Hepatitis B and C Viruses Linked to Increased Risk of Multiple Myeloma: New Meta-Analysis Reveals Crucial Insights
A groundbreaking systematic review and meta-analysis published in BMC Cancer has unveiled compelling evidence linking chronic infections with hepatitis B (HBV) and hepatitis C (HCV) viruses to an elevated risk of developing multiple myeloma (MM), a complex hematological malignancy. This comprehensive study synthesizes data spanning over three decades of epidemiological research to clarify the nature of this association, which has previously remained uncertain.
Multiple myeloma is characterized by the clonal proliferation of malignant plasma cells within the bone marrow, leading to severe clinical manifestations such as bone destruction, anemia, renal impairment, and immune dysfunction. Despite advances in treatment, MM remains largely incurable and is associated with poor long-term survival. The discovery of potential environmental and infectious risk factors is therefore critical to improving early detection and prevention strategies.
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The international research team conducted an exhaustive literature search across major biomedical databases, including PubMed, Scopus, Embase, Web of Science, and additional repositories, covering studies published from January 1990 to January 2025. The investigators focused exclusively on high-quality cohort and case-control studies that examined the risk of MM in populations infected with HBV and HCV.
In total, seventeen studies met the stringent inclusion criteria: one cohort study and sixteen case-control studies. Within this collection, nine studies focused on the relationship between HBV infection and MM risk, whereas fifteen addressed HCV infection. Employing a random-effects model allowed the researchers to account for variability across studies, enhancing the robustness of the pooled relative risk (RR) estimates.
The meta-analysis revealed that individuals with HBV infection face a modestly increased risk of developing MM, with a pooled RR of 1.25 (95% confidence interval [CI]: 0.99–1.58). Although this association approached statistical significance, the findings indicated moderate heterogeneity among the included studies, as quantified by an I² value of 56.52%. This measure reflects differences in study populations, designs, or diagnostic methods that could influence the observed effect sizes.
In contrast, the association between HCV infection and MM was more pronounced and statistically significant, with a pooled RR of 1.84 (95% CI: 1.27–2.67). This finding highlights a nearly twofold increase in MM risk among people chronically infected with HCV. The relatively stronger association underscores the distinct pathogenic mechanisms by which HCV may contribute to the development of hematological malignancies, potentially through chronic immune stimulation, direct viral oncogenic effects, or induction of systemic inflammation.
Subgroup analyses provided further insight into geographical and demographic trends. Notably, both HBV and HCV infections showed a stronger correlation with MM risk in European populations compared to other regions. For HBV, the risk elevation reached an RR of 1.67 (95% CI: 1.05–2.66), while HCV-infected individuals in Europe displayed an RR of 2.27 (95% CI: 1.21–4.25). These geographic disparities may reflect differences in viral genotypes, healthcare infrastructure, screening practices, or genetic susceptibility factors intrinsic to these populations.
Importantly, the systematic review employed rigorous methodological quality assessments using the Newcastle-Ottawa Scale (NOS), ensuring that only studies of adequate quality informed the meta-analysis findings. Statistical techniques were also utilized to evaluate potential publication bias, with Egger’s test indicating no significant bias, thereby strengthening the credibility of the results.
The pathophysiological mechanisms linking HBV and HCV infections to MM are still under investigation. However, prevailing hypotheses suggest that chronic viral infections elicit persistent antigenic stimulation of B cells, particularly plasma cells, potentially leading to malignant transformation. Additionally, viral proteins may interfere with cellular regulatory pathways, promoting genomic instability and oncogenesis in susceptible individuals.
These revelations bear significant clinical implications. They suggest that patients with chronic hepatitis, especially those infected with HCV, should be closely monitored for early signs of hematological malignancies such as multiple myeloma. Enhanced screening protocols and vigilant follow-ups could facilitate timely diagnosis and intervention, potentially improving patient outcomes.
Furthermore, this study emphasizes the importance of integrating infectious disease history into oncological risk stratification models. It also highlights the pressing need for further mechanistic studies to unravel the intricate interactions between chronic viral infections and plasma cell neoplasms.
The findings also raise public health considerations, particularly in regions with high prevalence of HBV and HCV. Effective vaccination campaigns against HBV and antiviral treatment programs targeting HCV could indirectly reduce the burden of multiple myeloma by minimizing chronic infection rates, thereby averting long-term oncogenic sequelae.
In conclusion, this landmark meta-analysis elucidates a critical link between hepatitis B and C virus infections and the risk of developing multiple myeloma. The stronger association observed with HCV infection calls for heightened awareness and proactive clinical management of at-risk populations. These insights pave the way for multidisciplinary strategies combining virology, oncology, and epidemiology to combat the complex interplay between chronic infections and cancer.
As the global healthcare community continues to grapple with the multifaceted challenges posed by hepatitis viruses and hematological malignancies, this research offers a timely reminder of the interconnectedness of infectious diseases and cancer biology. Ongoing research efforts must strive to deepen our understanding and translate these findings into improved patient care and preventative public health policies.
Subject of Research: Relationship between Hepatitis B (HBV) and Hepatitis C (HCV) virus infections and the risk of developing multiple myeloma (MM).
Article Title: Hepatitis B and C virus infection and risk of multiple myeloma: a systematic review and meta-analysis
Article References:
Zamani, K., Rostami, P., Darehbagh, R.R. et al. Hepatitis B and C virus infection and risk of multiple myeloma: a systematic review and meta-analysis.
BMC Cancer 25, 998 (2025). https://doi.org/10.1186/s12885-025-14420-5
Image Credits: Scienmag.com
DOI: https://doi.org/10.1186/s12885-025-14420-5
Tags: cancer prevention and infectious diseases.chronic infections and hematological malignanciesearly detection strategies for multiple myelomaenvironmental risk factors for multiple myelomaepidemiological research on hepatitis virusesHepatitis B virus and multiple myeloma riskHepatitis C virus and cancer associationimmune dysfunction in multiple myelomalong-term survival in cancer patientsmeta-analysis on multiple myelomaplasma cell proliferation and bone marrowsystematic review of HBV and HCV studies
