Dysregulation of the Immune System in HIV/HCV-Coinfected Patients According to Liver Stiffness Status

García-Broncano, Pilar; Medrano, Luz María; Berenguer, Juan; González-García, Juan; Jimenez-Sousa, Ma Ángeles; Carrero, Ana; Hontañón, Víctor; Guardiola, Josep M.; Crespo, Manuel; Quereda, Carmen; Sanz, José; García-Gómez, Ana; Jiménez, José Luís; Resino, Salvador

doi:10.3390/cells7110196

Cited by 16 publications

(11 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although cART might help reduce the plasma inflammatory marker levels in HIV–HCV-coinfected patients, the markers may still remain much higher than healthy controls [ 23 ]. In line with our findings, elevated liver fibrosis was previously linked to increased biomarkers of inflammation in HIV–HCV-coinfected patients [ 24 , 25 ]. In the present study, we identified a mixed profile of elevated circulating inflammatory cytokines, chemokines, and growth factors, including IL-6, IL-10, IFN-γ, GM-CSF, and FGF-basic, among HIV–HCV-coinfected patients with advanced liver fibrosis.…”

Section: Discussionsupporting

confidence: 92%

Plasma Inflammatory Biomarkers Associated with Advanced Liver Fibrosis in HIV–HCV-Coinfected Individuals

Chen

Liu

Duan³

et al. 2020

IJERPH

View full text Add to dashboard Cite

Background: HIV and HCV coinfection leads to accelerated liver fibrosis, in which microbial translocation and systemic inflammation might play important roles. Objective: This study aimed to provide an extensive profile of the plasma microbial translocation and inflammation biomarkers associated with advanced liver fibrosis among HIV–HCV-coinfected patients. Methods: This cross-sectional study recruited 343 HIV–HCV-coinfected patients on combination antiretroviral therapy (cART) from a rural prefecture of Yunnan province in Southwest China. The plasma concentrations of sCD14 and 27 cytokines and chemokines were assayed and compared against advanced or mild levels of liver fibrosis. Results: Of the 343 HIV–HCV-coinfected patients, 188 (54.8%) had severe or advanced liver fibrosis (FIB-4 > 3.25). The patients with advanced liver fibrosis (FIB-4 > 3.25 vs. FIB-4 ≤ 3.25) had higher plasma levels of interleukin (IL)-1β, IL-6, IL-7, IL-9, IL-12, IL-15, IL-17, granulocyte macrophage colony stimulating factor (GM-CSF), Interferon-γ (IFN-γ), tumor necrosis factor (TNF-α), IL-4, IL-10, IL-13, fibroblast growth factor 2 (FGF-basic), and Monocyte chemoattractant protein-1 (MCP-1). Multivariable logistic regression models showed that advanced liver fibrosis was associated with an increased plasma level of IL-1β, IL-6, IL-7, IL-12, IL-17, GM-CSF, IFN-γ, IL-4, IL-10, MCP-1, Eotaxin, and FGF-basic, with FGF-basic continuing to be positively and significantly associated with advanced liver fibrosis, after Bonferroni correction for multiple comparisons (adjusted odds ratio (aOR) = 1.92; 95%CI: 1.32–2.81; p = 0.001). Plasma sCD14 was also significantly associated with advanced liver fibrosis (aOR = 1.13; 95%CI: 1.01–1.30; p = 0.049). Conclusions: HIV–HCV-coinfected patients are living with a high prevalence of advanced liver fibrosis which coexists with a mixture of elevated plasma inflammation and microbial translocation biomarkers. The significant associations of advanced liver fibrosis with FGF-basic and sCD14 may reveal pathogenic mechanisms and potential clinical intervention targets for liver fibrosis in HCV–HIV coinfection.

show abstract

Section: Discussionsupporting

confidence: 92%

Plasma Inflammatory Biomarkers Associated with Advanced Liver Fibrosis in HIV–HCV-Coinfected Individuals

Chen

Liu

Duan³

et al. 2020

IJERPH

View full text Add to dashboard Cite

show abstract

“…The search for non-invasive parameters to predict the fibrosis progression becomes an important goal for monitoring HIV/HCV co-infected patients. As indicated, co-infection with HIV and HCV demonstrated an immunosuppressive profile compared to HIV-mono-infection, and in advanced cirrhosis patients, (stiffness > 25 kPa), was associated with the lowest plasma values of T-helper 1 and T-helper 17 response[27]. Furthermore, transient elastography evaluated in a prospective study on a cohort of 154 HCV/HIV co-infected patients identified that elevated alanine amino aspartate (AST) level and liver stiffness at the baseline were increased in individuals under the risk of fibrosis progression[28].…”

Section: Hiv/hcv Co-infection Induced Liver Injurymentioning

confidence: 99%

Human immunodeficiency virus and hepatotropic viruses co-morbidities as the inducers of liver injury progression

Ganesan¹,

Poluektova²,

Kharbanda³

et al. 2019

WJG

View full text Add to dashboard Cite

Hepatotropic viruses induced hepatitis progresses much faster and causes more liver- related health problems in people co-infected with human immunodeficiency virus (HIV). Although treatment with antiretroviral therapy has extended the life expectancy of people with HIV, liver disease induced by hepatitis B virus (HBV) and hepatitis C virus (HCV) causes significant numbers of non-acquired immune deficiency syndrome (AIDS)-related deaths in co-infected patients. In recent years, new insights into the mechanisms of accelerated fibrosis and liver disease progression in HIV/HCV and HIV/HBV co-infections have been reported. In this paper, we review recent studies examining the natural history and pathogenesis of liver disease in HIV-HCV/HBV co-infection in the era of direct acting antivirals (DAA) and antiretroviral therapy (ART). We also review the novel therapeutics for management of HIV/HCV and HIV/HBV co-infected individuals.

show abstract

“…Sixteen studies have evaluated the effect of both HIV mono‐infection and HIV/HCV co‐infection on inflammatory biomarkers. (Table and Table S4) The majority of studies have found that HCV co‐infection further increases the serum levels of IL‐6, IL‐10, and sTNFRI but decreases levels of CRP or hsCRP irrespective of liver function . Shah et al found that CRP levels fell with increasing IL‐6 levels suggesting attenuation of the CRP‐related IL‐6 response .…”

Section: Special Populationsmentioning

confidence: 99%

“…(Table 3 and Table S3) Among CHC patients, elevated levels of BNP, NT-proBNP, 50,51,67,99,[125][126][127][128][129] TnT, and TnI 103,128 have been observed compared to healthy controls. ( Table 4 and Table S4) The majority of studies have found that HCV co-infection further increases the serum levels of IL-6, 133-138 IL-10, 139 and sTNFRI 138 but decreases levels of CRP or hsCRP 133,134,136,[140][141][142] irrespective of liver function. 133 Shah et al found that CRP levels fell with increasing IL-6 levels suggesting attenuation of the CRP-related IL-6 response.…”

Section: Biomarkers Of Cardiac Dysfunctionmentioning

confidence: 99%

Inflammatory and cardiovascular diseases biomarkers in chronic hepatitis C virus infection: A review

Babiker

Hassan

Muhammed

et al. 2019

Clinical Cardiology

View full text Add to dashboard Cite

Hepatitis C virus (HCV) infects 180 million people worldwide and over 4 million people in the United States. HCV infection is a major cause of chronic liver disease and is recognized as a risk factor for clinical cardiovascular disease (CVD). Many studies have shown increased prevalence of cardiac and inflammatory biomarkers in patients with chronic HCV infection (CHC), and though these markers may be used to risk stratify people for cardiac disease in the general population their role in the HCV population is unknown. Patients with CHC have elevated cardiac and inflammatory biomarkers compared to noninfected controls which may play a role in CVD risk stratification. We undertook a systematic review of inflammatory and cardiac biomarkers in people with HCV infection with a focus on the effect of CHC on serum levels of these markers and their utility as predictors of CVD in this population. Medline, EMBASE, and Cochrane databases were searched for relevant articles until June 2019. A total of 2430 results were reviewed with 115 studies included. Our review revealed that HCV infection significantly alters serum levels of markers of inflammation, endothelial function, and cardiac dysfunction prior to HCV treatment, and some of which may change in response to HCV therapy. Current risk stratification tools for development of CVD in the general population may not account for the increased inflammatory markers that appear to be elevated among HCV‐infected patients contributing to increased CVD risk.

show abstract

Dysregulation of the Immune System in HIV/HCV-Coinfected Patients According to Liver Stiffness Status

Cited by 16 publications

References 66 publications

Plasma Inflammatory Biomarkers Associated with Advanced Liver Fibrosis in HIV–HCV-Coinfected Individuals

Plasma Inflammatory Biomarkers Associated with Advanced Liver Fibrosis in HIV–HCV-Coinfected Individuals

Human immunodeficiency virus and hepatotropic viruses co-morbidities as the inducers of liver injury progression

Inflammatory and cardiovascular diseases biomarkers in chronic hepatitis C virus infection: A review

Contact Info

Product

Resources

About