Because the noncytolytic process for virus clearance does not completely eliminate viral RNA from neurons, a mechanism for long-term immunologic control of virus replication is needed to prevent virus reactivation or progressive disease [27, 28] . Antibody is likely to participate in control, as well as initial clearance. Maintaining adequate levels of antibody in the CNS for continued control of virus replication requires either passage of antibody from the blood into the brain parenchyma or local production by resident antibody-secreting cells. The BBB restricts the entry of proteins from the blood into the CNS, and although this function is compromised during the acute phase of infection, it is quickly repaired. Under normal conditions, levels of antibody in the brain are sustained at 1% of plasma levels that are likely to be inadequate for long-term prevention of virus reactivation. Therefore, resident long-lived antibody-secreting cells that can continue to produce antiviral antibody for a lifetime are a feature of recovery from most CNS virus infections [29] . Long-term immune control of virus replication is not always successful, leading to recurrent or progressive neurologic disease [30] [31] [32] .