※ 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 ============================================================1 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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