What Causes Cervical Cancer

Cervical cancer develops when abnormal cells in the cervix—the lower part of the uterus—grow uncontrollably and form tumors. The primary cause is a persistent infection with human papillomavirus (HPV), a common sexually transmitted virus. However, several other risk factors—such as smoking, weakened immunity, and reproductive history—can increase a person’s vulnerability to developing this disease.

HPV infections are extremely common; most sexually active individuals will contract at least one strain during their lifetime. In many cases, the body clears the virus naturally within two years. Problems arise when high-risk HPV types—particularly HPV-16 and HPV-18—persist, causing precancerous changes in cervical cells that can progress to cancer over time.

Human Papillomavirus (HPV)

HPV is the most significant and well-established cause of cervical cancer. There are over 100 types of HPV, but about 14 are classified as high-risk because of their cancer-causing potential. These viruses infect the epithelial cells of the cervix and interfere with normal cell regulation, leading to genetic mutations and malignant growth.

The virus spreads primarily through sexual contact, including vaginal, anal, or oral sex. Condoms can lower the risk but do not provide full protection since HPV can infect areas not covered by condoms.

HPV infection often shows no symptoms. That’s why regular cervical screening (Pap smears and HPV testing) plays a vital role in detecting early cell changes before they turn cancerous.

How HPV Leads to Cervical Cancer

When a high-risk HPV strain infects cervical cells, it may integrate its genetic material into the host’s DNA. This integration disrupts two major tumor-suppressor proteins in the body—p53 and retinoblastoma (Rb)—which normally control cell division and prevent tumor growth.

Without these regulatory mechanisms, infected cells begin to divide uncontrollably, creating precancerous lesions known as cervical intraepithelial neoplasia (CIN). Over time, if left untreated, CIN can progress to invasive cervical cancer.

Persistent HPV infection is the key factor—temporary infections rarely cause harm. The risk increases with multiple sexual partners, early sexual activity, and other factors that increase exposure or reduce immune defense.

HPV Types and Cancer Risk

Not all HPV strains carry the same danger. The high-risk strains, especially HPV-16 and HPV-18, are responsible for about 70% of cervical cancer cases globally. Other high-risk types—like HPV-31, 33, 45, 52, and 58—also contribute to the remaining percentage.

On the other hand, low-risk HPV types (such as HPV-6 and HPV-11) typically cause benign conditions like genital warts but rarely lead to cancer. Understanding the difference helps guide screening, vaccination, and prevention strategies.

The HPV vaccine, available worldwide, targets the most dangerous strains and has drastically reduced HPV infection rates and cervical abnormalities in countries with strong vaccination programs.

Other Viral and Infectious Causes

Although HPV is the leading cause, co-infections with other sexually transmitted infections (STIs) may increase cervical cancer risk. For instance:

  • Chlamydia trachomatis infection can cause chronic inflammation, making it easier for HPV to persist.

  • Herpes simplex virus (HSV-2) has also been linked to increased cervical dysplasia.

  • Chronic bacterial vaginosis may alter the vaginal microbiome, affecting the body’s natural defenses against HPV.

Maintaining good sexual health, using protection, and undergoing regular STI screening can help reduce these compounding risks.

Smoking and Cervical Cancer

Smoking doubles the risk of cervical cancer. Tobacco byproducts are known to damage the DNA of cervical cells and weaken the immune system, making it harder to clear HPV infections.

Studies have found that nicotine and carcinogens from cigarettes concentrate in cervical mucus, where they can directly damage cell DNA. Moreover, smokers tend to have lower levels of antioxidants and immune-supporting nutrients, making them more vulnerable to infection and cancer development.

Quitting smoking is one of the simplest yet most powerful ways to reduce cervical cancer risk and improve overall reproductive health.

Weakened Immune System

A healthy immune system usually eliminates HPV infections before they cause harm. However, when the immune system is compromised—whether by HIV infection, long-term use of immunosuppressive medications (for autoimmune disease or organ transplant), or chronic stress—the body loses its ability to control HPV replication.

Women living with HIV, for instance, are up to five times more likely to develop cervical cancer compared to HIV-negative women. This makes regular Pap and HPV tests essential for immunocompromised individuals.

Reproductive and Sexual History

Certain reproductive factors can also elevate cervical cancer risk:

  • Early sexual activity: The cervix in adolescents is still developing, making it more susceptible to HPV infection.

  • Multiple sexual partners: Increases exposure to high-risk HPV strains.

  • Long-term use of oral contraceptives (over 5 years): Some studies suggest a slight increase in cervical cancer risk due to hormonal effects on cervical cells.

  • High number of pregnancies: Repeated cervical trauma during childbirth and hormonal changes may play a role.

While these factors alone don’t cause cervical cancer, they can amplify the impact of persistent HPV infection.

Genetic and Family History

Although cervical cancer is primarily caused by infections, genetic susceptibility also matters. Women with close relatives (mother, sister) who had cervical cancer may have a higher risk.

Researchers believe that certain genetic variations in immune response genes affect how effectively the body clears HPV infections. Inherited differences in DNA repair mechanisms may also make some women more prone to developing precancerous lesions after HPV exposure.

Family history should always be considered during regular checkups, particularly if multiple relatives have had gynecological cancers.

Socioeconomic and Environmental Factors

Access to healthcare plays a crucial role in cervical cancer prevention. Women from lower socioeconomic backgrounds often face limited access to Pap tests, HPV vaccination, and treatment for early lesions—leading to higher mortality rates.

Environmental exposures such as chemical carcinogens, poor nutrition, and chronic stress can further increase susceptibility. Nutrient deficiencies—particularly vitamins A, C, E, and folate—have been associated with impaired immune responses against HPV.

Public health initiatives that expand screening and vaccination access are essential to reducing global cervical cancer disparities.

Hormonal Influences

Hormonal factors also interact with HPV to influence cancer risk. Estrogen and progesterone, the main female sex hormones, can affect how cervical cells grow and respond to infections.

Long-term exposure to estrogen, whether from oral contraceptives or pregnancy, can make cervical tissue more receptive to HPV infection. In women with persistent HPV infection, these hormonal effects may accelerate the development of precancerous lesions.

Diet, Nutrition, and Lifestyle

A balanced diet plays a surprisingly strong role in cervical cancer prevention. Diets rich in antioxidants, vitamins, and carotenoids strengthen the body’s ability to fight infections and repair DNA damage.

Research suggests that low levels of folate, vitamin B12, vitamin C, and vitamin E may contribute to persistent HPV infection and abnormal Pap test results. Additionally, high consumption of processed foods, alcohol, and red meat can contribute to systemic inflammation—further increasing cancer risk.

Adopting a nutrient-dense, plant-based diet and staying physically active can enhance immune function and lower cancer risk overall.

Age and Long-Term HPV Infection

Age is another crucial factor. Most HPV infections occur in women under 30 and clear on their own. However, when infection persists beyond the age of 30–40, the likelihood of cellular transformation rises sharply.

This is why regular screening becomes increasingly important as women age. Early detection through Pap tests can identify precancerous changes, allowing timely treatment before they progress to cancer.

Hormone Replacement Therapy (HRT) and Oral Contraceptives

Studies on hormone replacement therapy (HRT) show mixed findings. While HRT is mainly associated with endometrial and breast cancers, prolonged use may also slightly influence cervical cancer risk in HPV-positive women.

Similarly, oral contraceptives used for more than five years may alter cervical cells’ hormonal environment, making them more vulnerable to viral persistence. Discussing birth control options with healthcare providers is recommended, especially for women with other risk factors.

Pregnancy and Childbirth

Having multiple full-term pregnancies has been linked to an increased risk of cervical cancer. Scientists believe this is due to hormonal shifts, immune changes, and cervical trauma during labor that make infection more likely to persist.

During pregnancy, immune suppression allows the body to tolerate the fetus, but it may also hinder its ability to clear HPV. After childbirth, tissue repair processes in the cervix may create opportunities for abnormal cell growth.

However, this does not mean pregnancy causes cancer—only that it may compound other risks when combined with chronic HPV infection.

Previous Precancerous Lesions or Conditions

Women with a history of cervical dysplasia (precancerous changes) or human immunodeficiency virus (HIV) infection have a higher risk of recurrence or progression. That’s why follow-up screening is crucial after treatment for abnormal Pap results.

Medical history, including prior cancers, should also be discussed with healthcare providers, as it can influence ongoing monitoring and prevention plans.

Can Cervical Cancer Be Prevented?

Yes—most cases are preventable. Prevention strategies focus on reducing HPV exposure, improving immunity, and regular screening. Key preventive measures include:

  • HPV vaccination: Highly effective against high-risk HPV types 16 and 18.

  • Routine Pap and HPV tests: Detect early cell changes before cancer develops.

  • Safe sex practices: Condom use and limiting sexual partners lower exposure.

  • Quit smoking: Reduces immune suppression and DNA damage.

  • Healthy diet and exercise: Support immune function and hormone balance.

Public education, access to vaccination, and awareness about screening remain the cornerstones of cervical cancer prevention worldwide.

Key Takeaways

  • Persistent infection with high-risk HPV is the primary cause of cervical cancer.

  • Risk is increased by smoking, immunosuppression, poor nutrition, and reproductive factors.

  • HPV vaccination and regular screening are the most effective prevention tools.

  • Lifestyle modifications—such as quitting smoking and improving diet—also play a vital role.

  • Early detection and prompt treatment can prevent nearly all cases from progressing to invasive cancer.