PHILADELPHIA, PA — New research from The Wistar Institute and the Perelman School of Medicine has identified the RSAD2/Viperin gene as a potential target for future HIV treatments. This discovery could reshape strategies in the ongoing search for a cure by focusing on HIV reservoirs, which are cells where the virus persists despite treatment.
HIV reservoirs are the main challenge in curing the virus because they resist elimination from the body, even with antiretroviral therapy (ART). Myeloid cells, which include macrophages, serve as significant reservoirs since they survive the virus’s replication process. These cells can cause neurocognitive issues in HIV-positive individuals, even those on ART.
Researchers, led by Paul M. Lieberman and Ronald G. Collman, found that RSAD2/Viperin, a gene known for its antiviral properties, was highly expressed in HIV-infected macrophages. This unexpected finding suggested that the gene might actually support the virus’s persistence.
To explore this, the team used siRNA techniques to suppress RSAD2/Viperin in infected macrophages. This reduction led to a decrease in indicators of HIV activity, such as viral transcripts and protein production, suggesting a novel role for the gene in maintaining HIV latency.
“Looking closely at RSAD2/Viperin in these HIV-infected macrophages, we’ve identified yet another paradox of HIV infection,” said Lieberman. “While this gene fights against the virus initially, it also seems to help the virus persist, making it a compelling target for further research.”
Collman added, “We’re hopeful that these findings will aid in developing therapeutic interventions to eliminate the viral reservoir or reduce the negative effects of chronic HIV infection.”
This research highlights the complexity of HIV and offers new directions for developing cures, potentially reducing the long-term impacts of the virus on patients.
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