Evasive strategies by paramyxoviruses

Of the many ways viruses can evade host immune responses, there are two well-documented strategies employed by some members of the Paramyxoviridae family. First, best exemplified by measles virus, is modulation of the immune response of the host. It has been long recognized that measles virus infection results in a nonspecific suppression of cell-mediated immune responses during both acute and convalescent stages of the disease. Suppression may be related to measles infection of monocytes and macrophages. This suppression has also been recently linked to the binding of the measles virus H protein to the CD46 receptor. This binding signals a downregulation of the expression of interleukin 12 (IL-12) production which could account for a general suppression of cell-mediated immunity.

Sendai virus and bovine parainfluenza virus have been shown to infect alveolar macrophages, which may account for decreased resistance of infected animals to bacterial pulmonary infections.

A second evasive mechanism employed by some paramyxoviruses is the establishment of persistent infection. Again this phenomenon is perhaps best studied with measles virus since the disease SSPK (subacute sclerosing panencephalitis), a rare fatal neurological disease that is a sequela of acute measles infection, is the result of measles virus persistent infections. The establishment of persistent infections by these normally lytic viruses is probably due to incompletely understood cellular as well as viral factors as well as virus-specific antibody. Viruses present in persistently infected cells are usually mutants of the wild-type virus responsible for acute infections. Mutations most frequently associated with persistence seen in SSPE are in the attachment protein, the fusion protein, or the M protein, although alterations which result in decreased expression of these proteins are also associated with persistent viruses. Expression of these proteins at infected cell surfaces as well as virus budding are usually considerably reduced or absent. Infection in immunologically privileged sites may also account for the persistence of the virus.

Paramyxoviruses, typical of RNA viruses, arc replicated by an RNA-dependent RNA polymerase which has no proofreading mechanism. Thus the frequency of mutation is high, allowing for variants in a population which may be less reactivc to immune responses. However, for reasons that arc not entirely clear, the antigenic drift observed in some other RNA viruses such as influenza viruses does not appear to play nearly as significant a role in the epidemiology of paramyxoviruses.

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