Journal
FUTURE VIROLOGY
Volume 6, Issue 1, Pages 85-99Publisher
FUTURE MEDICINE LTD
DOI: 10.2217/FVL.10.70
Keywords
CNS; fever; heat-shock protein; Innate immunity; measles virus; neuroinvasiveness; neurovirulence
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Funding
- NIAID NIH HHS [R21 AI071174-02, R21 AI071174] Funding Source: Medline
- NINDS NIH HHS [R01 NS031693, R01 NS031693-13] Funding Source: Medline
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Measles virus is highly neuroinvasive, yet host immune responses are highly effective at limiting neurovirulence in humans. We know that neurons are an important target of infection and that both IFN-gamma and -beta expression are observed in the measles virus-infected human brain. Rodent models can be used to understand how this response is orchestrated. Constitutive expression of the major inducible 70-kDa heat-shock protein is a feature of primate tissues that is lacking in mice. This article examines the importance of addressing this difference when modeling outcomes of brain infection in mice, particularly in terms of understanding how infected neurons may activate uninfected brain macrophages to produce IFN-beta and support T-cell production of IFN-gamma, a mediator of noncytolytic viral clearance. New and historical data suggest that the virus heat-shock protein 70 relationship is key to a protective host immune response and has potential broad relevance.
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