Can an STD Cause Cancer? Which Ones Increase Cancer Risk?

Several sexually transmitted infections are established causes of cancer, and together they account for a staggering share of the global cancer burden. A 2024 worldwide analysis estimated that about 2.3 million new cancer cases that year were attributable to infections, representing roughly one in eight of all cancers diagnosed globally.¹ The link between STDs and cancer goes well beyond human papillomavirus, though HPV is the most widely recognized culprit. Hepatitis B, hepatitis C, HIV, human herpesvirus 8, and HTLV-1 all raise cancer risk through distinct biological routes, and emerging evidence points to bacterial and parasitic STDs playing supporting roles as well.

How Big Is the Problem Worldwide

The infections most responsible for cancer cases globally follow a clear hierarchy. Helicobacter pylori (a stomach bacterium, not an STD) and HPV each drive roughly 750,000 or more new cancer cases a year. After those two, hepatitis B accounts for about 360,000 cancers, Epstein-Barr virus for around 260,000, hepatitis C for roughly 160,000, and Kaposi sarcoma herpesvirus for about 35,000.¹ HIV itself contributes an additional estimated 81,300 cancer cases per year, largely through cervical cancer, Kaposi sarcoma, and non-Hodgkin lymphoma.² Those numbers make infectious causes of cancer a far larger problem than most people realize, and the majority of the relevant infections spread through sexual contact or blood-to-blood exposure.

Human Papillomavirus and Cancer

HPV is the sexually transmitted infection most strongly tied to cancer. It is considered a necessary cause of cervical cancer, meaning the disease essentially does not develop without it. But cervical cancer is only part of the story. HPV is also linked to roughly 90% or more of anal cancers, about a third to two-fifths of penile cancers, around 40–50% of vulvar cancers, and a significant share of oropharyngeal (throat) cancers, where the fraction attributed to HPV varies widely in different studies.³ The virus has also been linked to vaginal cancer.⁴

What makes HPV dangerous at a cellular level is a pair of viral proteins called E6 and E7. When high-risk strains of HPV persist in tissue, those proteins interfere with two of the body’s most important tumor-suppressing systems. E6 promotes the destruction of p53, a protein that normally halts cell division when DNA damage is detected. E7 disables the retinoblastoma protein (pRb), which acts as a brake on cell growth.⁵ With both brakes knocked out, infected cells can keep dividing even when they accumulate genetic errors, and over years that unchecked growth can become cancer.

In most HPV-related cervical cancers, the viral DNA has actually integrated itself into the host cell’s chromosomes. Analysis of cervical cancer genomes shows that HPV integration occurs in more than 80% of HPV-positive cases. The integration rate differs by HPV type: about three-quarters of HPV16-positive tumors have integrated viral DNA, while all HPV18-positive tumors show integration.⁶ Once integrated, the virus’s E6 and E7 genes can be expressed continuously, driving cells further toward malignancy.⁷

Hepatitis B and Hepatitis C

Both hepatitis B virus (HBV) and hepatitis C virus (HCV) primarily threaten the liver. Each can become chronic, and chronic infection sets the stage for cirrhosis and, ultimately, hepatocellular carcinoma, the most common form of liver cancer. Globally, HCV is estimated to account for about a quarter of all cirrhosis cases and a similar share of liver cancer.⁸

The age at which someone catches HBV makes a dramatic difference in cancer risk. The virus is extremely efficient at establishing chronic infection in babies and young children: infection around birth leads to chronic carriage in over 90% of cases. Adults who contract HBV sexually or through blood exposure, by contrast, clear the virus on their own more than 95% of the time, with only about 1–5% developing a chronic infection.⁹ That distinction matters for understanding who is most at risk: the heaviest liver-cancer burden from HBV falls on people infected in infancy in high-prevalence regions, not on adults who acquire the virus later in life.

HCV spreads most efficiently through blood contact (shared needles, transfusions before screening was routine) and less efficiently through sex, but sexual transmission does occur. Unlike HBV, there is no vaccine for HCV. The good news is that HCV is now curable in most people with direct-acting antiviral drugs, and clearing the virus reduces, though does not eliminate, subsequent liver cancer risk.

HIV and the Shifting Cancer Landscape

HIV does not directly transform cells the way HPV does. Instead, it raises cancer risk primarily by weakening the immune system, which normally keeps other cancer-causing viruses in check and eliminates abnormal cells before they become tumors. Three cancers are so tightly linked to advanced HIV that they are classified as “AIDS-defining”: Kaposi sarcoma, non-Hodgkin lymphoma, and cervical cancer. But as people with HIV live longer on effective antiretroviral therapy, a new pattern has emerged. Non-AIDS-defining cancers now make up the majority of cancers diagnosed in this population, with rising rates of Hodgkin lymphoma, liver cancer, and head and neck cancers.¹⁰

The relationship between immune suppression and cancer risk is dose-dependent. People with HIV whose CD4 counts drop below 200 have far higher cancer rates than those who maintain higher counts. For anal cancer, the risk compared to HIV-negative people was about 34 times higher even when CD4 counts remained above 500, and jumped to over 90 times higher when counts fell below 200. Hodgkin lymphoma followed a similar pattern.¹¹ Even among people on antiretroviral therapy, the overall rate of non-AIDS-defining cancers remains roughly double what would be expected in the general population.¹²

Some research suggests that beyond CD4 count alone, the ratio of CD4 to CD8 immune cells is an independent predictor of non-AIDS cancers. People on antiretroviral therapy whose ratio stayed below 0.5 had roughly double the risk of developing such cancers compared to those with higher ratios.¹³ This raises the possibility that lingering immune dysfunction, even when CD4 counts look respectable, continues to fuel cancer risk.

How HIV Amplifies HPV’s Damage

HIV and HPV interact in ways that go beyond simple immune suppression. The HIV Tat protein can directly boost the activity of HPV’s cancer-driving genes. Tat binds to regulatory regions in the HPV genome and increases the production of E6 and E7, the same viral proteins that disable the body’s tumor-suppression machinery. In effect, HIV infection turns up the volume on HPV’s cancer-causing signals, accelerating the breakdown of p53 and pRb and pushing cells more rapidly toward malignancy.¹⁴ This helps explain why cervical cancer progresses faster and is diagnosed at later stages in women living with HIV.

Co-infection with other STDs can compound the problem further. Evidence from studies of women with multiple simultaneous infections shows that STI co-infections may help HPV persist by suppressing local immune defenses, disrupting the cervical mucosal barrier, fueling chronic inflammation, and reducing the body’s ability to clear the virus.¹⁵

Kaposi Sarcoma Herpesvirus

Human herpesvirus 8 (HHV-8), also called Kaposi sarcoma-associated herpesvirus, is the direct cause of Kaposi sarcoma, a cancer that forms in the lining of blood and lymph vessels and often appears as purplish lesions on the skin. The virus spreads primarily through sexual contact between men, though it also circulates in certain regions of sub-Saharan Africa through non-sexual routes. In one long-running study, among men co-infected with both HIV and HHV-8, the ten-year probability of developing Kaposi sarcoma was close to 50%.¹⁶ Seropositivity for HHV-8 was strongly correlated with the number of male sexual partners and a history of other STDs, reinforcing its sexual transmission route. Antiretroviral therapy has reduced the rate of Kaposi sarcoma in people with HIV, but the cancer has not disappeared, and it remains the most common cancer in several African countries.

HTLV-1 and Adult T-Cell Leukemia

Human T-lymphotropic virus type 1 (HTLV-1) is less widely discussed than HPV or hepatitis, but it causes a rare and aggressive cancer called adult T-cell leukemia/lymphoma. HTLV-1 spreads through sexual contact, blood transfusions, shared needles, and breastfeeding. Sexual transmission is relatively inefficient: one prospective study found a rate of about 0.9 transmissions per 100 person-years for HTLV-1 among discordant couples.¹⁷ Most people who carry the virus never develop leukemia, but for the roughly 5% who do, the prognosis is poor. HTLV-1 is endemic in parts of Japan, the Caribbean, Central Africa, and South America, yet it remains underdiagnosed because routine screening is uncommon outside of blood-donation settings.

Epstein-Barr Virus

Epstein-Barr virus (EBV) infects the vast majority of the world’s population, usually during childhood or adolescence (it is the virus behind most cases of mononucleosis). While EBV is not typically classified as a traditional STD, it spreads through saliva and intimate contact and is worth noting because of its broad cancer implications. A large prospective study of nearly 74,000 adults in Southern China found that people with antibodies indicating active EBV replication had markedly higher risks of several cancers. The strongest association was with nasopharyngeal carcinoma, where seropositive individuals faced a risk roughly 26 times that of seronegative individuals. Elevated risks also appeared for lymphoma (about three times higher), lung cancer, and liver cancer.¹⁸ EBV is also implicated in certain forms of gastric cancer and Burkitt lymphoma. The global incidence analysis cited above attributed around 260,000 cancers per year to EBV.¹

Bacterial STDs and Emerging Cancer Links

The bacterial STDs do not cause cancer as directly as viral STDs do, but growing evidence suggests they may raise risk through chronic inflammation and tissue damage. The clearest example involves Chlamydia trachomatis and ovarian cancer. A systematic review and meta-analysis found that chlamydia infection increased the overall risk of ovarian cancer by about 34%.¹⁹ Two population-based studies looking at antibodies against a key chlamydia protein found even stronger associations: when antibody levels were high, the risk of ovarian cancer roughly doubled compared to women without chlamydia exposure.²⁰ A large European cohort study found similar patterns, with chlamydia seropositivity linked to elevated risk of the serous and mucinous subtypes of ovarian cancer specifically.²¹

The proposed mechanism is pelvic inflammatory disease (PID). Chlamydia frequently causes PID, which produces chronic inflammation in the reproductive tract. That persistent inflammatory environment may damage DNA in ovarian tissue and create conditions favorable for tumor development. Researchers are careful to note that this remains an association rather than a confirmed causal chain, and chlamydia is treatable with antibiotics, so screening and early treatment could plausibly reduce this risk.

Trichomonas and Prostate Cancer

Trichomonas vaginalis, a parasitic STD, has attracted attention as a possible contributor to prostate cancer risk, though the evidence is mixed. A population-based case-control study found that exposure to T. vaginalis was associated with a roughly six-fold higher risk of prostate cancer.²² However, a separate study using a nationally representative sample found no statistically significant differences in prostate-specific antigen (PSA) levels between T. vaginalis-seropositive and seronegative men, though slightly higher PSA concentrations appeared in men with the strongest antibody responses.²³ The relationship, if it exists, likely involves chronic low-grade inflammation of the prostate rather than direct transformation of cells. More research is needed before trichomoniasis can be called a confirmed cancer risk factor, but the question is not closed.

The Vaginal Microbiome as a Modifier

An unexpected player in STD-related cancer risk is the vaginal microbiome. The composition of bacteria in the vaginal tract appears to influence whether an HPV infection clears on its own or sticks around long enough to cause precancerous changes. A systematic review and meta-analysis found that vaginal dysbiosis, a shift away from a healthy Lactobacillus-dominated environment toward a more diverse bacterial mix, was associated with a roughly 33% increase in the risk of acquiring HPV. For high-grade cervical lesions and cancer specifically, women with vaginal dysbiosis had about double the risk.²⁴

More recent research has zeroed in on specific bacterial shifts. The transition from communities dominated by Lactobacillus crispatus to dysbiotic states enriched with bacteria like Gardnerella and Sneathia appears to alter local immune function and promote epigenetic changes in both host cells and viral genomes, helping HPV evade immune detection.²⁵ Studies have also identified Prevotella bivia as enriched in women with persistent HPV, suggesting it may play a role in chronic infection.²⁶ This research is still in its early stages, but it raises the intriguing possibility that maintaining vaginal health through probiotics or other interventions could one day become part of cervical cancer prevention strategies.

Vaccines That Prevent Cancer

Two of the most cancer-relevant STDs are already preventable by vaccination. The hepatitis B vaccine has been available since 1982 and is now given routinely to newborns in most countries. In highly endemic countries like China, the prevalence of chronic HBV carriage has fallen from about 10% to 1–2% in vaccinated cohorts, and liver cancer rates in children have already dropped dramatically in places like Taiwan that adopted early universal vaccination.²⁷ The HPV vaccine, introduced more recently, has proven highly effective at preventing HPV infection, precancerous cervical lesions, and genital warts. Countries with high vaccine coverage are already seeing significant drops in the prevalence of the HPV types the vaccine targets and in rates of high-grade cervical lesions.²⁸

Both vaccines are most effective when given before exposure to the virus, which is why childhood and adolescent vaccination is the primary strategy.²⁹ The quadrivalent and nine-valent HPV vaccines also prevent precancerous anal lesions in men, extending cancer prevention beyond cervical cancer alone. For adults who missed the vaccination window, catch-up vaccination is still recommended up to age 26 in the United States, and in some cases up to 45 after discussion with a clinician.

Socioeconomic Disparities in STD-Related Cancers

STD-related cancers do not fall evenly across populations. In the United States, lower socioeconomic status is associated with both higher rates of HPV-associated cancers and worse outcomes once diagnosed.³⁰ For head and neck cancers linked to HPV, patients living in higher-income census tracts have 12–15% higher survival rates than those in lower-income areas, partly because wealthier patients are less likely to be diagnosed at a distant stage and more likely to start treatment quickly.³¹

Stigma also acts as a barrier. Research among women living with HIV in India found that fear of discrimination and concerns about disclosing their HIV status prevented many from seeking gynecological care and cervical cancer screening.³² This is a pattern replicated in many countries: the populations at highest risk of STD-related cancers are often the same populations with the least access to screening, vaccination, and treatment. Closing those gaps through targeted vaccination programs, reducing barriers to STD testing, and integrating cancer screening into routine HIV care could prevent tens of thousands of cancer cases each year.³³

The Economic Weight of HPV-Related Disease

Beyond the human toll, HPV-related diseases carry substantial financial costs. Based on U.S. cancer registry data, roughly 34,800 new HPV-associated cancers occurred in the United States in a single year, and the overall annual direct medical costs for all HPV-related diseases were estimated at about $8 billion. The largest share of that cost, over 80%, went to routine cervical cancer screening and follow-up rather than to treating cancers or warts themselves.³⁴ That breakdown illustrates an underappreciated point: even before cancer develops, the surveillance required to catch HPV-related disease early is enormously expensive. Widespread vaccination, by reducing the pool of people who need intensive screening, could ultimately save billions in healthcare costs on top of the lives saved.