Báo cáo hóa học: " Herpes Simplex Virus Type 1 Us3 Gene Deletion Influences Toll-like Receptor Responses in Cultured Monocytic Cells"

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: Herpes Simplex Virus Type 1 Us3 Gene Deletion Influences Toll-like Receptor Responses in Cultured Monocytic Cells | Virology Journal BioMed Central Open Access Herpes Simplex Virus Type I Us3 Gene Deletion Influences Toll-like Receptor Responses in Cultured Monocytic Cells Piritta Peri1 Riikka K Mattila2 Helena Kantola1 Eeva Broberg1 Heidi S Karttunen1 Matti Waris1 Tytti Vuorinen1 and Veijo Hukkanen 1 2 Address Department of Virology University of Turku Kiinamyllynkatu 13 20520 Turku Finland and 2Department of Medical Microbiology University of Oulu Aapistie 5A 90014 Oulu Finland Email Piritta Peri - Riikka K Mattila - Helena Kantola - Eeva Broberg - ebroberg@ Heidi S Karttunen - Matti Waris - Tytti Vuorinen - Veijo Hukkanen - Corresponding author Published 21 November 2008 Received I October 2008 Accepted 21 November 2008 Virologyjournal 2008 5 140 doi 1743-422X-5-140 This article is available from http content 5 1 140 2008 Peri 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 Toll-like receptors have a key role in innate immune response to microbial infection. The toll-like receptor TLR family consists of ten identified human TLRs of which TLR2 and TLR9 have been shown to initiate innate responses to herpes simplex virus type 1 HSV-1 and TLR3 has been shown to be involved in defence against severe HSV-1 infections of the central nervous system. However no significant activation of the TLR3 pathways has been observed in wild type HSV-1 infections. In this work we have studied the TLR responses and effects on TLR gene expression by HSV-1 with Us3 and ICP4 gene deletions which also subject infected cells to apoptosis in human .

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