Unravelling the Complex Interplay in Viral-Induced Cancer Pathogenic Mechanisms

Costin Indovina^*
*Correspondence: Costin Indovina, Department of Microbiology and Immunology, Drexel University, College of Medicine, Philadelphia, USA, Email:

Keywords

Viral-induced cancers • Pathogenic mechanisms • Oncogenesis • Viral oncogenes • Immune evasion • Cellular transformation

Introduction

Viral-induced cancers represent a substantial proportion of malignancies worldwide, contributing to significant morbidity and mortality. Several well-known viruses, such as Human Papillomavirus (HPV), Epstein - Barr virus (EBV), Hepatitis B Virus (HBV) and Hepatitis C virus (HCV) have been implicated in the development of various cancers. The complex interplay between these viruses and host cells leads to cellular transformation and tumor initiation. Understanding the pathogenic mechanisms by which viruses induce cancer is essential for advancing our knowledge of oncogenesis and developing effective therapeutic interventions. Viruses can exert oncogenic effects through various mechanisms. Some viruses possess viral oncogenes that directly manipulate host cell signaling pathways, leading to uncontrolled cell proliferation. For example, the E6 and E7 oncoproteins of high-risk HPV strains interfere with tumor suppressor proteins, promoting cellular transformation. Other viruses induce chronic inflammation, which creates an environment conducive to carcinogenesis. HBV and HCV are known to cause persistent inflammation in the liver, increasing the risk of hepatocellular carcinoma.

Viral-induced oncogenesis involves intricate molecular interactions between viral components and host cellular machinery. Viruses may integrate their genetic material into the host genome, disrupting normal gene expression and contributing to malignant transformation. For instance, EBV encodes latent membrane proteins that activate cellular signaling pathways, leading to cell survival and proliferation. Additionally, viruses can dysregulate cellular apoptosis mechanisms, allowing infected cells to evade programmed cell death and accumulate genetic mutations. Viruses exploit various strategies to subvert critical cellular processes, facilitating their survival and propagation. They can modulate immune responses by evading immune surveillance or manipulating immune checkpoints. For instance, the Human T-cell Leukemia Virus (HTLV-1) evades immune recognition by downregulating Major Histocompatibility Complex (MHC) class I molecules. Furthermore, viruses can disrupt DNA repair mechanisms, increasing the accumulation of DNA damage and promoting genomic instability, a hallmark of cancer [1,2].

Literature Review

Understanding the pathogenic mechanisms of viral-induced cancers holds significant therapeutic implications. Targeted therapies that directly inhibit viral oncoproteins or disrupt virus-host interactions show promise in combating these cancers. For example, specific inhibitors have been developed to target the oncoproteins E6 and E7 in HPV-associated cancers. Additionally, preventive measures, such as vaccination against oncogenic viruses like HPV, can substantially reduce the incidence of associated malignancies. Viral-induced cancers result from complex interactions between viruses and host cells, involving various pathogenic mechanisms. Unraveling these mechanisms is crucial for developing effective therapeutic strategies to combat viral-induced malignancies. Continued research in this field will pave the way for improved diagnosis, prevention and treatment options, ultimately reducing the global burden of viral-induced cancers. The study of pathogenic mechanisms in viralinduced cancers provides valuable insights into the intricate interplay between viruses and host cells. By understanding how viruses induce oncogenesis, researchers can develop targeted therapies and preventive measures to combat these devastating diseases effectively. Continued research in this field holds immense promise for improving patient outcomes and reducing the global impact of viral-induced cancers. Furthermore, advancements in technologies such as genomic sequencing and molecular profiling offer new opportunities to unravel the complex molecular landscape of viral-induced cancers and identify potential therapeutic targets [3].

One area of ongoing research is the development of antiviral therapies that specifically target viral components involved in oncogenesis. For instance, inhibitors targeting viral oncoproteins, such as E6 and E7 in HPV-associated cancers, have shown promising results in preclinical and clinical studies. These inhibitors aim to disrupt the interaction between viral oncoproteins and cellular proteins, effectively inhibiting their oncogenic activities and restoring normal cellular function. Similarly, drugs targeting viral enzymes involved in viral replication, such as polymerases or proteases, are being explored as potential therapeutic options. Complex molecular interactions exist between viral parts and host cellular machinery during virally-induced oncogenesis. Viruses may incorporate their genetic material into the genome of the host, altering regular gene expression and assisting in the development of cancer [4].

Discussion

Additionally, immune-based therapies have gained considerable attention in the field of viral-induced cancers. Immunotherapeutic approaches, such as immune checkpoint inhibitors, aim to enhance the immune response against infected or transformed cells. These therapies work by blocking inhibitory checkpoints on immune cells, thereby unleashing the immune system's ability to recognize and eliminate cancer cells. Immune-based therapies have shown remarkable success in various cancer types, including those associated with viral infections, highlighting the potential of harnessing the immune system to target viral-induced cancers. Prevention also plays a crucial role in reducing the burden of viral-induced cancers. Vaccination programs targeting oncogenic viruses, such as HPV and HBV, have been implemented in many countries with notable success. HPV vaccination has demonstrated remarkable efficacy in reducing the incidence of HPV-related cervical, anal, and oropharyngeal cancers. Similarly, HBV vaccination has shown a significant impact on reducing the incidence of hepatocellular carcinoma in regions with high endemicity. Expanded vaccination efforts, especially in resource-limited settings, can further reduce the global burden of viral-induced cancers [5,6].

Conclusion

Understanding the pathogenic mechanisms underlying viral-induced cancers is essential for developing effective therapeutic interventions and preventive strategies. The intricate interplay between viruses and host cells involves a range of mechanisms, including viral oncogenes, disruption of cellular processes and immune evasion. Ongoing research aims to decipher the molecular intricacies of these interactions, leading to the development of targeted therapies and immunotherapies. Additionally, preventive measures such as vaccination hold tremendous potential in reducing the incidence of viral-induced malignancies. Continued efforts in this field will undoubtedly contribute to better outcomes for patients affected by viral-induced cancers and ultimately lead to a reduction in the global burden of these diseases.

Acknowledgement

We thank the anonymous reviewers for their constructive criticisms of the manuscript.

Conflict of Interest

The author declares there is no conflict of interest associated with this manuscript.

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