| Autor: |
León K; Infettare, Facultad de Medicina, Universidad Cooperativa de Colombia, Medellín, Colombia. leonbacter@hotmail.com., Marín-Palma D; Infettare, Facultad de Medicina, Universidad Cooperativa de Colombia, Medellín, Colombia; Grupo de Inmunovirología, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia. bleidy1122@gmail.com., Gallego S; Grupo de Investigaciones Biomédicas Uniremington, Programa de Medicina, Facultad de Ciencias de la Salud, Corporación Universitaria Remington, Medellín, Colombia. salomon.sgq@gmail.com., Yepes C; Grupo de Inmunovirología, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia. cristinaypz0@gmail.com., Vélez J; Grupo de Inmunovirología, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia. jhonatan-2611@hotmail.com., Castro GA; Grupo de Inmunovirología, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia. gustavoandresc@gmail.com., Jaimes F; Dirección de Investigaciones, Fundación Hospitalaria San Vicente de Paúl, Medellín, Colombia; Departamento de Medicina Interna, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia. fabian.jaimes@udea.edu.co., Taborda N; Grupo de Inmunovirología, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia; Grupo de Investigaciones Biomédicas Uniremington, Programa de Medicina, Facultad de Ciencias de la Salud, Corporación Universitaria Remington, Medellín, Colombia. natalia.taborda@uniremington.edu.co., Rugeles MT; Grupo de Inmunovirología, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia. maria.rugeles@udea.edu.co., Hernández JC; Infettare, Facultad de Medicina, Universidad Cooperativa de Colombia, Medellín, Colombia. juankhernandez@gmail.com. |
| Abstrakt: |
Introduction: HIV-1 infection induces a chronic inflammatory state in which inflammasomes participate. The increase in inflammatory parameters is higher in individuals with active viral replication (progressors) than in those with viral control (HIV-1 controllers). This process triggers metabolic alterations related to changes in the lipid profile, which could increase the risk of cardiovascular events, even in patients with antiretroviral therapy. Objective: To establish whether there was a correlation between the expression of inflammasome components and cardiovascular risk markers in HIV-1 controllers and progressors with or without antiretroviral therapy. Materials and methods: We studied 13 HIV-1 controllers and 40 progressors (19 without antiretroviral therapy and 31 with therapy) and evaluated in them classic markers of cardiovascular risk. Using RT-PCR we quantified the expression of inflammasome components (NLRP1, NLRP3, NLRC4, AIM2, ASC, IL-1β, IL-18, and caspase-1), TLR2, TLR4, TGF-β, and IL-10. Results: Progressors with antiretroviral therapy had an increased expression of TLR2, TLR4, and IL-18 compared to HIV-1 controllers. They also showed high levels of triglycerides and VLDL, which positively correlated with the expression of the inflammasome components NLRP1, NLRP3, NLRC4, AIM2, ASC, and caspase-1. Conclusion: Progressors receiving antiretroviral therapy exhibited an increased expression of the inflammasome components, which correlated with the levels of triglycerides and VLDL. This supports the role of inflammation in cardiovascular risk during HIV-1 infection. |
