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Abstract #3623


Napapon Sailasuta1, Michelle L. D’Antoni2, Philip Chan3, Thep Chalermchai4, Pasiri Sithinamsuwan5, Somporn Tipsuk4, Suteeraporn Pinyakorn5, Bonnie Slike4, Shelly Krebs4, Vedbar Khadka6, Eugene Kroon4, Robert Paul7, Serena Spudich8, Victor Valcour9, Jintanat Ananworanich5,10, and Lishomwa Ndhlovu2

1Tropical Medicine, University of Hawaii, kapolei, HI, United States, 2Tropical Medicine, University of Hawaii, Honolulu, HI, United States, 3Memory and Aging Center, Department of Neurology, University of California, San Francisco, CA, United States, 4SEARCH, The Thai Red Cross AIDS Research Centre, Bangkok, Thailand, 5U.S. Military HIV Research Program, Silver Spring, MD, United States, 6Office of Biostatistics & Quantitative Health Sciences, University of Hawaii, Honolulu, HI, United States, 7Missouri Institute of Mental Health, St. Louis, MO, United States, 8Neurology, Yale University, New Haven, CT, United States, 9Memory and Aging Center, San Francisco, CA, United States, 10Henry M. Jackson Foundation for the Advancement of Military Medicine, Bethesda, MD, United States

Proton MRS was performed in 51 acute HIV participants. We observed Inverse correlations between sCD163 and markers of neuronal integrity (BG and PCG NAA) in select brain regions suggests regional variability to neuronal injury in AHI. Further, correlations between CSF sCD163 and BG Cho and mI reveal that membrane turnover activity and glia activation that occur early in infection remain susceptible to CNS neuroinflammation. Our observation suggests select brain injury linked to myeloid activation persists even early ART in AHI arguing for additional interventions to halt detrimental neuroinflammation.

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