Clinicn Investigator, Full Prf Pathology, Mass General Research Institute

Professor of Pathology Harvard Medical School

Pathologist Pathology, Massachusetts General Hospital

Physician Infectious Disease, Massachusetts General Hospital

MD Mount Sinai School of Medicine 1991

antiretroviral therapy highly active; cd4; cd4+ helper cells; cd4-positive t-lymphocytes; cd8-positive t-lymphocytes; hiv; hiv infections; hiv-1; t-lymphocytes cytotoxic; viremia

In the vast majority of individuals infected with HIV-1, infection is characterized by the inability of the immune system to control viral replication. This failure of containment of HIV-1 replication inevitably results in disease progression. The one notable exception to this observation is in persons with long-term non-progressive infection who appear to contain viral replication in the absence of antiretroviral therapy.

My laboratory investigates the mechanisms used by the cellular immune system in these individuals who are successful in mounting effective responses against HIV-1. Recent work has focused on characterizing CD4+ T helper cell function in individuals with long-term non-progressive infection and in a cohort of persons identified with acute HIV-1 infection prior to antibody seroconversion who when treated also generate functionally relevant immune responses.

Currently, we are studying immunologic and virologic mechanisms employed by both host and virus that result in success or failure of the host immune response. In particular, we are studying how HIV-specific CD4+T helper cell responses are generated and subsequently disarmed during acute HIV-1 infection.

In addition, we are studying the immunologic, virologic and clinical impact of antiretroviral therapy initiated during acute HIV-1 infection. Further investigation into the function of CD4+ T helper cells in these individuals will hopefully provide critical insight into the pathogenesis of HIV and support rationale for further immunotherapeutic interventions and vaccine development.