Evidence map›Paper›PMID 40258896›Full record

ArticleScientific reports2025

Lineage analysis of human papillomavirus types 33 and 35 based on E6 gene in cervical samples from Tehran, Iran.

Mohammad Shabanpour, Sima Taherkhani, Zabihollah Shoja, Mahtab Eftekhari, Somayeh Jalilvand

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Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Mohammad ShabanpourDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, 14155, Iran.
Sima TaherkhaniDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, 14155, Iran.
Zabihollah ShojaDepartment of Virology, Pasteur Institute of Iran, Tehran, Iran.
Mahtab EftekhariDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, 14155, Iran.
Somayeh JalilvandDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, 14155, Iran. sjalilvand@tums.ac.ir.

Funding

Tehran University of Medical Sciences and Health Services 68275 and 71552
6 · The paper itself

Abstract

Knowing the geographical distribution of lineages and sublineages of each HPV type is beneficial for the epidemiological and evolutionary studies of this virus. However, no studies have analyzed the variants of HPV 33 and 35 in Iranian women. To investigate the sequence variation of HPV 33 and 35 E6 gene, 42 and 92 samples were analyzed using nested PCR and sequencing, respectively. Sublineage analysis of HPV 33 showed that most of the samples belonged to the A2 sublineage (85.8%) and the remaining were classified to the A1 sublineage. Four mutations at positions A132C, A213C, A364C, and A480T were detected, among which two mutations A213C and A364C led to amino acid changes corresponding to positions K35N and N86H of amino acid, respectively, in 85.8% of samples. For HPV 35, two sublineages A1 and A2 were found in studied samples with a prevalence of 84.8 and 15.2%, respectively. Seven nucleotide changes were observed at positions of C127G/T, A130C, A131C, C136T, G249T, A326G, and C341T. Three of these mutations including A130C, G249T, and C341T resulted in amino acid changes at positions of E7D, C47F, and R78W in 4.4%, 3.3%, and 9.8% of samples, respectively. Concerning HPV 33 or 35 distinct lineages by histology/cytology status, no statistically significant differences were observed. Our results indicated that sublineages A2 of HPV 33 and A1 of HPV 35 were dominant in Tehran, Iran. However, more studies with larger sample sizes from different histopathological stages of cervix in various geographical regions of Iran are necessary to evaluate the pathogenicity risk of HPV 33 and 35 (sub)lineages in Iranian women with cervical cancer in the future.

Indexed as

Cervix UteriOncogene Proteins, ViralPapillomaviridaePapillomavirus InfectionsAdultFemaleHuman Papillomavirus VirusesHumansIranMiddle AgedMutationPhylogenyUterine Cervical NeoplasmsYoung AdultOncogene Proteins, ViralAnd cervical cancerHPV 33HPV 35Human papillomavirusLineageSublineage

Identifiers

PMID40258896
PMCPMC12012065

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