Genetic Polymorphisms Associated with Liver Disease Progression in HIV/HCV-Coinfected Patients.
The pathogenic mechanisms of the accelerated progression of liver injury in HIV/HCV coinfection are incompletely understood. The progression of liver disease is variable between individuals having similar risk factors, suggesting that genetic background is an important contributor. The aim of this review is to give a summary of all single nucleotide polymorphisms associated with the severity of liver disease in patients coinfected with HIV and HCV reported in the literature. Therefore, a systematic search for articles published was made, 17 of which were selected for this review. In summary, a large number of single nucleotide polymorphisms have been associated with the severity of liver disease in HIV/HCV-coinfected patients. These genes are involved in different biological processes, including seven that correspond to cytokine genes (IFNL3-4, CXCL9-11, IL15, TNF), two to receptor genes (IL7R, TLR8), and three are genes related to metabolism (PNPLA3, FTO, GSTM1). In addition, two combinations of polymorphisms (cirrhosis risk score and mitochondrial haplogroups) have also been related to severity of liver disease in HIV/HCV-coinfected patients. Although determinants other than genetics, such as environmental and viral factors, may be implicated in liver disease progression, information about genetic variation might be useful in clinical practice, allowing prioritization of patients with a genetic background that predispose to a worse evolution of HCV-related liver disease.
Viral Infection and Immunity Unit, National Centre for Microbiology, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.
Luz M
LM
Medrano
Viral Infection and Immunity Unit, National Centre for Microbiology, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.
María A
MA
Jiménez-Sousa
Viral Infection and Immunity Unit, National Centre for Microbiology, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.
Amanda
A
Fernández-Rodríguez
Viral Infection and Immunity Unit, National Centre for Microbiology, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.
Salvador
S
Resino
D015415:Biomarkers; D054370:Chemokine CXCL9 / Q000235:genetics; D060085:Coinfection / Q000150:complications*; D018450:Disease Progression; D015658:HIV Infections / Q000150:complications*; D006526:Hepatitis C / Q000150:complications*; D006801:Humans; D007372:Interferons; D007378:Interleukins / Q000235:genetics; D008107:Liver Diseases / Q000209:etiology / Q000235:genetics* / Q000276:immunology; D020641:Polymorphism, Single Nucleotide; D020395:Receptors, Interleukin-7 / Q000235:genetics; D051200:Toll-Like Receptor 8 / Q000235:genetics; D000095022:Interferon Lambda
D015415:Biomarkers; D054370:Chemokine CXCL9; D007372:Interferons; D007378:Interleukins; D020395:Receptors, Interleukin-7; D051200:Toll-Like Receptor 8; C080810:CXCL9 protein, human; C000624353:interferon-lambda, human; D000095022:Interferon Lambda; C579163:IFNL4 protein, human; C495349:TLR8 protein, human