Etude de co-facteurs pouvant moduler la replication du virus de l'immunodeficience humaine de type 1 (VIH-1) et analyse de proteines de signalisation

Abstract

Au cours du processus d'envahissement de l'organisme par le virus d'immunodéficience humaine de type 1 (VIH-1), celui-ci induit un important déficit immunitaire qui permet à la maladie d'avoir le champ libre pour se développer. La faiblesse du système immunitaire prédispose la personne atteinte du SIDA à des infections opportunistes causées par des bactéries, virus et parasites. Nous avons identifié 2 nouveaux co-facteurs, potentiels (Leishmania donovani et Mycobacterium tuberculosis ) pouvant moduler une infection causée par le VIH-1. Cette identification nous a conduit à l'analyse des différentes cascades biochimiques et physiologiques menant à l'activation de plusieurs événements intracellulaires dont la phosphorylation. Nous croyons que ce type d'événement induit par des signaux intracellulaires a pour conséquence la réactivation et la perpétuation du virus et donc possiblement une détérioration plus rapide du système immunitaire.

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During the process of invasion of the body by the human immunodeficiency virus type 1 (HIV-1), it induces a significant immune deficiency which allows the disease to have free rein to develop. A weak immune system predisposes a person with AIDS to opportunistic infections caused by bacteria, viruses and parasites. We have identified 2 new potential co-factors (Leishmania donovani and Mycobacterium tuberculosis) that can modulate an infection caused by HIV-1. This identification led us to the analysis of the different biochemical and physiological cascades leading to the activation of several intracellular events including phosphorylation. We believe that this type of event induced by intracellular signals results in the reactivation and perpetuation of the virus and therefore possibly a more rapid deterioration of the immune system.