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:

Molesworth S.J., Lake, C.M., Borza, C.M., Turk, S.M., Hutt-Fletcher, L.M. 2000. Epstein-Barr virus gH is essential for penetration of B cells but also plays a role in attachment of virus to epithelial cells.  J. Virol. 74:6324-6332.

Lake, C.M., Hutt-Fletcher, L.M. 2000. Epstein-Barr virus that lacks glycoprotein gN is impaired in assembly and infection.  J. Virol. 74:11162-11172.

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.

Lake, C.M. and Hutt-Fletcher, L.M.  2004. The Epstein-Barr virus BFRF1 and BFLF2 proteins interact and coexpression alters their cellular localization, Virology, 320:99-106.

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.

Hutt-Fletcher, L.M.  2005. EBV entry and epithelial infection.  In “Infection, Pathogenesis, Molecular Biology and Control of Epstein-Barr Virus”, Ed. Robertson, E. S., Caister Academic Press, Norfolk, England, p359-378.

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.

Turk, S.M., Jiang, R., Chesnokova, L.S., and Hutt-Fletcher, L.M.  2006  Antibodies to gp350/220 enhance the ability of Epstein-Barr virus to infect epithelial cells.  J. Virol.  80:9628-9633.

Wu, L., and Hutt-Fletcher, L.M.  2007.  Compatibility of the gH homologs of Epstein-Barr virus and related lymphocryptoviruses.  J. Gen Virol., 88:2129-2136.

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