Blood Type Offers No Shield Against Common Skin Warts, Study Finds

For decades, researchers have suspected that the sugars displayed on the surface of our red blood cells, the same molecular flags that define the ABO and Rh blood group systems, might quietly shape our vulnerability to infectious diseases. From norovirus outbreaks that sweep through group O populations to the COVID-19 susceptibility debates of the pandemic era, the idea that blood type could tip the scales of infection has proven remarkably persistent. Now, a retrospective case-control study from Turkey has tested that hypothesis against one of the most common viral infections of the human skin: the humble cutaneous wart. The verdict, published in the Archives of Dermatological Research, is a clear null result. Among more than 360 people analyzed, the researchers found no statistically significant relationship between a person’s ABO blood group or Rh status and their likelihood of developing viral warts caused by human papillomavirus.

The study, led by dermatologist Zekiye Kanat and colleagues at Inonu University School of Medicine in Malatya, drew on clinical records spanning nearly six years, from January 2020 to November 2025. The researchers identified 113 patients who had presented to the dermatology outpatient clinic and received a clinical diagnosis of verrucae, the medical term for the rough, raised lesions that human papillomavirus induces when it infects keratinocytes in the epidermis. As a comparison group, they assembled 250 age- and sex-matched healthy individuals. Matching by age and sex was a deliberate methodological choice, since both factors are known to influence wart prevalence, and any imbalance between the groups could have masqueraded as a blood group effect. Ethical approval for the retrospective design was granted by the Inonu University Health Sciences Research Ethics Committee in November 2025.

The numbers tell a straightforward story. In the patient group, the most common blood group was O, accounting for 44.2 percent of cases, while in the control group blood group A predominated at 45.6 percent. On its face, that difference might look intriguing, but statistical testing told a different tale. A chi-square comparison of the ABO distributions between the two groups yielded a p-value of 0.293, well above the conventional threshold of 0.05, meaning the observed variation was entirely compatible with random sampling noise. Rh status told the same story: positive and negative blood types were distributed almost identically between wart patients and controls, with a p-value of 0.534. Even age, the variable most carefully controlled in the design, showed no difference between the groups, with a p-value of 0.387 confirming the success of the matching procedure.

To go beyond simple comparisons, the team built a multiple logistic regression model, a statistical technique that estimates the independent contribution of each variable, blood group, Rh status, sex, and age, to the probability of having warts while holding the others constant. The results were striking in what they failed to find. No variable reached statistical significance. The closest contender was male sex, which carried an odds ratio of 1.573, suggesting that men in this cohort were somewhat more likely to have warts than women, but the p-value of 0.057 fell just short of the significance threshold. More telling still was the model’s explanatory power: a Nagelkerke R-squared of 0.033 means the entire set of variables explained barely three percent of the variation in wart occurrence. In practical terms, blood type and demographics were nearly useless for predicting who develops warts.

The clinical details of the cohort add texture to the statistical findings. Wart lesions were most commonly located on the hands, which accounted for 45.1 percent of cases, followed by the feet at 39.8 percent. That distribution is consistent with what dermatologists see in everyday practice and with the biology of transmission. Cutaneous warts spread through direct contact and through autoinoculation, and the hands and feet are the body surfaces most exposed to microtrauma, small breaks in the skin barrier that give papillomavirus particles access to the basal keratinocytes they must infect to establish a lesion. Swimming pools, communal showers, and occupational handling are classic routes of exposure, and the anatomic distribution of lesions in this study mirrors those routes rather than any immunogenetic pattern.

The null result matters because the hypothesis it tested was biologically plausible. ABO blood group antigens are carbohydrate structures synthesized by specific glycosyltransferase enzymes, and they are expressed not only on red blood cells but also on the surface of many epithelial and endothelial cells. Viruses, in turn, often rely on specific surface glycans as attachment factors or receptors. Norovirus strains, for example, bind histo-blood group antigens in the gut, which is why secretor status and blood group shape susceptibility to that virus. Helicobacter pylori exploits Lewis antigens, and some influenza strains show blood group-dependent binding patterns. A 2023 systematic review and meta-analysis published in BMC Infectious Diseases found associations between ABO type and the risk of several infections, and studies during the COVID-19 pandemic reported that group O individuals appeared at somewhat lower risk of SARS-CoV-2 infection, possibly because circulating anti-A and anti-B antibodies or differences in glycan expression modulate viral entry and immune recognition.

There is even a dermatological thread to this literature. Earlier studies have explored links between ABO blood groups and skin conditions ranging from lichen planus and pemphigoid to psoriasis vulgaris and acne severity, with mixed and often inconsistent results. One Turkish study published in 2019 examined blood groups and anogenital wart development, and researchers have also investigated blood type associations with nonmelanoma skin cancers. Recent work has added mechanistic depth: a 2024 study in Biology Research showed that H antigen expression, the glycan precursor shared by group O individuals, modulates the integrity and differentiation of epidermal keratinocytes, the very cells that papillomavirus infects. That finding made the wart hypothesis genuinely worth testing, since altered keratinocyte differentiation could theoretically change the permissiveness of the skin to viral replication.

Why, then, did no association emerge? The authors point toward the established drivers of wart pathogenesis, which operate on a different biological level. Immunosuppression is the single most powerful risk factor for cutaneous warts; transplant recipients on calcineurin inhibitors and people with advanced HIV infection can develop extensive, recalcitrant lesions, and immunodeficiency is associated with a dramatically elevated burden of HPV-related disease. Local trauma determines where lesions appear and whether inoculation succeeds. And above all, HPV genotype matters: more than 200 papillomavirus types have been described, and the alpha, beta, gamma, and mu genera infect different body sites with different clinical consequences. The interplay between a specific viral type and the local immune microenvironment of the skin likely dwarfs any subtle effect of red cell surface glycans. A retrospective design also has limits; blood group was extracted from existing records, wart diagnosis was clinical rather than HPV-genotype-confirmed, and a cohort of 113 cases may simply lack the statistical power to detect a small true effect, if one exists.

For the public, the takeaway is refreshingly simple. Knowing your blood type will not tell you whether you are likely to catch warts, and no blood group confers protection against them. Prevention still rests on the familiar pillars: avoiding direct contact with lesions, not picking or shaving over existing warts, keeping skin intact and moisturized in high-exposure settings, and seeking treatment early, since options from salicylic acid and cryotherapy to newer immunotherapies work best before lesions become large and established. For researchers, the study adds a well-designed negative result to a literature often criticized for chasing weak associations across dozens of diseases. Negative findings like this one help discipline the field, redirecting attention toward the factors that demonstrably drive infection, the virus itself, the state of the host immune system, and the microenvironment of the skin barrier. In the ongoing effort to map human genetic susceptibility to viral disease, the ABO and Rh systems, at least for cutaneous warts, can now be crossed off the list.

Subject of Research: The association between ABO/Rh blood groups and cutaneous viral warts caused by human papillomavirus

Article Title: The relationship between cutaneous viral warts and ABO/RH blood groups: a retrospective case-control study

Article References: Kanat, Z., Türkmen, D., Altunişik, N., Şener, S., Kayhan Teti̇k, B., & Güner, M. E. (2026). The relationship between cutaneous viral warts and ABO/RH blood groups: a retrospective case-control study. Archives of Dermatological Research, 318(1), Article 397. https://doi.org/10.1007/s00403-026-04858-3

Image Credits: AI Generated

DOI: 10.1007/s00403-026-04858-3

Keywords: viral warts, human papillomavirus, ABO blood groups, Rh factor, dermatology, case-control study, verrucae, host susceptibility, immunosuppression, skin barrier, logistic regression, blood group antigens