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Multiple sclerosis drugs show promise for HIV prevention and treatment

 


New research announced today PLOS pathogen Shows a promising alternative for those taking currently available antiretroviral therapy (ART) to control viral load of human immunodeficiency virus (HIV). Researchers at George Washington University in DC and colleagues have found that a drug called fingolimod, which is approved for the treatment of multiple sclerosis, also blocks HIV infection and infection of human cells.

Because the HIV virus has the ability to establish a latent period by integrating its genome into the genome of human host cells, people infected with HIV must stay in ART for life. This means that because ART drugs can’t target latent infections, by establishing latency, the HIV virus manages to survive despite treatment. About 40 million people live with HIV in the world.

With these hurdles in mind, scientists are looking for ways to discover new strategies that specifically target HIV latency and infection. Albert Bosque, the lead author of this study and associate professor at George Washington University, took a different approach by targeting what is known as the fingosine-1-phosphate (S1P) receptor.

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These receptors are key components of the immune system that are specifically involved in the progression of infection. The researchers decided to focus on fingolimod, a US FDA-approved drug known to block the S1P receptor.

In addition, they discovered that using fingolimod, the drug works by blocking infection of human immune cells called CD4 + T cells and interrupting multiple steps of the HIV life cycle. The drug has the ability to reduce the density of CD4, a protein on the surface of T cells, while at the same time preventing viral binding and fusion.

The researchers observed that the drug, fingolimod, was able to prevent HIV infection between cells as well as reduce the detectable latent virus by 65.85%. In addition, PCR tests revealed that this reduced level of infection resulted in a 60.4% reduction in integrated DNA.

“These results show that fingolimod deserves further investigation as an exciting new treatment for HIV,” the authors of the study said.

They further argued that this was the first study of the potential role of S1P signaling in the process of establishing HIV infection. The study also explores the potential of regulating this pathway to alter the infection pathway and prevent the establishment of a potential reservoir of CD4 + T cells.

The compound is clinically approved for the treatment of multiple sclerosis and has no significant side effects when taken orally daily. However, further research in both humans and animals, to prove its efficacy, is far from a potential solution for the prevention and treatment of HIV.

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