Coxsackievirus B3 Protease 3C Induces Cell Death in Eukaryotic Cells

Message:
Abstract:
Background And Aims
Coxsackievirus B3 (CVB3) is the most common agent known to cause viral myocarditis. The viral genome encodes a single polyprotein that is cleaved to produce several proteins by virally encoded proteases. Most of this proteolytic processing is catalyzed by a cysteine protease called 3C. The 3C protease plays major role in viral replication and cellular damage.
Methods
To understand the mechanism of 3C function in virus infected cells and also development of antiviral agents against the virus, a 3C expressing plasmid was constructed. The cDNA of 3C protease was synthesized using CVB3 infected cells through reverse transcription process and was cloned in pcDNA3.1-. The constructed plasmid was confirmed by sequencing and restriction enzyme analysis. By transfection of the constructed plasmid into HeLa and MCF-7 cells.
Results
We showed that 3C protease induced cell death through multiple converging pathways, such as down regulation of cellular factors and decreasing of mRNA transcripts. This affect on HeLa cells as stronger than MCF-7 cells.
Conclusion
This study, suggests that 3C protease is thought to be a suitable target for antiviral chemotherapy.
Language:
English
Published:
Iranian Journal of Virology, Volume:3 Issue: 1, 2009
Page:
1
magiran.com/p752547  
دانلود و مطالعه متن این مقاله با یکی از روشهای زیر امکان پذیر است:
اشتراک شخصی
با عضویت و پرداخت آنلاین حق اشتراک یک‌ساله به مبلغ 1,390,000ريال می‌توانید 70 عنوان مطلب دانلود کنید!
اشتراک سازمانی
به کتابخانه دانشگاه یا محل کار خود پیشنهاد کنید تا اشتراک سازمانی این پایگاه را برای دسترسی نامحدود همه کاربران به متن مطالب تهیه نمایند!
توجه!
  • حق عضویت دریافتی صرف حمایت از نشریات عضو و نگهداری، تکمیل و توسعه مگیران می‌شود.
  • پرداخت حق اشتراک و دانلود مقالات اجازه بازنشر آن در سایر رسانه‌های چاپی و دیجیتال را به کاربر نمی‌دهد.
In order to view content subscription is required

Personal subscription
Subscribe magiran.com for 70 € euros via PayPal and download 70 articles during a year.
Organization subscription
Please contact us to subscribe your university or library for unlimited access!