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Characterization of human papillomavirus genotypes and their coverage in vaccine delivered to Ethiopian women – Scientific Reports

The results of this study revealed that 139 (46.8%) of the study participants had an overall prevalence of HPV. This finding was in line with the results of another Ethiopian study that found 53.0% of women with cervical abnormalities being infected with HPV13. This finding is also consistent with research conducted in South Africa, where the total prevalence of HR-HPV DNA was 48.1%14, and Europe, where the study population’s overall HPV prevalence was reported to be 50.8%15.

Our finding indicated overall, there were 56 (18.85%) study participants with CIN II+ (classified as diseased) with pathology examination. Of CIN II+, 54/56 (96.43%) had HPV infection whereas two out of fifty six (3.57%) did not have HPV infection. The prevalence of HPV among women with CIN II+ was higher compared to women with CIN II. This finding is similar with another study conducted in South Africa which detected HPV infection in 84.2% (383/455) of women16.

This result is also in line with a Chinese study that found women with abnormal cervical lesions and cervical cancer as having high HPV prevalence compared to women with normal cervical histology 10.5% for the Negative for Intraepithelial Lesion or Malignancy (NILM), 73.9% for CIN1, 89.5% for CIN2, and 91.5% for ≥ CIN317. The study conducted in India also reported the prevalence of high risk HPV infection to be 93.3% in participants with invasive cervical cancer and 46.1% in those with precancerous lesions, indicating that HPV is a significant risk factor for cervical cancer18.

In our study, HPV-16 genotype, which was detected in 43 cases (14.48%), was the most common genotype. Its frequency rises as cervical cancer becomes more severe. The second most common genotype was HPV-58, which accounted for 21 (7.07%). HPV-18, -35, and -52 were the next in descending order accounting for 17 (5.72%), 14 (4.71%), and 12 (4.04%), respectively. This result has similar finding with study done in Ethiopia, which found that HPV-16 (37.3%), HPV-52 (6.8%), HPV-35 (4.8%), HPV-18 (4.4%), and HPV-56 (3.9%) were the most frequently detected genotypes19.

HPV-16 is the most prevalent genotype that is regularly mentioned as a major contributor to cervical abnormalities worldwide A systematic review study indicated that the pooled prevalence of the five most prevalent high-risk HPV types in Africa were HPV-16 (35.3%), HPV-52 (14.2%), HPV-35 (12.4%), HPV-18 (10.4%), and HPV-58 (10.0%)20. A different result is observed from a study done in Togo which reported HPV-16 as the least common genotype even though HPV-16 is the most frequent genotype in the world, according to this study the most prevalent genotypes were HPV-56 (22.7%), followed by HPV-51 (20.3%), HPV-31 (19.5%), HPV-52 (18.8%) and HPV-35 (17.2%)21.

The distribution of HPV genotypes is different in different parts of the world and among different studies22,23,24,25,26,27,28. The heterogeneity observed in the HPV genotype distribution among the studies could be attributed to variations in the spread of the HPV virus, sociodemographic composition of the study population, the degree of cervical lesions, and the diagnostic techniques used when examining women with abnormalities.

In the present study, the most common HPV type in patients with CIN II+ was HPV-16 which accounts 26 (46.4%), followed by HPV-53, HPV-58, HPV-18, HPV-52, and HPV-35 infections, accounting for 9 (16.1%), 9 (16.1%), 7 (12.5%), and 6 (10.7%) respectively. Infection by a specific type of HPV significantly increases the chance of developing cervical abnormalities. The risk that an HPV infection will progress to cervical cancer varies according to the HPV genotype. Among patients with CIN II, HPV-16 was the most common type, followed by HPV-58, HPV-53, HPV-18, and HPV-35. HPV-16 was associated with the highest risk of CIN II+, (AOR = 15.42; 95% CI 6.81–34.91). In addition, HPV-52, -18, -53, and -58, in descending order, were significantly associated with an increased risk of CIN II+, (AOR = 7.38 (1.73–31.54), 5.42 (1.61–18.31), 4.08 (1.53–10.87), and 3.17 (1.00–10.03)) respectively.

Our results are supported by a Korean study, which showed that HPV-16 was linked to the highest risk of high grade squamous intraepithelial lesion and carcinoma (OR = 11.75; 95% CI 8.55–16.15). Furthermore, there was a significant correlation between an elevated risk of HSIL+ and HPV-33, -31, -52, -18, -58, -51, and -35 (OR ranging from 3.50 [HPV-33] to 2.62 [HPV-35])6. A study conducted in China which supports our finding reported HPV-16, -31, -33 and -58 were found to have considerably greater infection rates in patients with HSIL and higher lesions29.

The most significant approach both to prevent and eradicate cervical cancer is vaccination. The U.S. Food and Drug Administration (FDA) has approved three HPV vaccines: the bivalent HPV vaccine (Cervarix, 2vHPV), the quadrivalent HPV vaccine (Gardasil, 4vHPV), and the nonavalent HPV vaccine (Gardasil 9, 9vHPV). Ethiopia launched the quadrivalent vaccination for the first time in December 2018 targeting 14-year-old girls, with the support of the Global Alliance for Vaccine and Immunization (GAVI)30. The results of our study showed that 25% of the genotypes were covered by the bivalent vaccine (HPV-16/18). The quadrivalent (HPV-6, -11, -16, and -18) vaccination had a coverage rate of 27.1% and the nonavalent vaccine had a coverage rate of 45%. In line with our findings, a systematic review conducted among women in West Africa, found that 15.1% of the genotypes identified were covered by the bivalent vaccine (HPV-16/18). Furthermore, the nonavalent vaccine’s additional high-risk carcinogenic HPVs (HPV-31/33/45/52/58) showed a prevalence of 37.6%. Thus, the nonavalent vaccine had a coverage rate of 55.8%. The prevalence of the HPV-35/39/51/56/59/66/68 genotypes, which are not protected by a vaccine, was 44.2%30.

The findings of the current study was also similar with a study conducted in Korea, which found that 12.0% of HPV-positive patients had HPV-16 and -18, which are protected against by all HPV vaccines. HPV-31, -33, -45, -52, and -58, which are covered by the 9-valent vaccine, accounted for 19.8% of HPV-positive patients. The remaining HR types (31.7%) among HPV-positive individuals were HPV-35, -39, -51, -56, -59, -66, and -686. The 9-valent vaccine may have a significant impact on the prevention of cervical cancer in Ethiopia; nevertheless, for Ethiopian women, a polyvalent vaccine that protects against more prevalent genotypes (HPV-16/18/35/52/58/53) that cause cervical cancer is necessary.

In our study, the proportion of HPV genotypes non-covered by the existing vaccine was 132/240 (55%). This finding was consistent with a study conducted in Ethiopia that reported the prevalence of non‑vaccine‑targeted HPV was 56 (51.8%, 95% CI 0.42, 0.61)31.