Division of BioMedical Sciences
Faculty of Medicine
Memorial University
300 Prince Philip Drive
St. John's, NL, Canada A1B 3V6

mgrant@mun.ca

Description of Research

My laboratory studies the immunology of chronic viral infection, especially the role of CD8⁺ T cell responses in hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infection.  Our aim is to determine the role that factors such as peptide specificity, human leukocyte antigen (HLA)-restriction, T cell receptor (TCR) avidity, viral replication, antiretroviral therapy, immune activation and disease progression play in the phenotypic and functional evolution of CD8⁺ T cells in infected individuals.  Blood samples are collected from infected individuals at regular intervals and CD8⁺ T cell responses are evaluated by cytokine ELISPOT assays, flow cytometry, in vitro cell culture and chromium release assays.  Experimental and clinical data is integrated to better understand the immune pathogenesis of chronic infections and to inform the design of novel therapeutic interventions.
 

Current research grants

Subset distribution of HIV-specific CD8+ T cells and disease progression. CIHR 2006-2010.

The role of B1 B lymphocyte networks in the pathogenesis of HCV infection. CIHR 2006.

Impact of HIV infection on the immune response against HCV. CIHR 2004-2007.

Identification of broadly immunogenic HIV peptides selected by antiretroviral drugs. CANFAR 2005-2007.

Recent Publications

Enhanced IL-10 Production in Response to Hepatitis C Virus Proteins by Peripheral Blood Mononuclear Human Immunodeficiency Virus Mono-infected Individuals.  L. Barrett, M. Gallant, C. Howley, M.I. Bowmer, G. Hirsch, K. Peltekian and M. Grant.  In press in BM Immunology, 2008.

Reining in Inflammation:  Harnessing CD36 to Interleukin-10.  M. Parsons, L. Barrett, C. Little and M. Grant.  In press in Endocrine, Metabolic and Immune Disorders-Drug Targets, 2008.

Circulating CD14^-CD36⁺ Peripheral Blood Mononuclear Cells Constitutively Produce Interleukin-10.  L. Barrett, C.Dai, J. Gamberg, M. Gallant and M.D. Grant.  J. Leuk. Biol. 82:152-160, 2007.

A Therapy-related Point Mutation Changes the HLA Restriction of an HIV-1 Pol Epitope from A2 to B57 and Enhances its Recognition. R.D. Mason and M.D. Grant. AIDS 19:981-984, 2005.

Cross-reactive Cytotoxic T Lymphocytes Against Human Immunodeficiency Virus type 1 Protease and Interferon-g-inducible Protein 30. R.D. Mason, M.I. Bowmer, C.M. Howley, and M.D. Grant. J. Virol. 79:5529-5536, 2005.

Antiretroviral Drug Resistance Mutations Sustain or Enhance CTL Recognition of Common HIV-1 Pol Epitopes. R.D. Mason, M.I. Bowmer, C.M. Howley, M. Gallant, J.C.E. Myers and M.D. Grant. J. Immunol. 172:7212-7219, 2004.