Báo cáo y học: " Differential resistance to cell entry by porcine endogenous retrovirus subgroup A in rodent species"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: " Differential resistance to cell entry by porcine endogenous retrovirus subgroup A in rodent species. | Retrovirology BioMed Central Open Access Differential resistance to cell entry by porcine endogenous retrovirus subgroup A in rodent species Giada Mattiuzzo Magda Matouskova and Yasuhiro Takeuchi Address Wohl Virion Centre Division of Infection and Immunity University College London W1T 4JF London UK Email Giada Mattiuzzo - Magda Matouskova - Yasuhiro Takeuchi - Corresponding author Published 14 December 2007 Received 10 October 2007 Accepted 14 December 2007 Retrovirology 2007 4 93 doi l742-4690-4-93 p This article is available from http content 4 1 93 2007 Mattiuzzo 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 The risk of zoonotic infection by porcine endogenous retroviruses PERV has been highlighted in the context of pig-to-human xenotransplantation. The use of receptors for cell entry often determines the host range of retroviruses. A human-tropic PERV subgroup PERV-A can enter human cells through either of two homologous multitransmembrane proteins huPAR-l and huPAR-2. Here we characterised human PARs and their homologues in the PERV-A resistant rodent species mouse and rat muPAR and ratPAR respectively . Results Upon exogenous expression in PERV-A resistant cells human and rat PARs but not muPAR conferred PERV-A sensitivity. Exogenously expressed ratPAR binds PERV-A Env and allows PERV-A infection with equivalent efficiency to that of huPAR-l. Endogenous ratPAR expression in rat cell lines appeared to be too low for PERV-A infection. In contrast the presence of Pro at position l09 in muPAR was identified

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