Department of Neurology and Neuroscience, Cornell University Medical College/New York Presbyterian Hospital, 525 East 68th Street, New York, NY 10065-4885, USA.
J Neuroimmunol. 2011 Oct 28;239(1-2):21-7. doi: 10.1016/j.jneuroim.2011.09.001. Epub 2011 Sep 25.
Virus-induced spinal cord damage results from a cytolytic effect on anterior horn cells or from predominantly cellular immune-mediated damage of long white matter tracts. Infection with the hepatitis virus group, most notably hepatitis C virus, has infrequently been associated with the occurrence of myelitis. The pathogenesis of hepatitis virus-associated myelitis has not been clarified: virus-induced autoimmunity (humoral or cell-mediated, possibly vasculitic) seems the most likely disease mechanism. Limited available information offers no evidence of direct hepatitis virus infection of the spinal cord. Virus neuropenetration may occur after virus-infected mononuclear cells penetrate the blood-brain barrier, but a true neurolytic effect has not been demonstrated. Attacks of acute myelitis usually respond favorably to immunomodulatory therapy. Antiviral therapy plays no confirmed role in the treatment of acute bouts of myelitis, but may limit the relapsing course of HCV-associated myelitis.
病毒引起的脊髓损伤是由于前角细胞的细胞溶解作用，或主要由细胞免疫介导的长白质束损伤所致。肝炎病毒组（尤其是丙型肝炎病毒）感染偶尔与脊髓炎的发生有关。肝炎病毒相关性脊髓炎的发病机制尚未阐明：病毒诱导的自身免疫（体液或细胞介导，可能伴血管炎）似乎是最可能的疾病机制。有限的可用信息没有证据表明脊髓直接感染肝炎病毒。病毒神经穿透可能发生在病毒感染的单核细胞穿透血脑屏障后，但尚未证明有真正的神经溶解作用。急性脊髓炎发作通常对免疫调节治疗有良好反应。抗病毒治疗在急性脊髓炎发作的治疗中没有明确作用，但可能限制丙型肝炎病毒相关性脊髓炎的复发过程。
