Posters
Presenting Author Academic/Professional Position
Medical Student
Academic/Professional Position (Other)
Shizue Mito
Academic Level (Author 1)
Medical Student
Academic Level (Author 2)
Medical Student
Presentation Type
Poster
Discipline Track
Biomedical Science
Abstract Type
Research/Clinical
Abstract
Background: Varicella-zoster virus (VZV) is a highly prevalent pathogen primarily recognized for causing chickenpox during primary infection and herpes zoster (HZ), also known as shingles, upon reactivation. While post-infectious complications of VZV, such as encephalitis, pneumonia, and post-herpetic neuralgia, are well-established, recent large population-based studies suggest that HZ may increase the risk of occult cancers. Emerging evidence suggests that VZV may modulate key oncogenic pathways, such as the inhibition of apoptosis, alteration of cell cycle regulatory enzymes, and interference with immunosurveillance, which could potentially promote cancer development. These findings indicate that VZV’s role in cancer biology may involve direct cellular manipulation that facilitates oncogenesis. Understanding the interplay between VZV and cancer is critical for public health. Further exploration of the mechanisms of viral oncogenesis could provide valuable insights into how VZV contributes to cancer development and open avenues for targeted preventive and therapeutic strategies.
Methods: We conducted an extensive search across more than 70 recent and relevant studies concerning VZV in cancer, utilizing various online databases such as PubMed, Google Scholar, and Web of Science. Our aim was to synthesize essential insights gleaned from the latest available research, thereby establishing a comprehensive framework that encapsulates the current knowledge regarding the role of VZV in cancer. All statistical analyses mentioned in the literature were carried out by the respective study authors.
Results: VZV's genome encodes multiple proteins that help it evade the immune response, including IE62 and STPK, which manipulate host cell processes like IRF3 activation, inhibiting IFN-β production and weakening immune defenses. Additionally, VZV's glycoprotein C induces IL4I1, which suppresses anti-tumor immune responses by inhibiting T cell proliferation, inhibiting Th1 polarization, and promoting the differentiation of naive CD4+ T cells into FoxP3+ Tregs, thereby contributing to a tumor-friendly microenvironment. VZV infection disrupts the JAK-STAT pathway by decreasing the levels of JAK1, JAK2, and STAT1 proteins, preventing the phosphorylation and nuclear translocation of STAT1, which is essential for the transcriptional activation of IFN-γ-inducible genes, including those encoding MHC class II molecules. Furthermore, VZV modulates NF-κB activity by preventing the degradation of IκBα through the action of the ORF61 protein, leading to the cytoplasmic retention of NF-κB subunits and inhibition of NF-κB-dependent gene transcription. Finally, ORF66 disrupts the transport of MHC I molecules from the endoplasmic reticulum through the golgi apparatus, leading to their retention in the golgi compartment. This retention prevents MHC I molecules from reaching the cell surface.
Conclusions: Further investigation into how VZV interacts with cellular pathways, particularly those related to apoptosis and cell survival, may help clarify potential connections between the virus and tumorigenesis. Understanding how VZV manipulates host cell functions—such as inhibiting apoptosis or altering cell cycle regulation—could shed light on how normal cells might transform into cancerous ones. These insights are crucial in determining whether VZV is merely a viral pathogen or if it could also act as an oncogenic factor, contributing to cancer development in certain cells or conditions.
Recommended Citation
Cisneros, Fernando and Martin, Blake, "Exploring the Mechanisms of Varicella-Zoster Virus Pathogenesis and Its Potential Role in Oncogenesis" (2025). Research Symposium. 66.
https://scholarworks.utrgv.edu/somrs/2025/posters/66
Included in
Medical Biochemistry Commons, Medical Immunology Commons, Medical Microbiology Commons, Medical Pathology Commons
Exploring the Mechanisms of Varicella-Zoster Virus Pathogenesis and Its Potential Role in Oncogenesis
Background: Varicella-zoster virus (VZV) is a highly prevalent pathogen primarily recognized for causing chickenpox during primary infection and herpes zoster (HZ), also known as shingles, upon reactivation. While post-infectious complications of VZV, such as encephalitis, pneumonia, and post-herpetic neuralgia, are well-established, recent large population-based studies suggest that HZ may increase the risk of occult cancers. Emerging evidence suggests that VZV may modulate key oncogenic pathways, such as the inhibition of apoptosis, alteration of cell cycle regulatory enzymes, and interference with immunosurveillance, which could potentially promote cancer development. These findings indicate that VZV’s role in cancer biology may involve direct cellular manipulation that facilitates oncogenesis. Understanding the interplay between VZV and cancer is critical for public health. Further exploration of the mechanisms of viral oncogenesis could provide valuable insights into how VZV contributes to cancer development and open avenues for targeted preventive and therapeutic strategies.
Methods: We conducted an extensive search across more than 70 recent and relevant studies concerning VZV in cancer, utilizing various online databases such as PubMed, Google Scholar, and Web of Science. Our aim was to synthesize essential insights gleaned from the latest available research, thereby establishing a comprehensive framework that encapsulates the current knowledge regarding the role of VZV in cancer. All statistical analyses mentioned in the literature were carried out by the respective study authors.
Results: VZV's genome encodes multiple proteins that help it evade the immune response, including IE62 and STPK, which manipulate host cell processes like IRF3 activation, inhibiting IFN-β production and weakening immune defenses. Additionally, VZV's glycoprotein C induces IL4I1, which suppresses anti-tumor immune responses by inhibiting T cell proliferation, inhibiting Th1 polarization, and promoting the differentiation of naive CD4+ T cells into FoxP3+ Tregs, thereby contributing to a tumor-friendly microenvironment. VZV infection disrupts the JAK-STAT pathway by decreasing the levels of JAK1, JAK2, and STAT1 proteins, preventing the phosphorylation and nuclear translocation of STAT1, which is essential for the transcriptional activation of IFN-γ-inducible genes, including those encoding MHC class II molecules. Furthermore, VZV modulates NF-κB activity by preventing the degradation of IκBα through the action of the ORF61 protein, leading to the cytoplasmic retention of NF-κB subunits and inhibition of NF-κB-dependent gene transcription. Finally, ORF66 disrupts the transport of MHC I molecules from the endoplasmic reticulum through the golgi apparatus, leading to their retention in the golgi compartment. This retention prevents MHC I molecules from reaching the cell surface.
Conclusions: Further investigation into how VZV interacts with cellular pathways, particularly those related to apoptosis and cell survival, may help clarify potential connections between the virus and tumorigenesis. Understanding how VZV manipulates host cell functions—such as inhibiting apoptosis or altering cell cycle regulation—could shed light on how normal cells might transform into cancerous ones. These insights are crucial in determining whether VZV is merely a viral pathogen or if it could also act as an oncogenic factor, contributing to cancer development in certain cells or conditions.
