Abstract

Toxoplasma gondii is a protozoan parasite that is normally controlled by the host immune system and results in an asymptomatic chronic infection maintained by dormant cysts. Actually, animals and humans are simultaneously infected with T. gondii and by various micro-organisms during their life, and raise a specific protective immune response against each pathogen. The advent of immunosuppression related to concurrent viral infection such as human immunodeficiency virus (HIV) in humans or to the use of intensive immunosuppressive therapies is responsible for a profound alteration of protective immunity, and this often results in the recurrence of latent infections. Cerebral toxoplasmosis is one of the most common infections occurring in AIDS patients, especially in countries where T. gondii is highly endemic. However, other opportunistic infections due to protozoa, bacteria, and fungi are also commonly observed in these patients. Thus, co-infection with various pathogens is usual in patients with acquired immunodefiency syndrome (AIDS), and several lines of evidence suggest that interactions between the immune responses generated by each pathogen, due to cross-regulation of Th1- and Th2-activated CD4+ T lymphocytes, macrophages, neutrophils and natural killer (NK) cells can result in an aggravation of one or more infections (Mosier 1994). Furthermore, several of the pathogens infecting AIDS patients are intracellular (including HIV, T. gondii, Mycobacterium avium-intracellulare, MAI, and cytomegalovirus, CMV), giving rise to the hypothesis that possible interactions between these pathogens within the cell may occur and result in alterations of cell functions.

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