Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Shedding of soluble glycoprotein 1 detected during acute Lassa virus infection in human subjects | Branco et al. Virology Journal 2010 7 306 http content 7 1 306 VIROLOGY JOURNAL RESEARCH Open Access Shedding of soluble glycoprotein 1 detected during acute Lassa virus infection in human subjects f 1 f 3 5 5 Luis M Branco 1 Jessica N Grove Lina M Moses Augustine Goba Mohammed Fullah Mambu Momoh Randal J Schoepp4 Daniel G Bausch3 Robert F Garry Abstract Background Lassa hemorrhagic fever LHF is a neglected tropical disease with significant impact on the health care system society and economy of Western and Central African nations where it is endemic. With a high rate of infection that may lead to morbidity and mortality understanding how the virus interacts with the host s immune system is of great importance for generating vaccines and therapeutics. Previous work by our group identified a soluble isoform of the Lassa virus LASV GP1 sGP1 in vitro resulting from the expression of the glycoprotein complex GPC gene 1 2 . Though no work has directly been done to demonstrate the function of this soluble isoform in arenaviral infections evidence points to immunomodulatory effects against the host s immune system mediated by a secreted glycoprotein component in filoviruses another class of hemorrhagic fever-causing viruses. A significant fraction of shed glycoprotein isoforms during viral infection and biogenesis may attenuate the host s inflammatory response thereby enhancing viral replication and tissue damage. Such shed glycoprotein mediated effects were previously reported for Ebola virus EBOV a filovirus that also causes hemorrhagic fever with nearly 90 fatality rates 3-5 . The identification of an analogous phenomenon in vivo could establish a new correlate of LHF infection leading to the development of sensitive diagnostics targeting the earliest molecular events of the disease. Additionally the reversal of potentially untoward immunomodulatory functions mediated by sGP1 could potentiate the development of novel therapeutic intervention.
