Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Characterization of the Lassa virus GP1 ectodomain shedding: implications for improved diagnostic platforms | Virology Journal BioMed Central Research Characterization of the Lassa virus GP1 ectodomain shedding implications for improved diagnostic platforms Luis M Branco1 2 and Robert F Garry 1 Address Tulane University Health Sciences Center New Orleans LA USA and 2Autoimmune Technologies LLC New Orleans LA USA Email Luis M Branco - lbranco@ Robert F Garry - rfgarry@ Corresponding author Open Access Published 24 September 2009 Received 10 September 2009 Accepted 24 September 2009 Virologyjournal 2009 6 147 doi l743-422X-6-l47 This article is available from http content 6 l l47 2009 Branco and Garry 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 There is a significant requirement for the development and acquisition of reagents that will facilitate effective diagnosis treatment and prevention of Lassa fever. In this regard detection of early markers of Lassa virus LASV infection may improve diagnosis and ultimately successful treatment with antivirals. Characterization of LASV GPl ectodomain shedding is an important step toward developing sensitive diagnostics to detect circulating levels of this viral glycoprotein in infected patient sera. Results Secretion of GPl from mammalian cells expressing a native LASV GPC gene was not mediated by proteolytic cleavage as determined by treatment with a panel of matrix metalloprotease MMP inhibitors. The shedding of GPl was also not the result of over-expression of GPC under the control of a strong intron-A containing CMV promoter as the soluble component could be immunoprecipitated from supernatants of cells expressing low levels of GPC under the control of an intronless promoter. Cells transfected with GPC retained surface .
