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Determinants of measles virus (hamster neurotropic strain) replication in mouse brain
Abstract:
In newborn mice the hamster neurotropic strain of measles virus produces a severe meningoencephalitis with readily recoverable virus, while in weanling mice a fatal encephalopathy is produced with scant histopathology and no viral infectivity in brain homogenates. In this study various host factors that may change with maturation and determine the restriction of viral expression were investigated, including immune response, interferon production, host temperature, and the possible role of proteases. None of these factors appeared to be responsible for host restriction of viral expression. Recovery of virus from brains of weanling mice was not significantly enhanced by cocultivation with Vero cells, complementation with temperature-sensitive mutants, or phenotypic mixing with the Edmonston strain of measles virus. These data, combined with our previous observations of production of viral proteins including nucleocapsid proteins without development of recognizable nucleocapsids in neurons of weanling mice, suggest that with maturation the neural cells fail to replicate sufficient amounts of encapsidated viral ribonucleic acid.
Insights
Maturation restricts measles virus (MeV) replication in mouse brains, causing fatal encephalopathy. Host factors like immunity and interferon do not explain this restriction, suggesting a neural cell defect in viral RNA replication.
Area of Science:
- Virology
- Neuroscience
- Immunology
Background:
- Measles virus (MeV) causes severe meningoencephalitis in newborn mice.
- In weanling mice, MeV infection results in fatal encephalopathy with limited viral recovery and pathology.
Purpose of the Study:
- Investigate host factors influencing MeV restriction with maturation.
- Determine why viral expression is limited in weanling mouse brains.
Main Methods:
- Assessed immune response, interferon production, host temperature, and protease activity.
- Attempted to enhance viral recovery via cell cocultivation, mutant complementation, and phenotypic mixing.
Main Results:
- Host factors like immunity and interferon did not explain viral restriction.
- Viral recovery was not improved by cocultivation, complementation, or phenotypic mixing.
- Viral proteins were produced, but nucleocapsids did not form in weanling mouse neurons.
Conclusions:
- Neural cell maturation restricts measles virus replication.
- A failure in encapsidated viral RNA replication within neurons appears responsible for host restriction.