Mark Brockman, Simon Fraser University
Associate Professor
Molecular Biology and Biochemistry
Vancouver, British Columbia
mark_brockman@sfu.ca
Office:
(778) 782-3341
Bio/Research
The research in our laboratory aims to use molecular approaches to investigate key questions at the interface of virology, pathogenesis, and the human cellular immune response to human immunodeficiency virus (HIV) infection. Current studies focus on understanding the impact of viral immune escape...
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Bio/Research
The research in our laboratory aims to use molecular approaches to investigate key questions at the interface of virology, pathogenesis, and the human cellular immune response to human immunodeficiency virus (HIV) infection. Current studies focus on understanding the impact of viral immune escape mutations on cytotoxic T lymphocyte (CTL) recognition and on HIV protein function, measuring the ability of T cell receptors (TCR) to recognize and kill HIV-infected cells, and assessing the relevance of viral tropism and cellular compartments on disease progression.
We have developed recombination strategies to generate large panels of viral variants that encode patient-derived HIV sequences. Replication capacity of these variants is being measured to define codon-specific associations in the viral Gag and Pol genes with fitness and to identify potential relationships with immune selection pressure. Similar work assesses the impact of immune escape on function of viral accessory proteins, such as Nef and Vif. The host CTL response to HIV is determined in large part by interactions between TCR and MHC class I/viral peptide complexes. We are cloning and expressing full-length TCR from virus-specific CTL in order to examine the activity of TCR variants in greater detail. Finally, changes in viral tropism and related cell death may contribute to disease progression and AIDS. We are using virion immunocapture strategies to examine viral compartmentalization in plasma in order to determine the cellular sources of HIV in infected individuals over time.
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We have developed recombination strategies to generate large panels of viral variants that encode patient-derived HIV sequences. Replication capacity of these variants is being measured to define codon-specific associations in the viral Gag and Pol genes with fitness and to identify potential relationships with immune selection pressure. Similar work assesses the impact of immune escape on function of viral accessory proteins, such as Nef and Vif. The host CTL response to HIV is determined in large part by interactions between TCR and MHC class I/viral peptide complexes. We are cloning and expressing full-length TCR from virus-specific CTL in order to examine the activity of TCR variants in greater detail. Finally, changes in viral tropism and related cell death may contribute to disease progression and AIDS. We are using virion immunocapture strategies to examine viral compartmentalization in plasma in order to determine the cellular sources of HIV in infected individuals over time.
Click to Shrink <<