Many neurotropic viruses exist and may cause classical inflammation but also low-level neuroinflammation. However, viruses may be dormant within the CNS and become active later. The role of neurotropic virus infections in the causation of psychiatric disorders may be underestimated, because the diagnostic approach to the CNS is difficult and to dormant infections in general, but especially within the CNS. Evidence is increasing that infections increase the risk of psychiatric disorders, not only prenatal infections but also infections during the lifetime. The question how low level neuroinflammation may be involved in severe psychiatric disorders like affective and schizophrenic spectrum disorders is intriguing but remains to be studied. Experimental data clearly show that low-level neuroinflammation can be induced by viruses, but the definitions of inflammation and low level neuroinflammation appear to be blurred and apparently the previous classical definition of inflammation has to be widened. Virus infection itself or virus-related products or virus-induced autoimmunity may play a role in disease pathogenesis. More sensitive diagnostic approaches from neuroimaging and CSF investigations may hold the key to a better understanding and definition of CNS viral infections as an etiopathogenetic subgroup of severe psychiatric disorders.
