Microbiology: Current Research

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (202) 780-3397

Brief Report - Microbiology: Current Research (2024) Volume 8, Issue 5

The Role of Viruses in Cancer: Understanding Oncoviruses

Samuel Osei*

Department of Microbiology, University of Cape Coast, Ghana

*Corresponding Author:
Samuel Osei
Department of Microbiology
University of Cape Coast, Ghana
E-mail: samuel.osei@email.com

Received: 10-Oct-2024, Manuscript No. AAMCR-24-155100; Editor assigned: 11-Oct-2024, PreQC No. AAMCR-24-155100 (PQ); Reviewed: 22-Oct-2024, QC No. AAMCR-24-155100; Revised: 24-Oct-2024, Manuscript No. AAMCR-24-155100 (R); Published: 31-Oct-2024, DOI: 10.35841/aamcr-8.5.234

Citation: Osei S. The Role of Viruses in Cancer: Understanding Oncoviruses. J Micro Bio Curr Res. 2024;8(5):234

Visit for more related articles at Microbiology: Current Research

Introduction

Viruses are primarily known for causing infections, but some viruses can also lead to cancer by altering the genetic material of host cells. These cancer-causing viruses, known as oncoviruses, are responsible for a significant percentage of human cancers. Oncoviruses promote oncogenesis by disrupting normal cellular processes, leading to uncontrolled cell division, genetic mutations, and eventually, the formation of tumors. This article explores how oncoviruses cause cancer, the types of cancers associated with viral infections, and ongoing research aimed at preventing and treating virus-related cancers [1].

Oncoviruses are a group of viruses that can cause cancer in humans and animals. These viruses infect cells and integrate their genetic material into the host cell's DNA, leading to changes in cellular functions that can promote tumor formation. Oncoviruses are responsible for around 15-20% of human cancers worldwide. The major oncoviruses known to cause cancer in humans include human papillomavirus (HPV), Epstein-Barr virus (EBV), hepatitis B and C viruses (HBV and HCV), Kaposi's sarcoma-associated herpesvirus (KSHV), and human T-cell lymphotropic virus (HTLV-1). These viruses use different mechanisms to induce cancer, but they all disrupt normal cell regulation [2].

Oncoviruses cause cancer through several mechanisms. One common strategy is the integration of viral DNA into the host genome, which can activate oncogenes or inactivate tumor suppressor genes. For example, HPV encodes proteins like E6 and E7, which inactivate the tumor suppressor proteins p53 and retinoblastoma protein (pRb), leading to uncontrolled cell division. Another mechanism is chronic inflammation induced by viral infections, which can damage DNA and promote mutations. Hepatitis viruses, for instance, cause chronic liver inflammation, increasing the risk of liver cancer. Additionally, some viruses, like EBV, can induce immortalization of infected cells, allowing them to proliferate indefinitely [3].

One of the most well-known oncoviruses is human papillomavirus (HPV), which is responsible for the vast majority of cervical cancers. HPV is a sexually transmitted virus with more than 100 different strains, but only a few, such as HPV-16 and HPV-18, are classified as high-risk for cancer. HPV infects the epithelial cells of the cervix and integrates its DNA into the host genome. The viral proteins E6 and E7 inactivate the tumor suppressors p53 and pRb, leading to the accumulation of genetic mutations and the development of cancer. HPV is also associated with other cancers, including head and neck cancers, anal cancer, and penile cancer [4].

Epstein-Barr virus (EBV) is a herpesvirus that is commonly associated with infectious mononucleosis (also known as the “kissing disease”), but it is also linked to several cancers, particularly lymphomas. EBV can infect B cells, a type of immune cell, and establish a latent infection. In some cases, EBV infection can lead to the development of cancers like Burkitt’s lymphoma, Hodgkin’s lymphoma, and nasopharyngeal carcinoma. EBV-induced oncogenesis is mediated by viral proteins such as latent membrane protein 1 (LMP1), which mimics growth signals and promotes cell survival and proliferation. The virus can also promote genetic instability, increasing the likelihood of mutations that lead to cancer [5].

Hepatitis B virus (HBV) and hepatitis C virus (HCV) are leading causes of liver cancer, also known as hepatocellular carcinoma (HCC). These viruses cause chronic infections that lead to long-term inflammation of the liver, which increases the risk of developing cancer. Chronic hepatitis infection results in liver damage and attempts at tissue repair, which can lead to DNA mutations over time. HBV can also directly integrate into the host genome, promoting oncogenesis by disrupting cellular regulatory genes. Vaccinations against HBV and antiviral treatments for HCV have been effective in reducing the incidence of liver cancer, but it remains a major global health issue [6].

Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV-8), is linked to the development of Kaposi's sarcoma, a cancer that forms in the lining of blood vessels and is most commonly seen in immunocompromised individuals, such as those with HIV/AIDS. KSHV infects endothelial cells, promoting the growth of abnormal blood vessels and the formation of tumors. Viral proteins encoded by KSHV, such as the viral homolog of IL-6 (vIL-6) and the viral FLICE inhibitory protein (vFLIP), promote cell survival, proliferation, and angiogenesis, all of which contribute to tumor development [7].

Human T-cell lymphotropic virus type 1 (HTLV-1) is a retrovirus that can cause adult T-cell leukemia/lymphoma (ATLL), a rare and aggressive form of cancer. HTLV-1 infects T cells, a type of immune cell, and integrates its genetic material into the host genome. The viral protein Tax plays a crucial role in transforming infected T cells by activating oncogenes and inhibiting tumor suppressor genes. In addition to promoting uncontrolled cell proliferation, HTLV-1 can also suppress the immune response, allowing infected cells to evade immune surveillance. ATLL is difficult to treat, and infection with HTLV-1 remains a significant risk factor for this form of cancer [8].

One of the most effective ways to prevent virus-related cancers is through vaccination. The HPV vaccine has been widely successful in reducing the incidence of cervical cancer and other HPV-related cancers by protecting against high-risk strains of the virus. Similarly, the hepatitis B vaccine has been instrumental in reducing the global burden of liver cancer. In addition to vaccines, regular screening and early detection play a key role in preventing the progression of virus-associated cancers. For example, Pap smears are used to detect precancerous changes in the cervix caused by HPV, and liver function tests and imaging can help monitor individuals at risk for liver cancer due to chronic hepatitis infections [9].

The treatment of virus-induced cancers often involves a combination of surgery, chemotherapy, radiation, and antiviral therapy. For example, antiviral drugs like lamivudine and entecavir can be used to treat chronic HBV infection and reduce the risk of liver cancer progression. For patients with Kaposi’s sarcoma, highly active antiretroviral therapy (HAART) can control HIV infection and improve immune function, leading to the regression of Kaposi’s sarcoma lesions. Immunotherapy, which enhances the immune system’s ability to recognize and attack cancer cells, is also being explored as a potential treatment for virus-induced cancers, particularly those associated with HPV and EBV [10].

Conclusion

Research into oncoviruses continues to evolve, with scientists exploring new ways to prevent and treat virus-associated cancers. One area of focus is the development of therapeutic vaccines, which not only prevent infection but also treat existing infections by stimulating the immune system to target virus-infected cells. Advances in gene-editing technologies, such as CRISPR, hold promise for directly targeting and eliminating viral genomes from infected cells. Furthermore, understanding the interactions between oncoviruses and the host immune system is essential for developing new immunotherapies. As our knowledge of viral oncogenesis grows, so too does the potential to reduce the global burden of cancer through innovative treatments and preventive measures.

References

  1. Fowler JF, Lindstrom MJ. Loss of local control with prolongation in radiotherapy. Int J Radiat Oncol Biol Phys.1992;23(2):457-67.

    2. Indexed at, Google Scholar, Cross Ref

  2. Begg AC, Hofland I, Moonen L, et al. The predictive value of cell kinetic measurements in a European trial of accelerated fractionation in advanced head and neck tumors: an interim report. Int J Radiat Oncol Biol Phys. 1990;19(6):1449-53.

    3. Indexed at, Google Scholar, Cross Ref

  3. Haustermans KM, Hofland I, Van Poppel H, et al. Cell kinetic measurements in prostate cancer. Int J Radiat Oncol Biol Phys. 1997;37(5):1067-70.

    4. Indexed at, Google Scholar, Cross Ref

  4. Rew DA, Wilson GD. Cell production rates in human tissues and tumours and their significance. Part II: Clinical Data (EJSO). 2000;26(4):405-17.

    5. Indexed at, Google Scholar, Cross Ref

  5. Bernardini ML, Mounier J, d'Hauteville H, et al. Identification of icsA, a plasmid locus of Shigella flexneri that governs bacterial intra-and intercellular spread through interaction with F-actin. PNAS. 1989;86(10):3867-71.

    6. Indexed at, Google Scholar, Cross Ref

  6. Bielecki J, Youngman P, Connelly P, et al. Bacillus subtilis expressing a haemolysin gene from Listeria monocytogenes can grow in mammalian cells. Nature. 1990;345(6271):175-6.

    7. Indexed at, Google Scholar, Cross Ref

  7. Gaillard JL, Berche P, Sansonetti P. Transposon mutagenesis as a tool to study the role of hemolysin in the virulence of Listeria monocytogenes. Infection Immunity. 1986;52(1):50-5.

    8. Indexed at, Google Scholar, Cross Ref

  8. Gillmaier N, Götz A, Schulz A, et al. Metabolic responses of primary and transformed cells to intracellular Listeria monocytogenes. PLoS One. 2012;7(12):e52378.

    9. Indexed at, Google Scholar, Cross Ref

  9. Huang L, Kushner NL, Theriault ME, et al. The deconstructed granuloma: a complex high-throughput drug screening platform for the discovery of host-directed therapeutics against tuberculosis. Front cell Infect Mi. 2018;8:275.

    10. Indexed at, Google Scholar, Cross Ref

  10. Lustigman S, Prichard RK, Gazzinelli A, et al. A research agenda for helminth diseases of humans: the problem of helminthiases. PLoS Negl Trop Dis. 2012;6(4):e1582.

    11. Indexed at, Google Scholar, Cross Ref

Get the App