tailieunhanh - Báo cáo khoa học: "Deletions of neuraminidase and resistance to oseltamivir may be a consequence of restricted receptor specificity in recent H3N2 influenza viruses"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Deletions of neuraminidase and resistance to oseltamivir may be a consequence of restricted receptor specificity in recent H3N2 influenza viruses | Virology Journal BioMed Central Research Deletions of neuraminidase and resistance to oseltamivir may be a consequence of restricted receptor specificity in recent H3N2 influenza viruses Shelly Gulati1 David F Smith2 and Gillian M Air 1 Open Access Address Department of Biochemistry Molecular Biology University of Oklahoma Health Sciences Center Oklahoma City OK 73104 USA and 2Department of Biochemistry Emory University School of Medicine Atlanta GA 30322 USA Email Shelly Gulati - shelly-gulati@ David F Smith - dfsmith@ Gillian M Air - gillian-air@ Corresponding author Published 14 February 2009 Received 7 January 2009 Accepted 14 February 2009 Virology Journal 2009 6 22 doi l 743-422X-6-22 This article is available from http content 6 1 22 2009 Gulati et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Influenza viruses attach to cells via sialic acid receptors. The viral neuraminidase NA is needed to remove sialic acids so that newly budded virions can disperse. Known mechanisms of resistance to NA inhibitors include mutations in the inhibitor binding site or mutations in the hemagglutinin that reduce avidity for sialic acid and therefore reduce the requirement for NA activity. Results Influenza H3N2 isolates A Oklahoma 323 03 Fujian-like A Oklahoma 1992 05 California-like and A Oklahoma 309 06 Wisconsin-like lost NA activity on passage in MDCK cells due to internal deletions in the NA-coding RNA segment. The viruses grow efficiently in MDCK cells despite diminished NA activity. The full length NA enzyme activity is sensitive to oseltamivir but replication of A Oklahoma 323 03 and A Oklahoma 309 06 in MDCK cells was resistant to this inhibitor .

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