There is no evidence for persistent enterovirus infections in chronic medical conditions in humans

Enteroviruses, together with the rhinoviruses, aphthoviruses, and the cardioviruses, belong to the family of Picommiridme.' The genus enterovirus can be further divided into polio-, ECHO-, Coxsackie A and B-, and the enteroviruses 68 to 71. Enteroviruses are the prototype of positive-strand RNA viruses since the genome is similar to eukaryotic mRNA. A small virally encoded protein, Vpg, is covalently attached to the 5'end and a poly(A) tail is present at the 3'end of the viral RNA. Once the virus has entered the host cell, uncoating is completed and the viral RNA is released into the cytoplasm of the cell where the RNA is directly translated into a polyprotein' of M, about 200 000. Directly after infection, host cell protein synthesis is shut-off. Evidence for the mechanism of poliovirus shut-off points towards the inactivation of initiation complex eIF-4F, in which the cleavage of a cellular protein pZZO by the 2A protease is thought to be involved.' Virus progeny are released by cell-Iysis which is induced by the infection itself. The virus can subsequently spread throughout the body until neutralising antibodies arise that stop further spreading and eliminate the virus. At that point, virus cultures will become negative. The role of cellular immunity seems to be of less importance than that of antibody. This is consistent with an obligatory cell-lysis forming part of the in vivo infectious cycle. Thus, chronic enterovirus infections are only known to occur in patients with agammaglobulinaemia3 or neonates, in whom the immune system is still imrnat~re.~ It is possible to isolate virus from such patients, even in the chronic stage of the infection. In normal health, enteroviral infection may follow a biphasic course, with a secondary viraemia with dissemination of the infection to target organs such as heart, brain, pancreas, or