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※ 引述《jay0404 (yuga)》之銘言：
: Journal of NeuroVirology
: 11:256-264,2005
: Neuronal activity regulates viral replication of herps simplex virus type 1
: in the nervous system
: ISSn:1355-0284
: 我急需PDF檔
: 希望有善心人士能幫我找到
: 謝謝
我有找
可是全文要３０美金哩
我附上abstract希望有用
可以在NCBI的Pubmed上key in 標題
就有連結了
或是以下這個網址
http://journalsonline.tandf.co.uk/(hp4gcnf0rffj2155f5hhoc45)/app/home/
contribution.asp?referrer=parent&backto=issue,3,9;journal,3,32;
linkingpublicationresults,1:100968,1
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Journal of NeuroVirology
Publisher: Taylor & Francis
Issue: Volume 11, Number 3 / June 2005
Pages: 256 - 264
URL: Linking Options
DOI: 10.1080/13550280590952781
Neuronal activity regulates viral replication of herpes simplex virus type 1
in the nervous system
Cheryl X Zhang A1, Harrison Ofiyai A1, Ming He A1, Xuexian Bu A1, Yanhua Wen
A1, William Jia A1
A1 Department of Surgery and Brain Research Centre, University of British
Columbia, Vancouver, British Columbia, Canada
Abstract:
Herpes simplex virus types 1 and 2 (HSV-1, -2) infect and also establish
latency in neurons. In the present study, the authors investigated the
influence of neuronal activity on the replication of HSV-1. The results showed
that the sodium channel blocker tetrodotoxin (TTX) and the inhibitory
neurotransmitter gamma-aminobutyric acid (GABA) could significantly increase
viral replication in primary neuronal cultures, by two- to fourfold. In
contrast, KCl reduced viral production by at least 80% in the same
cultures. Inhibitors of GABAA receptors completely abolished the effects of
GABA. Intravitreously injected TTX in a mouse corneal scarification model
enhanced the viral titers > 10-fold in both the trigeminal ganglia and the
brain. At 2 h post infection, both TTX and GABA significantly up-regulated
the levels of transcription for the viral immediate early (IE) genes ICP0,
ICP4, and ICP27, as revealed by real time PCR. These results indicate that
the neuronal excitation status may dictate the efficiency
of HSV-1 viral replication, probably by regulating the levels of viral IE
gene expression. These are the first findings connecting neuronal activity to
the molecular mechanisms of HSV replication in the nervous system, which may
significantly influence our view of herpesvirus infection and latency.
Journal of NeuroVirology (2005) 11, 256–264.
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