<?xml version='1.0'?>
<!DOCTYPE art SYSTEM 'http://www.biomedcentral.com/xml/article.dtd'>
<art>
   <ui>ar985</ui>
   <ji>ARJ</ji>
   <fm>
      <dochead>Meeting abstract</dochead>
      <bibl>
         <title>
            <p>Viral infection of retinal pigment epithelium: a possible role for initiation of Beh&#231;et's disease</p>
         </title>
         <aug>
            <au id="A1">
               <snm>Irschick</snm>
               <fnm>EU</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A2">
               <snm>Huemer</snm>
               <fnm>HP</fnm>
               <insr iid="I2"/>
            </au>
            <au id="A3">
               <snm>Larcher</snm>
               <fnm>C</fnm>
               <insr iid="I2"/>
            </au>
            <au id="A4">
               <snm>Sgonc</snm>
               <fnm>R</fnm>
               <insr iid="I3"/>
            </au>
            <au id="A5">
               <snm>G&#246;ttinger</snm>
               <fnm>W</fnm>
               <insr iid="I1"/>
            </au>
         </aug>
         <insg>
            <ins id="I1">
               <p>Department of Ophthalmology, University of Innsbruck, Austria</p>
            </ins>
            <ins id="I2">
               <p>Institute for Hygiene and Sozialmedizin, University of Innsbruck, Austria</p>
            </ins>
            <ins id="I3">
               <p>Institute of Pathophysiology, University of Innsbruck, Austria</p>
            </ins>
         </insg>
         <source>Arthritis Res Ther</source>
         <supplement>
            <title>
               <p>1st Workshop of the International Society for Beh&#231;et's Disease (ISBD) on Pathophysiology and Treatment of Beh&#231;et's Disease</p>
            </title>
            <editor>S Assaad-Khalil, H Direskeneli, M Schirmer</editor>
            <sponsor>
               <note>This workshop was supported in part by Merck Austria and the Scientific Society of Hematology, Oncology and Immunology, Innsbruck Austria</note>
            </sponsor>
            <note>Meeting abstracts</note>
            <url>http://arthritis-research.com/supplements/notes/ar-5-s2-info.pdf</url>
         </supplement>
         <conference>
            <title>
               <p>1st Workshop of the International Society for Beh&#231;et's Disease (ISBD) on Pathophysiology and Treatment of Beh&#231;et's Disease</p>
            </title>
            <location>K&#252;htai, Austria</location>
            <date-range>2&#8211;5 April 2003</date-range>
            <url>http://www.behcet.ws</url>
         </conference>
         <issn>1478-6354</issn>
         <pubdate>2003</pubdate>
         <volume>5</volume>
         <issue>Suppl 2</issue>
         <fpage>10</fpage>
         <xrefbib>
            <pubid idtype="doi">10.1186/ar985</pubid>
         </xrefbib>
      </bibl>
      <history>
         <pub>
            <date>
               <day>9</day>
               <month>9</month>
               <year>2003</year>
            </date>
         </pub>
      </history>
   </fm>
   <bdy>
      <sec>
         <st>
            <p/>
         </st>
         <p>The <it>in vitro </it>susceptibility of human retinal pigment epithelial cells (RPE) to representative members of different groups of human pathogenic viruses was investigated in this study. Subacute viral infection is known to change the phenotype of infected cells, thereby causing immune-mediated tissue damage. Downregulation of cell surface antigens provides a means of long-term survival of viruses and persistent infection. Therefore the aim of this study was to investigate the capacity of in vitro infection with viruses and the expression of different cell surface molecules on human RPE cells following viral infection with special emphasis on those having immune regulatory functions. Primary cultures of RPE cells were infected with various viruses. We found infection with different neurotropic viruses, respiratory viruses and enteroviruses whereas no infection was observed with lymphotropic viruses. Cytomegalovirus (CMV) downregulated MHC class I antigens on RPE, whereas coxsackie virus (CVB) and HSV did not alter MHC class I antigen expression. No induction of class II antigens was observed in RPE cells infected with CVB, HSV or CMV. Adhesion molecule ICAM-1 (CD54) was slightly increased after virus infection and the other cell surface molecules did not alter.</p>
         <p>Several common human viruses could infect RPE cells. As even animal viruses, such as pseudorabies virus, could infect these cells, it might be possible that transient infections with animal viruses could act as a trigger for 'autoimmune' retinal diseases &#8211; and under certain circumstances like genetic predisposition or immunologic disorders this could lead to Beh&#231;et's disease in the eye.</p>
      </sec>
   </bdy>
</art>
