Immunorégulation et plasticité fonctionnelle des réponses lymphocytaires T CD4+ dans l'infection au VIH : vers l'identification de nouvelles cibles thérapeutiques.


Daniel Kaufmann

Centre de recherche du Centre hospitalier de l'Université de Montréal


Domaine : maladies infectieuses et immunitaires

Programme chercheurs-boursiers - Senior

Concours 2015-2016

The Human Immunodeficiency Virus, or HIV, is the cause of AIDS (Acquired Immunodeficiency Syndrome).  In the absence of antiviral treatment, the large majority of HIV-infected persons will develop major complications that can lead to death.  In spite of major progress in antiviral treatment over the past several years, there is currently no therapy capable of eradicating the virus or of leading to a durable control of viral replication once medication is interrupted.  Furthermore, in spite of optimal viral control on antiviral therapy, many persons present a chronic inflammation that leads to other diseases.  Development of treatments that overcome these limitations are hampered by the lack of understanding of the underlying mechanisms of defective immune responses against the virus in the large majority of HIV-infected people.

The goal of my research program is to study mechanisms that lead to the impairment of a key population of white blood cells called CD4 T lymphocytes.  I propose to study cells from the blood of individuals infected by HIV, as well as small samples of the mucosa of the intestine obtained by a procedure called endoscopy (colonoscopy) as well as biopsies of lymph nodes.  My goal is to identify the processes that make CD4 T cells incapable of fighting the virus and to find ways to restore effective immune responses against HIV.  We are also interested in the help that CD4 cells provide for the production of powerful antibodies against the virus.  The results of my studies could contribute to the discovery of more effective treatments against the AIDS virus, and maybe allow infected persons to stop medication without that the virus begins to multiply again.  My results could also contribute to the improvement of vaccine strategies against HIV.