Jeffrey P. Bombardier1, Eva-Maria Ratai1,2, Chan Gyu Joo1,2, Jeffrey D. Lifson3, Michael Piatak, Jr3, Elkan Halpern1, Susan V. Westmoreland4, Lakshmanan Annamalai4, Kenneth Williams5, Ramon Gilberto Gonzalez1,2
1Radiology, Massachusetts General Hospital, Charlestown, MA, USA; 2Radiology, Harvard Medical School, Charlestown, MA, USA; 3AIDS and Cancer Virus Program, SAIC-Frederick, National Cancer Institute, Frederick, MD, USA; 4New England regional Primate Research Center, Harvard Medical School, Southborough, MA, USA; 5Biology, Boston College, Chestnut Hill, MA, USA
We tested the hypothesis that brain injury is more closely related to SIV levels in blood rather than in cerebrospinal fluid. Neuronal injury was quantified by measuring N-acetylaspartate (NAA) levels with 1H-MRS in an accelerated SIV-infected macaque model of neuroAIDS. We found that NAA/Cr is correlated to the peripheral blood viral burden, and not to the viral levels in the CSF at later time points. This supports the theory that brain injury is primarily derived from activated/infected monocytes that traffic across the blood-brain barrier, rather than virus directly infecting the choroid plexus, then infecting the CSF, and finally the brain.
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