Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Modulation of viral replication in macrophages persistently infected with the DA strain of Theiler's murine encephalomyelitis virus | Virology Journal BioMed Central Research Modulation of viral replication in macrophages persistently infected with the DA strain of Theiler s murine encephalomyelitis virus Stephane Steurbaut Ellen Merckx Bart Rombaut and Raf Vrijsen Address Department of Pharmaceutical Biotechnology and Molecular Biology Vrije Universiteit Brussel Brussels Belgium Email Stephane Steurbaut - ssteurb@ Ellen Merckx - Bart Rombaut - brombaut@ Raf Vrijsen - rvrijsen@ Corresponding author Open Access Published 4 August 2008 Received 29 April 2008 Virology Journal 2008 5 89 doi 1743-422X-5-89 Accepted 4 August 2008 This article is available from http content 5 1 89 2008 Steurbaut 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 Demyelinating strains of Theiler s murine encephalomyelitis virus TMEV such as the DA strain are the causative agents of a persistent infection that induce a multiple sclerosis-like disease in the central nervous system of susceptible mice. Viral persistence mainly associated with macrophages is considered to be an important disease determinant that leads to chronic inflammation demyelination and autoimmunity. In a previous study we described the establishment of a persistent DA infection in RAW macrophages which were therefore named DRAW. Results In the present study we explored the potential of diverse compounds to modulate viral persistence in these DRAW cells. Hemin was found to increase viral yields and to induce cell lysis. Enviroxime and neutralizing anti-TMEV monoclonal antibody were shown to decrease viral yields whereas interferon-a .
