Cases of acute polyneuroradiculopathy mimicking Guillain-Barré syndrome (GBS) have been described in HIV infection, often associated with mild CSF pleocytosis. We report a 42-year-old HIV-positive patient with an acute inflammatory polyradiculoneuropathy associated with subclinical HCV infection. He presented with rapidly progressing sensorimotor symptoms 2 weeks after an episode of fever and asthenia. EMG/ENG study indicated a demyelinating damage of motor and sensory nerves. CSF findings revealed 20 WBC/mmc, IgG intrathecal synthesis and oligoclonal bands, but no increase in proteins. He underwent plasmapheresis, and the clinical course improved within 1 month. Quantitative analysis of the HIV-1 and HCV viral load in paired plasma/CSF samples showed detectable amounts of HCV-RNA in CSF on clinical presentation and a subsequent decrease below quantification limits after plasmapheresis. Conversely, plasma HIV-1 viral load was persistently high after plasmapheresis, too, while there was an increase in HIV-1 RNA in CSF immediately after plasmapheresis, even if symptoms were improving. Moreover, the lack of HIV-1 specific cytolytic activity in CSF-derived CD8+ cells suggests that a cellular immune response against HIV-1 antigens was an unlikely cause of the disease. HCV infection has been associated with acute GBS only in a handful of patients, and no direct demonstration of viral genome in CSF is available, though recent works suggest that HCV may enter the CSF. Molecular studies in our patient would indicate a more likely association with HCV rather than HIV-1 infection.
|Issue number||4 SUPPL.|
|Publication status||Published - 2000|
ASJC Scopus subject areas
- Clinical Neurology