[BK21 Plus Seminar]
  
    
 ▶Subject: The sphingolipid system in host defense and immunity to virus infections
        
 
 ▶Speaker: Bumsuk Hahm, Ph.D. (University of Missouri-Columbia School of Medicine)
          
 
 ▶Date: 4:00PM/July/21(Mon)/2014
         
   
 ▶Place: Auditorium(1F), Postech Biotech Center
         
 
        *Abctract
       Our research is focused on investigating the mechanisms of virus-host interaction and viral regulation of host innate and adaptive immune responses, and particularly the role of the sphingolipid system in these processes. The sphingolipids regulate diverse cellular conditions and display therapeutic potential in treating human diseases. However, the functions of sphingolipids and their metabolizing enzymes in host defense and immunity to virus infections remain unclear. In our investigations, we use two distinct viral infection models, lymphocytic choriomeningitis virus clone 13 (LCMV Cl 13) and influenza virus.
LCMV Cl 13 suppresses dendritic cells (DCs) and antiviral T cell immunity, which allows the virus to persist in mice. Therefore, LCMV Cl 13 infection represents an excellent model system for studying the interplay between chronic viral infections and host immunity. Sphingosine kinase (SK) mediates the generation of sphingosine 1-phosphate (S1P) from sphingosine. In this study, we demonstrate that SK plays a key role in virus-mediated immune suppression, viral immunopathology, and viral persistence. Further, the sphingosine analog AAL-R increased the activation of LCMV-infected DCs via type I IFN signaling, unlike its known immune suppressive activity. These results enhance our understanding of sphingosine regulation of the host immunity to virus infection and provide the basis for developing immunotherapeutic approaches to clear virus infections.
Influenza virus continues to threaten humans and remains a major worldwide health concern. Thus, identifying therapeutic targets and understanding the mechanisms of host-virus interactions are important biomedical goals. We have found that SK promotes the replication of influenza virus, whereas S1P-degrading enzyme S1P lyase inhibits influenza viral propagation and virus-induced cytopathic effects. While SK regulates influenza virus-induced intracellular signaling pathways, S1P lyase elevates type I IFN-induced antiviral signaling to inhibit virus replication. Thus, S1P-metabolizing enzymes are new therapeutic targets for the treatment of diseases caused by influenza virus infection.

 ▶Inquiry: Prof.Sung Key Jang(279-2298)
        
  
  * This seminar will be given in English