Because mature neurons are relatively resistant to virus-induced cell death [15] , noncytolytic mechanisms for virus clearance can be employed to control or eliminate infection. If infected cells are allowed to survive, the clearance of virus must include mechanisms for inhibiting intracellular synthesis of virus nucleic acid and protein, and for removing virus genomes from cells or preventing their replacement after degradation. Alphavirus encephalitis has been most thoroughly studied, and two noncytolytic clearance mechanisms have been identified: IFN-c and anti-viral antibody ( Figure 1) . However, not all types of neurons are equally responsive to virus clearance by these mechanisms. IFN-c acts through a Jak/STAT signaling pathway to activate an antiviral response that suppresses virus replication in motor neurons without toxicity, but the relevant antiviral proteins have not been identified [24] . Antibody to the E2 viral glycoprotein present on the surface of infected neurons suppresses virus replication in all populations of neurons through a pathway that requires bivalent antibody, but does not require complement or effector cells [25, 26] .