Several viruses have been suspected of causing or triggering vasculitis, with hepatitis B virus-related polyarteritis nodosa (HBV-PAN) and hepatitis C virus-related mixed cryoglobulinemic vasculitis (HCV-MCV) having the best demonstrated and confident proof for a causal link with viruses. Human immunodeficiency virus, erythrovirus B19, cytomegalovirus, varicella-zoster virus or human T-cell lymphotropic virus-1 can also induce mainly localized vasculitis. Conversely, no strong evidence indicates that viruses are implicated in the pathogenesis of other primary systemic vasculitides, like Kawasaki or Behcets diseases, or granulomatosis with polyangiitis (Wegeners). Treatment for all these virus-associated vasculitides should be two-pronged: one to control and clear the viral infection, using antiviral drugs; the other to rapidly control the clinical manifestations of vasculitis. Management of this second concomitant therapy is more delicate. It can rely on plasma exchange to clear immune complexes in HBV-PAN or rituximab in HCV-MCV, but sometimes it must include short durations of corticosteroids, and cytotoxic agents for most severe cases, both of which are potentially deleterious because they can hamper virus clearance and delay seroconversion.
Keywords: Vasculitis, HBV-related polyarteritis nodosa, HCV-associated cryoglobulinemic vasculitis, HIV infection, Behcet's diseases, leukocytoclastic vasculitis, vasculopathy, Retinitis, Erythrovirus B19, systemic vasculitis
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