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Research & Breakthroughs

The Cure for HIV May Lie in Our Body’s Own Defenses

The Cure for HIV May Lie in Our Body’s Own Defenses

Scientists are trying to figure out what makes HIV strong enough to break through our body's immune system. 



The human body is designed in such a way to ward off infection. Its main objective is to constantly find a way to heal itself — how else can you explain a sneeze? 

But every once in a while, our wonderful immune system gets corrupted. Certain strains of retroviruses manage to successfully break through the constructs our body uses to protect itself. So, what’s special about these certain kinds of viruses?  

In a study published in Proceedings of the National Academy of Sciences, scientists investigated characteristics of certain HIV strains hoping to figure out what it is that made them evade our immune systems so easily. 

Scientists looked at genital mucous, a membrane that prevents most bacteria from entering the body, hoping to find out how HIV is able to break in. As Medical Xpress reports, the team discovered that HIV strains that are able to replicate and spread do so because of an increased “transmission fitness.” They also found that the virus purposely selects these kinds of strains for reasons unknown. As a result, HIV research is made more difficult. 

Co-author Beatrice Hahn’s team collected 300 virus isolates from HIV-1 particles infecting both the donors and recipients, then compared the two. They discovered that recipient viruses are three times more infectious, had a 1.4 higher ability replicate, and were more resilient to antiviral effects than donor viruses.

The team also discovered that recipient isolates were released more efficiently from infected T cells than donor isolates, which suggests the production of cell free particles is important in order to transmit the virus. 

"Knowing the viral properties that confer the ability to transmit despite all of the human body's barriers to infection, might aid the development of vaccines against HIV-1," Hahn said. "But we still don't know which viral gene products render HIV-1 resistant to interferon and how they function. The next steps will be to dissect these mechanisms to define possible new targets for AIDS prevention and therapy."

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