A Viral–Host Immunogenetic Interaction Model in Hodgkin Lymphoma: Co-Association of HHV-6B Infection and IL-18 rs1946518 Polymorphism

Alheany, Aya Raed Abdulwahhab; Abdulkareem, Aws Zamil; Abdullah, Zahraa Ali; Al-Alwany, Shakir H. Mohammed

doi:10.31557/APJCP.2026.27.5.1931

A Viral–Host Immunogenetic Interaction Model in Hodgkin Lymphoma: Co-Association of HHV-6B Infection and IL-18 rs1946518 Polymorphism

Document Type : Research Articles

Authors

¹ Department of Microbiology, College of Medicine, Ibn Sina University of Medical and Pharmaceutical Sciences, Baghdad, Iraq.

² Department of Science, College of Basic Education, Diyala University, Diyala, Iraq.

³ Department of Biology, College of Science, Babylon University, Babylon, Iraq.

10.31557/APJCP.2026.27.5.1931

Abstract

Background: Hodgkin lymphoma (HL) arises from germinal center B cells through complex viral, genetic, and environmental factors. This study examines HHV-6B infection and the IL-18 rs1946518 polymorphism as potential contributors to inflammation-driven HL susceptibility and risk of disease progression. Methods: A case-control study of 180 venous blood samples was conducted, including 90 HL patients and 90 healthy controls. Viral and genomic DNA were isolated using the standard phenol-chloroform protocol, and polymerase chain reaction (PCR) amplification of HHV-6B genomes and the IL-18 rs1946518 single-nucleotide polymorphism (SNP) was performed. Variants of IL-18 rs1946518 were confirmed using Sanger sequencing. To compare genotype and allele frequencies between patient and control groups, statistical tests were conducted, including chi-square tests and logistic regression, as appropriate. Results: No significant difference in age was observed between HL patients (28.5 ± 9.7 years) and controls (30.6 ± 10.8 years; P > 0.05). Males represented 57.8% of HL patients compared to 42.2% females. The presence of HHV-6B DNA was detected in 25.6% (23/90) of HL patients, with 74.4% (67/90) testing negative. Analysis of IL-18 rs1946518 revealed a significant difference in the frequency of the TT genotype between HL patients and controls (P = 0.04, OR = 0.28, 95% CI: 0.09–0.87). The frequency of T and C alleles was observed to be higher in HL patients (T: 70, C: 40) and in controls (T: 60, C: 60), respectively, suggesting a potential increased risk of HL associated with the T allele and a possible protective effect of the C allele. Conclusions: Current evidence links HHV-6B infection and IL-18 rs1946518 variants to the pathogenesis of Hodgkin lymphoma, potentially influencing disease susceptibility and clinical outcomes. Further studies with larger cohorts are needed to clarify the underlying mechanisms.

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