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NEUROLOGY 2007;69:1781-1788
© 2007 American Academy of Neurology
Views & Reviews

Biomarkers of HIV-1 CNS infection and injury

R. W. Price, MD, L. G. Epstein, MD, J. T. Becker, MD, P. Cinque, MD, PhD, M. Gisslen, MD, PhD, L. Pulliam, PhD and J. C. McArthur, MBBS, MPH

From the Departments of Neurology (R.W.P.) and Laboratory Medicine and Medicine (L.P.), University of California, San Francisco; Department of Neurology (L.G.E.), Children’s Memorial Hospital, Chicago, IL; Departments of Neurology and Psychiatry (J.T.B.), University of Pittsburgh, PA; Clinic of Infectious Diseases (P.C.), San Raffaele Hospital, Milan, Italy; Department of Infectious Diseases (M.G.), Sahlgrenska University Hospital, Göteborg, Sweden; and Department of Neurology, Pathology, and Epidemiology (J.C.M.), Johns Hopkins University, Baltimore, MD.

Address correspondence and reprint requests to Dr. Richard W. Price, Neurology Service, Rm 4M62, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, CA 94117

While it is clear that HIV-1 can cause CNS dysfunction, current approaches to classification and diagnosis of this dysfunction rely on syndromic definitions or measures of abnormality on neuropsychological testing in the background context of HIV-1 infection. These definitions have been variably applied, offer only limited sensitivity or specificity, and do not easily distinguish active from static brain injury. Supplanting or augmenting these approaches with objective biologic measurements related to underlying disease processes would provide a major advance in classification, diagnosis, epidemiology, and treatment assessment. Two major avenues are now actively pursued to this end: 1) analysis of soluble molecular markers in CSF and, to a lesser degree, in blood, and 2) neuroimaging markers using anatomic, metabolic, and functional measurements. This review considers the rationale and prospects of these approaches.

GLOSSARY: ADC = AIDS dementia complex; BBB = blood–brain barrier; DTI = diffusion tensor imaging; FA = fractional anisotropy; fMRI = functional MRI; HAART = highly active combination antiretroviral therapy; HIVE = HIV-1 encephalitis; MCP-1 (CCL2) = monocyte chemoattractant protein 1; MRS = MR spectroscopy; MTR = magnetization transfer imaging; NAA = N-acetylaspartate; NFL = neurofilament light chain protein.

rwprice{at}sfgh.ucsf.edu

See also page 1789

Sponsored by Clinic of Infectious Diseases, San Raffele Scientific Institute, Milan, Italy; National Institute for Infectious Diseases, Lazzaro Spallanzani IRCCS, Rome, Italy; National Institute of Mental Health (NIMH); National Institute of Neurological Disease and Stroke (NINDS); Office of AIDS Research, National Institutes of Health, Bethesda, MD; Department of Neurology, University of North Carolina at Chapel Hill.

Disclosure: The authors report no conflicts of interest.

Presented in part at "HIV Infection and the Central Nervous System: Developed and Resource Limited Settings"; June 11–13, 2005; Frascati (Rome), Italy.

Received July 12, 2006. Accepted in final form May 4, 2007.


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A. Antinori, G. Arendt, J. T. Becker, B. J. Brew, D. A. Byrd, M. Cherner, D. B. Clifford, P. Cinque, L. G. Epstein, K. Goodkin, M. Gisslen, I. Grant, R. K. Heaton, J. Joseph, K. Marder, C. M. Marra, J. C. McArthur, M. Nunn, R. W. Price, L. Pulliam, K. R. Robertson, N. Sacktor, V. Valcour, and V. E. Wojna
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