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The Journal of Neuroscience, October 4, 2006, 26(40):10299-10304; doi:10.1523/JNEUROSCI.3135-06.2006

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Neurobiology of Disease
Establishment of a Rodent Model of HIV-Associated Sensory Neuropathy

Sanjay C. Keswani,¹ Christelene Jack,¹ Chunhua Zhou,¹ and Ahmet Höke^1,2

Departments of ¹Neurology and ²Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287

Correspondence should be addressed to Dr. Ahmet Höke, Johns Hopkins Hospital, 600 North Wolfe Street, Path 509, Baltimore, MD 21287. Email: ahoke{at}jhmi.edu

Human immunodeficiency virus (HIV)-associated sensory neuropathy (SN) is the most common neurological complication of HIV infection in the current highly active antiretroviral therapy era. The painful sensory neuropathy is associated with the use of dideoxynucleoside antiretrovirals, and its development limits the choice of antiretroviral drugs in affected patients. There are presently no effective therapies for HIV-SN, and moreover there has been no robust animal model of HIV-SN in which candidate therapeutic agents can be tested. In this paper, we show that we have established a rodent model of HIV-SN by oral administration of a dideoxynucleoside drug, didanosine, to transgenic mice expressing the HIV coat protein gp120 under a GFAP promoter. The neuropathy in these rodents is characterized by distal degeneration of unmyelinated sensory axons, similar to the "dying back" pattern of C-fiber loss seen in patients with HIV-SN. This model will be useful in examining mechanisms of distal axonal degeneration and testing potential neuroprotective compounds that may prevent development of the sensory neuropathy.

Key words: HIV; peripheral neuropathy; animal model; gp120; DDI; dideoxynucleoside

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Received July 23, 2006; revised Aug. 20, 2006; accepted Sept. 4, 2006.

Correspondence should be addressed to Dr. Ahmet Höke, Johns Hopkins Hospital, 600 North Wolfe Street, Path 509, Baltimore, MD 21287. Email: ahoke{at}jhmi.edu

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