It is admitted that viral infections can be responsible for systemic vasculitides. Viruses can be responsible for various types of vasculitis that affect vessels of different sizes. Clinical manifestations are the same as those observed in previously described vasculitides such as polyarteritis nodosa or cryoglobulinemia. When viral infection is diagnosed and considered to be responsible for vasculitis, a specific therapeutic approach must be prescribed. Treatment is based on the combination of antiviral agents and symptomatic or immunomodulating therapies. Antiviral therapy facilitates virus clearance and seroconversion to specific antibodies. In systemic vasculitides, plasma exchanges are a powerful treatment that clears circulating immune complexes. In the case of digital ischemia, vasodilators are also useful. Conversely, steroids and cytotoxic agents stimulate virus replication and favor disease chronicity and deleterious effects due to the presence of the virus. Hepatitis B virus-related polyarteritis nodosa can be cured with the combination of antiviral agents (mainly interferon alpha) and plasma exchanges. Hepatitis C virus-related cryoglobulinemia responds to interferon alpha and sometimes to plasma exchanges, but responses are usually partial and relapses occur in the majority of cases. In HIV-related vasculitides, currently available antiretroviral agents are not able to definitively eradicate the virus but their combination with plasma exchanges can cure the vasculitis. Due to common epidemiologic factors, several viruses can be present in the same patient, and determining their responsibility in the vasculitic process requires careful clinical and virologic analysis and then the selection of a specifically adapted therapeutic regimen. The therapeutic strategy applied in virus-associated vasculitides is therefore based on the etiologic investigations and the choice of a treatment is adapted to the pathogenetic mechanisms.