Abstract
Abstract Distal symmetrical polyneuropathy (DSP) is the most common form of HIV infection-associated peripheral neuropathy and is often associated with pain. C57BL/6 (B6) mice infected with LP-BM5, a murine retroviral isolate, develop a severe acquired immunodeficiency syndrome similar to humans infected with HIV, hence the term murine AIDS (MAIDS). We investigated the induction of peripheral neuropathy post- LP-BM5 infection (p.i.) in B6 mice. First, LP-BM5 infected mice displayed significant symmetrical hind paw mechanical hypersensitivity (behavioral sign of peripheral neuropathy) starting from week 6 p.i. up to the time of sacrifice at week 12. The density of PGP9.5+ (a pan-neuronal marker) intraepidermal nerve fibers (IENFs) was found to be significantly reduced at week 2 p.i. and this loss was gradually recovered with time. There were no significant differences between left and right paws. Also, significantly increased levels of viral gag RNA in all segments of spinal cord tissue were detected in infected mice via quantitative real-time PCR. Further, FACS analysis showed an early increase of lumbar spinal cord microglia p.i.. Altogether, LP-BM5 induced the development of peripheral neuropathy that occurred concurrently with the development of MAIDS and was correlated with viral infection of the spinal cord. The potential role of spinal cord microglia in LP-BM5-induced painful neuropathy will be further investigated.
Published Version
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