Journal
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
Volume 67, Issue 8, Pages 784-792Publisher
OXFORD UNIV PRESS INC
DOI: 10.1097/NEN.0b013e318180f0d5
Keywords
neuron infection; progressive multifocal leukoencephalopathy; rhesus monkey; simian virus 40
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Funding
- NCRR NIH HHS [P51 RR000163, P51 RR00163, U24 RR018107] Funding Source: Medline
- NINDS NIH HHS [R01 NS047029, R21 NS046243-02, R01 NS074995, R21 NS046243] Funding Source: Medline
- PHS HHS [R21 046243, U24 018107] Funding Source: Medline
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There currently is no animal model of JC virus-associated progressive multifocal leukoencephalopathy (PML). Reactivation of simian virus 40 (SV40) in immunosuppressed rhesus monkeys, however, rarely causes a PML-like illness. We sought to isolate a neurotropic clone of SV40 and determine its pathogenic potential in monkeys. The clone SV40(CNS1) was amplified by polymerase chain reaction from the brain DNA of a simian/human immunodeficiency virus-infected monkey that had developed PML and meningoencephalitis. Compared with the SV40 prototype 776, SV40(CNS1) had a small number of single-amino-acid mutations and caused a productive infection in monkey fibroblasts. It was inoculated into 2 SV40-negative, simian/human immunodeficiency virus-immunosuppressed monkeys. Both animals developed meningoencephalitis with productive SV40 infection of cerebral cortical neurons and glia in the superficial layers of the cortex and at the gray-white junction. Focal SV40-infected cells were also found in the cerebellar molecular and granule cell layers and white matter. Both animals also developed disseminated SV40 infection with nephritis and pneumonitis. Thus, SV40(CNS1) is infectious and pathogenic in immunosuppressed monkeys, but it induces encephalitis with fulminant productive infection in cortical neurons and systemic disease, rather than PML. These findings shed new light on SV40 neurotropism and expand the host cell range of this virus.
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