Virology journal · 2026
Genetic variation of human papillomavirus type 39 E6 and E7 genes in central China.
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Qin Keying, Yang Yang, Lin Zicong, Wu Yangying, Luo Ping, Gao Xiaoru, Mei Bing
Аннотация
BACKGROUND: Persistent infection with high-risk human papillomavirus (HR-HPV) is a key driver of cervical carcinogenesis. Human papillomavirus type 39 (HPV-39) infection is relatively prevalent in central China. However, data regarding the genetic variability of HPV-39 in this region remain limited.
METHODS: To characterize the genetic variation of the HPV-39 E6 and E7 genes in central China, samples with single type HPV-39 infection were identified by HPV genotyping prior to amplification. The E6 and E7 genes were amplified by polymerase chain reaction (PCR), followed by Sanger sequencing. The obtained sequences were subjected to variation, phylogenetic, selective pressure, and T-cell epitope analyses.
RESULTS: A total of 33 single nucleotide variants were identified in the E6 and E7 sequences, including 13 synonymous mutations and 20 non-synonymous mutations. Among which, six were novel non-synonymous mutations. Phylogenetic analysis based on HPV-39 E6 and E7 sequences demonstrated that most sequences (56/71) showed sequence similarity to lineage A. No positively selected site was detected in HPV-39 E6 or E7 genes. The predicted T-cell epitopes in the E6 sequence were influenced by non-conservative substitutions at positions H5Y, P7S, T19R, Q26H, E46D, A87G, L102S, and L151P; whereas those in the E7 sequence were affected by substitutions at positions L8V, D14H, D14E, H50Q, D57E, R87Q, Q88E, Q88D, L89V, Q91K, and F93C. A predicted candidate T-cell epitope spanning residues 70-78 (KFYAKIREL), restricted by HLA-C*06:02, was identified within the HPV-39 E6 sequence.
CONCLUSION: This study describes the genetic variations of HPV-39 E6 and E7 genes in central China and provides regional molecular epidemiological data on HPV-39 sequence diversity. The identified sequence variations may be useful for future studies investigating HPV-39 evolution and host immune interactions.
METHODS: To characterize the genetic variation of the HPV-39 E6 and E7 genes in central China, samples with single type HPV-39 infection were identified by HPV genotyping prior to amplification. The E6 and E7 genes were amplified by polymerase chain reaction (PCR), followed by Sanger sequencing. The obtained sequences were subjected to variation, phylogenetic, selective pressure, and T-cell epitope analyses.
RESULTS: A total of 33 single nucleotide variants were identified in the E6 and E7 sequences, including 13 synonymous mutations and 20 non-synonymous mutations. Among which, six were novel non-synonymous mutations. Phylogenetic analysis based on HPV-39 E6 and E7 sequences demonstrated that most sequences (56/71) showed sequence similarity to lineage A. No positively selected site was detected in HPV-39 E6 or E7 genes. The predicted T-cell epitopes in the E6 sequence were influenced by non-conservative substitutions at positions H5Y, P7S, T19R, Q26H, E46D, A87G, L102S, and L151P; whereas those in the E7 sequence were affected by substitutions at positions L8V, D14H, D14E, H50Q, D57E, R87Q, Q88E, Q88D, L89V, Q91K, and F93C. A predicted candidate T-cell epitope spanning residues 70-78 (KFYAKIREL), restricted by HLA-C*06:02, was identified within the HPV-39 E6 sequence.
CONCLUSION: This study describes the genetic variations of HPV-39 E6 and E7 genes in central China and provides regional molecular epidemiological data on HPV-39 sequence diversity. The identified sequence variations may be useful for future studies investigating HPV-39 evolution and host immune interactions.