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Báo cáo y học: "Retroviral superinfection resistance"

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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài:"Retroviral superinfection resistance | Retrovirology BioMed Central Review Retroviral superinfection resistance Micha Nethe Ben Berkhout and Antoinette C van der Kuyl Open Access Address Dept. of Human Retrovirology Academic Medical Centre University of Amsterdam Meibergdreef 15 1105AZ Amsterdam The Netherlands Email Micha Nethe - michanethe@hotmail.com Ben Berkhout - b.berkhout@amc.uva.nl Antoinette C van der Kuyl - a.c.vanderkuyl@amc.uva.nl Corresponding author Published 18 August 2005 Received 18 April 2005 Retrovirology 2005 2 52 doi 10.1186 1742-4690-2-52 Accepted 18 August 2005 This article is available from http www.retrovirology.cOm content 2 1 52 2005 Nethe 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 The retroviral phenomenon of superinfection resistance SIR defines an interference mechanism that is established after primary infection preventing the infected cell from being superinfected by a similar type of virus. This review describes our present understanding of the underlying mechanisms of SIR established by three characteristic retroviruses Murine Leukaemia Virus MuLV Foamy Virus FV and Human Immunodeficiency Virus HIV . In addition SIR is discussed with respect to HIV superinfection of humans. MuLV resistant mice exhibit two genetic resistance traits related to SIR. The cellular Fv4 gene expresses an Env related protein that establishes resistance against MuLV infection. Another mouse gene Fvl mediates MuLV resistance by expression of a sequence that is distantly related to Gag and that blocks the viral infection after the reverse transcription step. FVs induce two distinct mechanisms of superinfection resistance. First expression of the Env protein results in SIR probably by occupancy of the cellular receptors for FV entry. .

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