An oncogenic virus, or oncovirus, is a virus that can cause or contribute to the development of cancer in humans and animals. These viruses are responsible for an estimated 10% to 20% of all human cancers globally. The vast majority of viral infections do not result in cancer. However, a persistent infection in a susceptible host can disrupt normal cell growth and survival pathways, leading to the uncontrolled proliferation characteristic of malignancy.
The Major Oncogenic Viruses
A small group of viruses is responsible for the majority of virus-related human cancers and is classified as Group 1 human carcinogens by the International Agency for Research on Cancer (IARC). The Human Papillomavirus (HPV) is the primary cause of nearly all cervical cancers, accounting for approximately 99% of cases. High-risk HPV types, particularly HPV-16 and HPV-18, are also linked to cancers of the anus, vulva, vagina, penis, and oropharyngeal cancers.
The Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) are major causes of liver cancer, or Hepatocellular Carcinoma (HCC). These two viruses are implicated in approximately 80% of all HCC cases globally. Chronic infection with HBV or HCV leads to liver damage and cirrhosis, which increases the risk of developing this cancer.
The Epstein-Barr Virus (EBV), a common human herpesvirus, is associated with a diverse range of malignancies. These include nasopharyngeal carcinoma and several types of lymphomas. EBV is linked to certain forms of Hodgkin’s lymphoma and non-Hodgkin’s lymphomas, such as Burkitt’s lymphoma.
The Kaposi’s Sarcoma-associated Herpesvirus (KSHV), also known as Human Herpesvirus 8 (HHV-8), causes Kaposi’s Sarcoma. This cancer produces lesions on the skin, lymph nodes, and other organs. It is most frequently seen in individuals with weakened immune systems, such as those with Acquired Immunodeficiency Syndrome (AIDS). KSHV is also associated with primary effusion lymphoma.
The retrovirus Human T-lymphotropic Virus Type 1 (HTLV-1) is linked to Adult T-cell Leukemia/Lymphoma (ATLL). This is a rare but aggressive cancer of the T-lymphocytes. Its incidence is highest in certain endemic regions. The Merkel Cell Polyomavirus (MCV) is a recently identified oncovirus that causes Merkel cell carcinoma, an aggressive form of skin cancer.
Viral Mechanisms of Cancer Development
The transformation of a healthy cell into a malignant one involves several molecular mechanisms. One common mechanism is the direct action of viral proteins, called oncoproteins, which are encoded by the virus’s genes. For instance, high-risk HPV strains produce the oncoproteins E6 and E7.
The E6 protein targets and promotes the degradation of the host cell’s tumor suppressor protein, p53. P53 is responsible for initiating DNA repair or programmed cell death (apoptosis) in damaged cells. The E7 protein binds to and inactivates the Retinoblastoma (Rb) protein, another major tumor suppressor that acts as a brake on the cell cycle. Disabling both p53 and Rb removes the cell’s natural safeguards, allowing uncontrolled cell division.
Other oncogenic viruses, such as HBV, HCV, and HTLV-1, primarily cause cancer through indirect mechanisms, with chronic inflammation being a major driver. Persistent infection leads to continuous tissue damage and repair cycles, particularly in organs like the liver. This prolonged inflammation creates an environment rich in inflammatory signals and reactive oxygen species, which cause genetic mutations and promote abnormal cell growth.
Some viruses also integrate their genetic material directly into the host cell’s DNA. This integration can disrupt the function of host tumor suppressor genes or lead to the overexpression of host genes that promote cell growth, turning a normal cellular gene into an oncogene. Many oncogenic viruses also evade or suppress the host’s immune system, allowing infected cells to persist and proliferate. This immune suppression contributes to the chronic infection often required for cancer development.
Strategies for Viral-Induced Cancer Prevention
Preventing the initial viral infection is the most effective strategy for combating virus-associated cancers. The development of prophylactic vaccines against oncogenic viruses represents a major public health success. The Human Papillomavirus (HPV) vaccine is effective and targets the high-risk types, such as HPV-16 and HPV-18, which cause the majority of cervical and other related cancers.
Vaccination is most effective when administered to preteens, typically at age 11 or 12, before potential exposure to the virus. For those who have not been vaccinated, catch-up vaccination is generally recommended through age 26. The Hepatitis B Virus (HBV) vaccine is another successful preventative measure that significantly reduces the risk of Hepatocellular Carcinoma. This vaccine is routinely given to infants, and its widespread use has demonstrated a substantial reduction in liver cancer rates in vaccinated populations.
Screening and early detection programs are also a cornerstone of prevention for cancers linked to viral infection. Regular cervical cancer screening, such as the Pap test and HPV testing, allows for the detection and removal of precancerous lesions caused by HPV before they can progress to invasive cancer.
Similarly, individuals with chronic HBV or HCV infection are considered a high-risk population for liver cancer. These patients often undergo regular surveillance with imaging tests, such as ultrasound, to detect small tumors at an early, more treatable stage.
For chronic infections that do not yet have a vaccine, such as Hepatitis C Virus (HCV), antiviral treatments offer a powerful means of cancer prevention. The use of modern direct-acting antiviral (DAA) medications can cure over 95% of chronic HCV infections. By eliminating the virus, these treatments remove the source of chronic inflammation and liver damage, thereby drastically reducing the patient’s long-term risk of developing liver cancer.