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Age-Dependent Pathogenesis of Murine Gammaherpesvirus 68 Infection of the Central Nervous System

Authors
Cho, Hye-JeongKim, SungbumKwak, Sung-EunKang, Tae-CheonKim, Hee-SungKwon, Hyung-JooKim, Yoon-WonKim, Yong-SunChoi, Eun-KyungSong, Moon Jung
Issue Date
1월-2009
Publisher
KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
Keywords
age-dependency; gammaherpesvirus; multiple sclerosis; neurological diseases; proinflammatory cytokines
Citation
MOLECULES AND CELLS, v.27, no.1, pp.105 - 111
Indexed
SCIE
SCOPUS
KCI
Journal Title
MOLECULES AND CELLS
Volume
27
Number
1
Start Page
105
End Page
111
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/120858
DOI
10.1007/s10059-009-0011-5
ISSN
1016-8478
Abstract
Gammaherpesvirus infection of the central nervous system (CNS) has been linked to various neurological diseases, including meningitis, encephalitis, and multiple sclerosis. However, little is known about the interactions between the virus and the CNS in vitro or in vivo. Murine gammaherpesvirus 68 (MHV-68 or gamma HV-68) is genetically related and biologically similar to human gammaherpesviruses, thereby providing a tractable animal model system in which to study both viral pathogenesis and replication. In the present study, we show the successful infection of cultured neuronal cells, microglia, and astrocytes with MHV-68 to various extents. Upon intracerebroventricular injection of a recombinant virus (MHV-68/LacZ) into 4-5-week-old and 9-10-week-old mice, the 4-5-week-old mice displayed high mortality within 5-7 days, while the majority of the 9-10-week-old mice survived until the end of the experimental period. Until a peak at 3-4 days post-infection, viral DNA replication and gene expression were similar in the brains of both mouse groups, but only the 9-10-week-old mice were able to subdue viral DNA replication and gene expression after 5 days post-infection. Pro-inflammatory cytokine mRNAs of tumor necrosis factor-alpha, interleukin 1 beta, and interleukin 6 were highly induced in the brains of the 4-5-week-old mice, suggesting their possible contributions as neurotoxic factors in the age-dependent control of MHV-68 replication of the CNS.
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