MEASLES VIRUS, IMMUNE CONTROL, AND PERSISTENCE.

Tuesday, 3rd of September 2013 Print
[source]FEMS Microbiology Reviews[|source]

The frequency of measles virus (MeV) RNA persistence in the absence of disease is unknown. MeV has been identified by RT-PCR or morphologic analysis in tissues from normal individuals. In addition to SSPE, MeV antigen or RNA has been described as present and postulated to be playing an etiologic role in a large number of chronic diseases of unknown etiology (e.g. multiple sclerosis, Paget’s disease, otosclerosis, chronic active hepatitis, achalasia and Crohn’s disease). The authors conclude that none of these diseases has been convincingly linked to persistent MeV infection, but call for a better understanding of the immune mechanisms and their regulation necessary for clearance of virus and viral RNA. This understanding will hopefully ellucidate on how the virus or viral RNA persistence could help to determine if a causative role is plausible. If interested in this proposed research area, the details are available at:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319515/

 

Abstract

Measles remains one of the most important causes of child morbidity and mortality worldwide with the greatest burden in the youngest children. Most acute measles deaths are due to secondary infections that result from a poorly understood measles-induced suppression of immune responses. Young children are also vulnerable to late development of subacute sclerosing panencephalitis, a progressive, uniformly fatal neurologic disease caused by persistent measles virus (MeV) infection. During acute infection, the rash marks the appearance of the adaptive immune response and CD8+ T cell-mediated clearance of infectious virus. However, after clearance of infectious virus, MeV RNA persists and can be detected in blood, respiratory secretions, urine and lymphoid tissue for many weeks to months. This prolonged period of virus clearance may help to explain measles immunosuppression and the development of lifelong immunity to re-infection, as well as occasional infection of the nervous system. Once MeV infects neurons, the virus can spread transynaptically and the envelope proteins needed to form infectious virus are unnecessary, accumulate mutations and can establish persistent infection. Identification of the immune mechanisms required for clearance of MeV RNA from multiple sites will enlighten our understanding of the development of disease due to persistent infection.

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