Abstract:
:Viruses can induce progressive neurologic disorders associated with diverse pathological manifestations, and therefore, viral infection of the brain can impair differentiated neural functions, depending on the initial viral tropism. We have previously reported that canine distemper virus (CDV) targets certain mouse brain structures, including the hypothalamus, early and selectively. Infected mice exhibit acute encephalitis, with late disease, characterized by motor impairment or obesity syndrome, appearing in some of the surviving mice several months after the initial viral replication. In the present study, we show viral persistence in the hypothalami of obese mice, as demonstrated by low, but still significant, levels of CDV nucleoprotein transcripts, associated with a dramatic decrease in F gene mRNAs. Given the pivotal role of the hypothalamus in obesity (eating behavior, energy consumption, and neuroendocrine function) and that of leptin, the adipose tissue-derived satiety factor acting through hypothalamic receptors, we analyzed the leptin networks in both obese and nonobese mice. The discrepancy found between the chronic and dramatic increase in blood leptin levels and the occurrence of obesity may be due to leptin resistance in the brain. In fact, expression of the long leptin receptor isoform, representing the functional leptin receptor, was specifically downregulated in the hypothalami of obese mice, explaining their inability to generate an adequate response to leptin in the brain. Intriguingly, during the acute phase of infection, its expression was increased in CDV-targeted structures in all infected mice and remained high in obese mice in all CDV-targeted structures, except for the hypothalamus. The biphasic change in hypothalamic leptin receptor expression seen during the progression of CDV-induced obesity provides a new paradigm for understanding mechanisms of neuroendocrinological, virus-induced abnormalities.
journal_name
J Viroljournal_title
Journal of virologyauthors
Bernard A,Cohen R,Khuth ST,Vedrine B,Verlaeten O,Akaoka H,Giraudon P,Belin MFdoi
10.1128/JVI.73.9.7317-7327.1999subject
Has Abstractpub_date
1999-09-01 00:00:00pages
7317-27issue
9eissn
0022-538Xissn
1098-5514journal_volume
73pub_type
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.70.10.7219-7223.1996
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journal_title:Journal of virology
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doi:10.1128/JVI.65.12.6553-6561.1991
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.62.1.91-99.1988
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journal_title:Journal of virology
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journal_title:Journal of virology
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doi:10.1128/JVI.54.1.58-64.1985
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journal_title:Journal of virology
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doi:10.1128/JVI.43.2.749-752.1982
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journal_title:Journal of virology
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.68.8.5108-5116.1994
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journal_title:Journal of virology
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.3.1.17-24.1969
更新日期:1969-01-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.51.3.656-661.1984
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.70.5.2861-2868.1996
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pub_type: 杂志文章
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journal_title:Journal of virology
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journal_title:Journal of virology
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pub_type: 杂志文章
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journal_title:Journal of virology
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.18.3.904-910.1976
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.68.4.2347-2354.1994
更新日期:1994-04-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2002-10-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.61.12.3832-3840.1987
更新日期:1987-12-01 00:00:00