TAILIEUCHUNG - Báo cáo khoa học: "Impaired antiviral activity of interferon alpha against hepatitis C virus 2a in Huh-7 cells with a defective Jak-Stat pathway"

Impaired antiviral activity of interferon alpha against hepatitis C virus 2a in Huh-7 cells with a defective Jak-Stat pathway | Hazari et al. Virology Journal 2010 7 36 http content 7 1 36 VIROLOGY JOURNAL RESEARCH Open Access Impaired antiviral activity of interferon alpha against hepatitis C virus 2a in Huh-7 cells with a defective Jak-Stat pathway 1 11 12 3 Sidhartha Hazari Partha K Chandra Bret Poat Sibnarayan Datta Robert F Garry Timothy P Foster Gus Kousoulas3 Takaji Wakita4 Srikanta Dash1 Abstract Background The sustained virological response to interferon-alpha IFN-a in individuals infected with hepatitis C virus HCV genotype 1 is only 50 but is about 80 in patients infected with genotype 2-6 viruses. The molecular mechanisms explaining the differences in IFN-a responsiveness between HCV 1 and other genotypes have not been elucidated. Results Virus and host cellular factors contributing to IFN responsiveness were analyzed using a green fluorescence protein GFP based replication system of HCV 2a and Huh-7 cell clones that either possesses or lack a functional Jak-Stat pathway. The GFP gene was inserted into the C-terminal non-structural protein 5A of HCV 2a full-length and sub-genomic clones. Both HCV clones replicated to a high level in Huh-7 cells and could be visualized by either fluorescence microscopy or flow cytometric analysis. Huh-7 cells transfected with the GFP tagged HCV 2a genome produced infectious virus particles and the replication of fluorescence virus particles was demonstrated in naive cells after infection. IFN-a effectively inhibited the replication of full-length as well as sub-genomic HCV 2a clones in Huh-7 cells with a functional Jak-Stat pathway. However the antiviral effect of IFN-a against HCV 2a virus was not observed in Huh-7 cell clones with a defect in Jak-Stat signaling. HCV infection or replication did not alter IFN-a induced Stat phosphorylation or ISRE promoter-luciferase activity in both the sensitive and resistant Huh-7 cell clones. Conclusions The cellular Jak-Stat pathway is critical for a successful IFN-a antiviral .

TÀI LIỆU LIÊN QUAN
TAILIEUCHUNG - Chia sẻ tài liệu không giới hạn
Địa chỉ : 444 Hoang Hoa Tham, Hanoi, Viet Nam
Website : tailieuchung.com
Email : tailieuchung20@gmail.com
Tailieuchung.com là thư viện tài liệu trực tuyến, nơi chia sẽ trao đổi hàng triệu tài liệu như luận văn đồ án, sách, giáo trình, đề thi.
Chúng tôi không chịu trách nhiệm liên quan đến các vấn đề bản quyền nội dung tài liệu được thành viên tự nguyện đăng tải lên, nếu phát hiện thấy tài liệu xấu hoặc tài liệu có bản quyền xin hãy email cho chúng tôi.
Đã phát hiện trình chặn quảng cáo AdBlock
Trang web này phụ thuộc vào doanh thu từ số lần hiển thị quảng cáo để tồn tại. Vui lòng tắt trình chặn quảng cáo của bạn hoặc tạm dừng tính năng chặn quảng cáo cho trang web này.