Astrocyte Apoptosis and HIV Replication Are Modulated in Host Cells Coinfected with Trypanosoma cruzi

• Published in: Frontiers in cellular and infection microbiology Vol. 7; p. 345
• Main Authors: Urquiza, Javier M, Burgos, Juan M, Ojeda, Diego S, Pascuale, Carla A, Leguizamón, M Susana, Quarleri, Jorge F
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 02.08.2017
• Subjects: apoptosis; Apoptosis - drug effects; astrocytes; Astrocytes - immunology; Astrocytes - parasitology; Astrocytes - virology; Cell Death; Cell Line; Chagas Disease - complications; Chagas Disease - immunology; Chagas Disease - virology; Chagasic meningoencephalitis; Coinfection; Cytokines - metabolism; Herpesvirus 2, Human - physiology; HIV; HIV - physiology; HIV Infections - complications; HIV Infections - immunology; Humans; Interleukin-6; Microbiology; Nitroimidazoles - pharmacology; Th1 Cells - immunology; Th17 Cells - immunology; Th2 Cells - immunology; Trypanosoma cruzi; Trypanosoma cruzi - genetics; Trypanosoma cruzi - immunology; Trypanosoma cruzi - physiology; Virus Replication - physiology; apoptosis; astrocytes; HIV; coinfection; Chagasic meningoencephalitis; Trypanosoma cruzi
• ISSN: 2235-2988; 2235-2988
• DOI: 10.3389/fcimb.2017.00345

The protozoan is the etiological agent of Chagas disease. In immunosuppressed individuals, as it occurs in the coinfection with human immunodeficiency virus (HIV), the central nervous system may be affected. In this regard, reactivation of Chagas disease is severe and often lethal, and it accounts for meningoencephalitis. Astrocytes play a crucial role in the environment maintenance of healthy neurons; however, they can host HIV and . In this report, human astrocytes were infected with both genetically modified-pathogens to express alternative fluorophore. As evidenced by fluorescence microscopy and flow cytometry, HIV and coexist in the same astrocyte, likely favoring reciprocal interactions. In this context, lower rates of cell death were observed in both monoinfected-astrocytes and HIV- coinfection in comparison with those infected only with HIV. The level of HIV replication is significantly diminished under coinfection, but without affecting the infectivity of the HIV progeny. This interference with viral replication appears to be related to the multiplication rate or its increased intracellular presence but does not require their intracellular cohabitation or infected cell-to-cell contact. Among several Th1/Th2/Th17 profile-related cytokines, only IL-6 was overexpressed in HIV- coinfection exhibiting its cytoprotective role. This study demonstrates that and HIV are able to coinfect astrocytes thus altering viral replication and apoptosis.