previous finding that the replicative capacity of the newly established virus drives how quickly infected individuals' levels of CD4 T cells declined. People infected with viruses with high replicative capacity had more signs of acute inflammation in the first few months of infection. Their T cells displayed more signs of "exhaustion," which sets the stage for faster disease progression.
20 February 2015 | Emory University press release