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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: Functional inaccessibility of quiescent herpes simplex virus genomes | Virology Journal BioMed Central Research Functional inaccessibility of quiescent herpes simplex virus genomes Rebecca L Minaker1 Karen L Mossman1 2 and James R Smiley 1 Open Access Address department of Medical Microbiology Immunology University of Alberta Edmonton Alberta T6G 2S2 Canada and 2Center for Gene Therapeutics Department of Pathology and Molecular Medicine McMaster University Hamilton Ontario L8N 3Z5 Canada Email Rebecca L Minaker - minaker@ualberta.ca Karen L Mossman - mossk@mcmaster.ca James R Smiley - jim.smiley@ualberta.ca Corresponding author Published 21 November 2005 Received 21 September 2005 Accepted 21 November 2005 Virology Journal 2005 2 85 doi 10.1186 1743-422X-2-85 This article is available from http www.virologyj.com content 2 1 85 2005 Minaker 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 Background Newly delivered herpes simplex virus genomes are subject to repression during the early stages of infection of human fibroblasts. This host defence strategy can limit virus replication and lead to long-term persistence of quiescent viral genomes. The viral immediate-early protein ICP0 acts to negate this negative regulation thereby facilitating the onset of the viral replication cycle. Although few mechanistic details are available the host repression machinery has been proposed to assemble the viral genome into a globally inaccessible configuration analogous to heterochromatin blocking access to most or all trans-acting factors. The strongest evidence for this hypothesis is that ICP0-deficient virus is unable to reactivate quiescent viral genomes despite its ability to undergo productive infection given a sufficiently high multiplicity of infection. However recent studies have shown .
