Serum complements C3 and C4 in chronic HCV infection and their correlation with response to pegylated interferon and ribavirin treatment

Hanno, A; Mohiedeen, Khaled Mahmoud; Deghedy, Akram; Sayed, R

doi:10.1016/j.ajg.2014.04.005

Cited by 9 publications

(2 citation statements)

References 18 publications

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“…To our knowledge, this is the first report of HCV co-infection with HIV being associated with increased complement activation. A previous report showed lower serum C3 and C4 levels in HCV-infected subjects compared with uninfected controls 26 , potentially reflecting complement activation and consumption or decreased component synthesis in the liver. Additionally, it has been shown that elevated C3a in HCV-infected patients is associated with the development of hepatocellular carcinoma 27 .…”

Section: Discussionmentioning

confidence: 84%

Effects of Well-Controlled HIV Infection on Complement Activation and Function

Rossheim

Cunningham

Hair

et al. 2016

JAIDS Journal of Acquired Immune Deficiency Syndromes

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INTRODUCTION Uncontrolled HIV infection is known to activate the complement system, leading to an increase in chronic inflammation. Whether or not this activation of complement persists and contributes to chronic inflammation in subjects with HIV infection that is well-controlled through use of antiretroviral therapy has not been studied. METHODS We conducted an observational, cross-sectional study using sera from 305 adults with well-controlled HIV infection and 30 healthy controls. Sera was tested for markers of complement activation (C3a and C5a levels), complement function (CH50 assay), and immunoglobulin levels (IgG1-IgG4) as IgG can activate complement. We evaluated the association of well-controlled HIV infection with C3a, C5a, CH50, IgG1-IgG4, and total IgG levels using both univariate and multivariate analyses, controlling for factors such as age, gender race, comorbidities (including hepatitis C co-infection), smoking status, and statin use. RESULTS Well-controlled HIV infection was associated with a 54% increase in complement activation as measured by C3a levels compared with healthy controls (p<0.0001). Hepatitis C co-infection was associated with a further 52% increase in complement activation, as measured by C3a levels, over HIV alone (p = 0.003). CONCLUSION These results suggest that complement activation may contribute to a pro-inflammatory state even in well-controlled HIV infection. Further, HCV-co-infection may be even more pro-inflammatory, in terms of complement activation, compared with HIV infection alone.

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Section: Discussionmentioning

confidence: 84%

Effects of Well-Controlled HIV Infection on Complement Activation and Function

Rossheim

Cunningham

Hair

et al. 2016

JAIDS Journal of Acquired Immune Deficiency Syndromes

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“…The studies revealed that mRNA and protein levels of complement C4 were significantly increased after anti-HCV treatment. A positive alteration in C4 level represents as an independent predictor for treatment response and reflects viral clearance after anti-HCV therapy in CHC patients (98)(99)(100). Further studies revealed that hepatitis C virus proteins [HCV core; non-structural (NS) 5A] render transcriptional suppression of the expression of complement C4.…”

Section: Infection Of Hepatitis Cmentioning

confidence: 99%

Complement C4, Infections, and Autoimmune Diseases

Wang

Liu

2021

Front. Immunol.

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Complement C4, a key molecule in the complement system that is one of chief constituents of innate immunity for immediate recognition and elimination of invading microbes, plays an essential role for the functions of both classical (CP) and lectin (LP) complement pathways. Complement C4 is the most polymorphic protein in complement system. A plethora of research data demonstrated that individuals with C4 deficiency are prone to microbial infections and autoimmune disorders. In this review, we will discuss the diversity of complement C4 proteins and its genetic structures. In addition, the current development of the regulation of complement C4 activation and its activation derivatives will be reviewed. Moreover, the review will provide the updates on the molecule interactions of complement C4 under the circumstances of bacterial and viral infections, as well as autoimmune diseases. Lastly, more evidence will be presented to support the paradigm that links microbial infections and autoimmune disorders under the condition of the deficiency of complement C4. We provide such an updated overview that would shed light on current research of complement C4. The newly identified targets of molecular interaction will not only lead to novel hypotheses on the study of complement C4 but also assist to propose new strategies for targeting microbial infections, as well as autoimmune disorders.

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Complement Regulation and Immune Evasion by Hepatitis C Virus

Kwon

Ray

2018

Methods in Molecular Biology

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Serum complements C3 and C4 in chronic HCV infection and their correlation with response to pegylated interferon and ribavirin treatment

Cited by 9 publications

References 18 publications

Effects of Well-Controlled HIV Infection on Complement Activation and Function

Effects of Well-Controlled HIV Infection on Complement Activation and Function

Complement C4, Infections, and Autoimmune Diseases

Complement Regulation and Immune Evasion by Hepatitis C Virus

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