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The interactions of Kaposi's sarcoma-associated herpesvirus with human toll-like receptors and human papillomavirus and pdz-domain containing proteins

James, Claire Deborah (2011)
M.Res. thesis, University of Birmingham.

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Approximately 15-20% of human cancers are associated with viral agents (Parkin, 2006). The human tumour virus Kaposi’s sarcoma associated herpesvirus (KSHV) is one such virus. It is the aetiological agent of the AIDS-defining malignancy Kaposi’s sarcoma (KS) and primary effusion lymphoma (PEL), and is linked to the development of multi-centric Castleman’s disease (MCD). As a herpesvirus, KSHV resides in a latent state within infected host cells, evading various innate and adaptive immune mechanisms. The widely expressed and highly conserved toll-like receptor (TLR) family plays a major role in binding of pathogen-associated molecular patterns (PAMPs), thus identifying pathogens and leading to the stimulation of relevant host immune responses. Members of the Herpesviridae family are known to act upon, interact with and/or be detected by certain TLRs. Based on this precedence, we have investigated the interaction of KSHV on human TLRs in the human epithelial kidney cell line, 293. We evaluated the initial effect of ectopic TLR expression on KSHV infection level and the effect of KSHV infection on ectopic TLR transcript levels. Using flow cytometry, we found that KSHV infection is sensitive to the expression of TLRs 2, 3, 4 and 5, presumably via KSHV PAMP recognition, and is not sensitive to the ectopic expression of TLRs 1, 6, 7, 8 and 9. Semi-quantitative PCR revealed that TLR 7 mRNA levels are decreased by KSHV infection. We suggest that this result indicates that KSHV utilises some mechanism to decrease mRNA levels in order to evade potential antiviral responses triggered by the receptor.

Type of Work:M.Res. thesis.
Supervisor(s):Chanos, Simon
School/Faculty:Colleges (2008 onwards) > College of Medical & Dental Sciences
Department:School of Cancer Studies
Subjects:RC0254 Neoplasms. Tumors. Oncology (including Cancer)
Institution:University of Birmingham
ID Code:3167
This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder.
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