Angiogenesis, Inflammation & Therapeutics | Online ISSN  2207-872X
RESEARCH ARTICLE   (Open Access)

Elevated Co-infection in Hepatitis C Virus and Toxoplasmosis Patients With IL-32, IL-33 and TNF-α

Amjad T. Hameed  1*, Nazar Sh. Mohammed 1, Amani M. Jasim 1

+ Author Affiliations

Journal of Angiotherapy 8 (4) 1-9 https://doi.org/10.25163/angiotherapy.849566

Submitted: 04 March 2024 Revised: 03 April 2024  Published: 06 April 2024 


Abstract

Background: Hepatitis C virus (HCV) infection is a major global health concern, often leading to chronic liver diseases such as hepatitis, cirrhosis, and hepatocellular carcinoma. Toxoplasmosis, caused by Toxoplasma gondii, primarily affects the central nervous system but can also cause severe symptoms when co-infected with HCV, particularly in the liver. The relationship between these two infections and their impact on cytokine levels, especially interleukins (IL-32, IL-33) and tumor necrosis factor alpha (TNF-α), remains poorly understood. Methods: A case-control study was conducted involving 100 HCV-infected patients, 20 of whom were co-infected with both HCV and Toxoplasma. Blood samples were collected, and serological assays were performed to measure levels of HCV and Toxoplasma antibodies (IgM and IgG). Additionally, cytokine levels (IL-32, IL-33, TNF-α) were quantified using enzyme-linked immunosorbent assays (ELISA). DNA sequencing was performed to analyze gene variations associated with cytokine production. Results: Co-infected patients exhibited significantly higher levels of HCV and Toxoplasma antibodies compared to HCV-infected individuals without Toxoplasma co-infection (p < 0.001). Furthermore, levels of IL-32, IL-33, and TNF-α were elevated in co-infected patients, indicating a potential role of these cytokines in disease severity. The mean levels of IL-32, IL-33, and TNF-α were 10.110±0.596, 24.914±2.308, and 12.356±1.369, respectively, in co-infected patients. Conclusion: Co-infection with HCV and toxoplasmosis is associated with elevated levels of pro-inflammatory cytokines IL-32, IL-33, and TNF-α, suggesting a dysregulated immune response. These findings highlight the importance of understanding cytokine dynamics in co-infected patients for targeted therapeutic interventions and improved clinical management. DNA sequencing revealed variations in genes encoding cytokines, suggesting a genetic predisposition to elevated cytokine levels and disease progression.

Keywords: Hepatitis C Virus (HCV), Toxoplasmosis, Cytokine Levels, Interleukins (IL-32, IL-33), Tumor Necrosis Factor Alpha (TNF-α)

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