Faculty List

Research Interests



Professor

Contact Information:
Email: lhuttf@lsuhsc.edu
Office Phone: 318-675-4948
Laboratory Phone: 318-675-4976
Office Fax: 318-675-5764

Education/Training:
Postdoctoral Study, University of North Carolina at Chapel Hill
Ph.D., Virus Immunology, 1973, University of London
B.Sc., Bacteriology, 1968, University of Liverpool

Major Research Interests:  Virus cell interactions, pathogenesis of oncogenic EBV

Long standing research interests are in virus cell interactions and virus pathogenesis, particularly in the biology of Epstein-Barr virus (EBV).  EBV is an oncogenic human herpesvirus that establishes persistent infections in almost 100% of the world's population.  Most people are infected subclinically in childhood.  However, the virus also causes infectious mononucleosis, oral hairy leukoplakia and immunoblastic lymphoma and is strongly implicated in the development of Burkitt's lymphoma, nasopharyngeal carcinoma, gastric carcinoma and Hodgkin's Disease.   EBV has two major cellular targets, B lymphocytes and epithelial cells.  Our long term goal is to understand how the virus enters and exits these target cells and how it spreads within and between its human hosts.  Studies focus on the functions of the envelope glycoproteins critical to these processes and on the cellular proteins with which they interact. 

Representative Publications:

Borza, C.M., and Hutt-Fletcher, L.M. 2002. Alternate replication in B cells and epithelial cells switches Epstein-Barr virus tropism.  Nature Medicine, 8:594-599.

Borza, C.M., Morgan A.J., Turk, S.M. and Hutt-Fletcher L.M. 2004. Use of gHgL for attachment of Epstein-

Barr virus to epithelial cells compromises infection,  J. Virol.  78:5007-5014.


Wu, L., Borza, C.M., and Hutt-Fletcher.  2005.  Mutations of Epstein-Barr virus gH that are differentially able to support fusion with B cells or epithelial cells.  J. Virol.  79:10923-10930.

Jiang, R., Scott, R.S. and Hutt-Fletcher, L.M.  2006.  Epstein-Barr virus shed in saliva is high in the B cell tropic glycoprotein gp42.  J. Virol.  80:7281-7283.

Hutt-Fletcher, L.M.  2007.  Epstein-Barr virus entry.  J. Virol., 81:7825-7832.


Gore, M., and Hutt-Fletcher, L.M.  2009.  The BDLF2 protein of Epstein-Barr virus is a type II glycosylated envelope protein whose processing is dependent on coexpression with the BMRF2 protein.  Virology, 383:162-167.

Chesnokova, L.S.,  Nishimura, S.L., and Hutt-Fletcher, L.M.  2010.  Fusion of epithelial cells by Epstein-Barr virus proteins is triggered by binding of viral glycoproteins gHgL to integrins αvβ6 or αvβ8.  Proc. Natl. Acad. Sci. USA, 106:20464-20469. 

Chesnokova, L.S., and Hutt-Fletcher, L.M. 2011. Fusion of EBV with epithelial cells can be triggered by αvβ5 in addition to αvβ6 and αvβ8 and integrin binding triggers a conformational change in gHgL  J. Virol., 85:13214-13223, 2011.

Valencia, S.M. and Hutt-Fletcher, L.M.  2012.  Important but differential roles for actin in trafficking of EBV in B cells and epithelial cells.  J. Virol., 86:2-10.

 

Jiang, R., Gu, X., Moore-Medlin, T., Nathan, C., and Hutt-Fletcher, L.M.  2012. Oral dysplasia and squamous cell carcinoma: correlation between increased expression of CD21, Epstein-Barr virus and CK19.  Oral Oncology, in press.

All Publications: PubMed  

 

 


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