HLA-G liver expression in chronically HIV/hepatitis C-coinfected individuals
Fernando Crivelenti Vilar1, Eduardo Donadi1, Benedito Antônio Lopes da Fonseca1
1Department of Internal Medicine, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.
Insights
Human leukocyte antigen G (HLA-G) expression is linked to more severe liver disease in HIV/HCV-coinfected patients. This suggests HLA-G may worsen immune response and disease progression in coinfection.
Area of Science:
- Immunology
- Hepatology
- Virology
Background:
- Hepatitis C (HCV) significantly impacts survival in people with HIV.
- HIV/HCV coinfection accelerates cirrhosis development compared to HCV monoinfection.
- The role of Human Leukocyte Antigen G (HLA-G) in chronic hepatitis C progression is under investigation.
Purpose of the Study:
- To investigate HLA-G expression in liver specimens from HIV/HCV-coinfected patients.
- To correlate HLA-G expression with clinical and histopathological features of chronic hepatitis C.
- To understand the potential role of HLA-G in disease progression in coinfection.
Main Methods:
- Analysis of HLA-G expression in 59 liver specimens.
- Stratification of findings based on clinical and histopathological data.
- Assessment of correlation with treatment response to pegylated-IFN-α plus ribavirin.
Main Results:
- HLA-G expression was detected in 64% of liver specimens.
- HLA-G was significantly more frequent in severe stages of chronic hepatitis (94.1%) versus milder stages (55%; p<0.01).
- No correlation was found between HLA-G expression and antiviral response to therapy.
Conclusions:
- HLA-G expression in HIV/HCV coinfection is complex and multifactorial.
- HLA-G may contribute to disease progression and immune deterioration against HCV in coinfected individuals.
- Further research is needed to elucidate the precise mechanisms of HLA-G in HIV/HCV pathogenesis.
Introduction And Objectives:
Hepatitis C-induced liver disease represents a significant threat to the survival of people living with HIV. HIV/HCV-coinfected individuals have a more rapid progression to cirrhosis and its complications than HCV monoinfected patients. Although the underlying mechanisms remain unclear, HLA-G, a non-classical class I HLA molecule, has a well-recognized property to down-regulate the immune response against viruses and may favor the progression of chronic hepatitis C.
Materials And Methods:
We analyzed HLA-G expression in 59 liver specimens of patients harboring chronic HCV and HIV coinfection and stratified the findings according to clinical and histopathological features.
Results:
Genotype 1 was the most prevalent (88%); the HLA-G expression was observed in 38 (64%) liver specimens, and it was more frequent in more severe stages than in milder stages of chronic hepatitis (94,1% x 55%; p<0.01). HLA-G expression in the liver was not correlated to antiviral response to hepatitis C therapy with pegylated-IFN-α plus ribavirin.
Conclusions:
HLA-G expression in the context of HCV/HIV coinfection is a complex process modulated by many factors. HLA-G expression may play a role in the mechanisms that facilitate disease progression and may contribute to the deterioration of the immune response against HCV in individuals living with HIV.
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