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Updated: Feb 12, 2026

Acute and Chronic Tactile Sensory Testing after Spinal Cord Injury in Rats
Published on: April 4, 2012
HIV and spinal cord disease
Seth N Levin1, Jennifer L Lyons2
1Department of Neurology, Massachusetts General Hospital, Boston, MA, United States; Department of Neurology, Brigham and Women's Hospital, Boston, MA, United States; Harvard Medical School, Boston, MA, United States.
Abstract:
The epidemiology of spinal cord disease in human immunodeficiency virus (HIV) infection is largely unknown due to a paucity of data since combination antiretroviral therapy (cART). HIV mediates spinal cord injury indirectly, by immune modulation, degeneration, or associated infections and neoplasms. The pathologies vary and range from cytotoxic necrosis to demyelination and vasculitis. Control of HIV determines the differential for all neurologic presentations in infected individuals. Primary HIV-associated acute transverse myelitis, an acute inflammatory condition with pathologic similarities to HIV encephalitis, arises in early infection and at seroconversion. In contrast, HIV vacuolar myelopathy and opportunistic infections predominate in uncontrolled disease. There is systemic immune dysregulation as early as primary infection due to initial depletion of gut-associated lymphoid tissue CD4 cells and allowance of microbial translocation across the gut that never fully recovers throughout the course of HIV infection, regardless of how well controlled. The subsequent proinflammatory state may contribute to spinal cord diseases observed even after cART initiation. This chapter will highlight an array of spinal cord pathologies classified by stage of HIV infection and immune status.
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