My primary research interests are to understand the determinants of virus-specific T cell responses to persistent viral infections with neurological manifestations, the co-evolution of the pathogen and the human immune response and how a better understanding of these interactions might lead to a better treatment of these infections.
The main focus has been on human immunodeficiency virus (HIV) because the rapid evolution of this virus allows real-time evaluation of the interplay between the virus and the infected human host, but my group also works on hepatitis C virus (HCV) and human polyomavirus JC (JCV).
Neurological disturbances are frequent in patients with HIV or AIDS. They occur in 30-50% of HIV-infected individuals and can present as the initial symptom, throughout the course of the disease or in advanced AIDS.
HIV might affect the nervous system directly or may act indirectly by weakening the immune system so that tumors of the nervous system or other infections develop. One example is reactivation of JCV, which cases Progressive Multifocal Leukoencephalopathy (PML) in about 5% of untreated AIDS patients and an immune reconstitution inflammatory syndrome (IRIS) in HIV infected patients receiving antiretroviral therapy. Because a JCV-specific T-cell response is associated with PML survival it is necessary to better understand the determinants of these responses and how they might be reinforced.
HIV-infected sex workers with beneficial HLA-variants are potential hubs for selection of HIV-1 recombinants that may affect disease progression.
Chang C-H. et al, (2015), Sci Rep, 5
Possible footprints of APOBEC3F and/or other APOBEC3 deaminases, but not APOBEC3G, on HIV-1 from patients with acute/early and chronic infections.
Armitage AE. et al, (2014), J Virol, 88, 12882 - 12894
HIV-1 Adaptation to Antigen Processing Results in Population-Level Immune Evasion and Affects Subtype Diversification
Tenzer S. et al, (2014), Cell Reports, 7, 448 - 463
HIV-1 adaptation to antigen processing results in population-level immune evasion and affects subtype diversification.
Tenzer S. et al, (2014), Cell Rep, 7, 448 - 463
APOBEC3G-induced hypermutation of human immunodeficiency virus type-1 is typically a discrete "all or nothing" phenomenon.
Armitage AE. et al, (2012), PLoS Genet, 8