Meningoencephalitis and demyelination are pathologic manifestations of primary polyomavirus infection in immunosuppressed rhesus monkeys

被引:19
作者
Axthelm, MK
Koralnik, IJ
Dang, X
Wüthrich, C
Rohne, D
Stillman, IE
Letvin, NL
机构
[1] Harvard Univ, Div Viral Pathogenesis, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA
[2] Harvard Univ, Dept Neurol, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA
[3] Harvard Univ, Dept Pathol, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA
[4] Oregon Hlth & Sci Univ, Vaccine & Gene Therapy Inst, Oregon Natl Primate Res Ctr, Beaverton, OR USA
[5] Oregon Hlth & Sci Univ, Div Pathobiol & Immunol, Oregon Natl Primate Res Ctr, Beaverton, OR USA
关键词
primate model; progressive multifocal leukoencephalopathy (PML); SV40;
D O I
10.1093/jnen/63.7.750
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The human polyomavirus JC (JCV) is the etiologic agent of progressive multifocal leukoencephalopathy (PML), a demyelinating disease of the CNS that occurs in immunosuppressed individuals. Because polyomavirus-induced CNS pathology usually occurs as a result of the reactivation of latent virus, little is known about the disease manifestations of a primary polyomavirus-induced disease in man. To model such a primary infection, SV40-negative rhesus monkeys were immunosuppressed by infection with the virus SHIV-89.6P and then superinfected with the polyomavirus SV40. The animals developed CNS pathology characterized by both demyelination and meningoencephalitis. This observation suggests that a primary polyomavirus infection can be associated with an inflammatory CNS process. These data shed new light on the pathogenic mechanisms of primate polyomaviruses in the immunocompromised host.
引用
收藏
页码:750 / 758
页数:9
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