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Long-term follow-up of elite controllers: Higher risk of complications with HCV coinfection, no association with HIV disease progression

To estimate the effect of hepatitis C virus (HCV) coinfection on the development of complications and progression of human immunodeficiency virus (HIV) disease among HIV-infected elite controllers. Single-center retrospective cohort. Kaplan–Meier methods, prevalence ratios, and Cox proportional-haza...

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Detalles Bibliográficos
Autores principales: Stafford, Kristen A., Rikhtegaran Tehrani, Zahra, Saadat, Saman, Ebadi, Maryam, Redfield, Robert R., Sajadi, Mohammad M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer Health 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5500077/
https://www.ncbi.nlm.nih.gov/pubmed/28658155
http://dx.doi.org/10.1097/MD.0000000000007348
Descripción
Sumario:To estimate the effect of hepatitis C virus (HCV) coinfection on the development of complications and progression of human immunodeficiency virus (HIV) disease among HIV-infected elite controllers. Single-center retrospective cohort. Kaplan–Meier methods, prevalence ratios, and Cox proportional-hazards models were used. In all, 55 HIV-infected elite controllers were included in this study. Among them, 45% were HIV/HCV coinfected and 55% were HIV mono-infected. Median follow-up time for the cohort was 11 years. Twenty-five patients experienced a complication and 16 lost elite controller status during the study period. HCV coinfected patients were 4.78 times (95% confidence interval 1.50–15.28) more likely to develop complications compared with HIV mono-infected patients. There was no association between HCV coinfection status and loss of elite control (hazard ratio 0.75, 95% confidence interval 0.27–2.06). Hepatitis C virus coinfection was significantly associated with the risk of complications even after controlling for sex, injecting drug use, and older age. HCV coinfected patients had higher levels of cellular activation while also having similar levels of lipopolysaccharide and soluble CD14. HCV coinfection was not associated with loss of elite controller status. Taken together, this suggests that HCV coinfection does not directly affect HIV replication dynamics or natural history, but that it may act synergistically with HIV to produce a greater number of associated complications. Continued follow-up will be needed to determine whether HCV cure through the use of direct-acting antivirals among HIV/HCV coinfected elite controllers will make the risk for complications among these patients similar to their HIV mono-infected counterparts.