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Báo cáo hóa học: " Human cytomegalovirus UL27 is not required for viral replication in human tissue implanted in SCID mice"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Human cytomegalovirus UL27 is not required for viral replication in human tissue implanted in SCID mice | Virology Journal BioMed Central Short report Open Access Human cytomegalovirus UL27 is not required for viral replication in human tissue implanted in SCID mice Mark N Prichard 1 Debra C Quenelle1 Deborah J Bidanset1 Gloria Komazin3 Sunwen Chou2 John C Drach3 and Earl R Kern1 Address Department of Pediatrics University of Alabama School of Medicine Birmingham AL USA 2Medical and Research Services VA Medical Center and Oregon Health and Science University Portland OR and 3Department of Biologic and Materials Sciences University of Michigan Ann Arbor MI USA Email Mark N Prichard - mprichard@peds.uab.edu Debra C Quenelle - dquenelle@peds.uab.edu Deborah J Bidanset - debbie@uab.edu Gloria Komazin - gloria_komazin@hms.harvard.edu Sunwen Chou - chous@ohsu.edu John C Drach - jcdrach@umich.edu Earl R Kern - ekern@peds.uab.edu Corresponding author Published 29 March 2006 Received 03 February 2006 Accepted 29 March 2006 VirologyJournal2006 3 18 doi l0.ll86 l743-422X-3-18 This article is available from http www.virologyj.cOm content 3 1 18 2006Prichard et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Inhibition of the human cytomegalovirus UL97 kinase by maribavir is thought to be responsible for the antiviral activity of this compound. Some mutations that confer resistance to maribavir map to UL97 however additional mutations that also confer resistance to the drug were mapped to UL27. These open reading frames share a low level of homology yet the function of pUL27 remains unknown. A recombinant virus with a deletion in the UL27 open reading frame was reported previously to exhibit a slight replication deficit but a more important function in vivo was hypothesized given its homology to the UL97 kinase. The potential .