Discussion: K93N of HPV-33 E6, K93R of HPV-52 Discussion: The N86H, R145I of HPV-33 E6 and D86E, R145K of HPV-58 E6 occurred in the same positions; K93N of HPV-33 E6, K93R of HPV-52 E6 and K93N of HPV-58 E6 all located in the 93rd of the E6 protein; those amino acid substitutions located in protein active region, can cause the E6 terminal and the trend of the carboxyl end structure disorder.
Prevalence and distribution of human papillomavirus (HPV) in Luoyang city of Henan province during 2015-2021 and the genetic variability of HPV16 and 52.
Abstract: The K93R mutation was observed in most HPV52 E6 protein.
Result: The most prevalent non-synonymous mutations in E6 genes was A379G (14/15) and cause the amino acid to change from Lysine to arginine (K93R).
Discussion: Compared with the HPV52 reference sequence (NC 001,592), the K93R was the only one non-synonymous mutation.
Discussion: The K93R mutation was also observed in other HPV52 isolates in China.
Discussion: Though the K93R mutation did not increase the cell immortalization ability of HPV52, a higher colony formation and greater cell migration ability was observed when compared to HPV52 prototype.
Genetic variation of E6 and E7 genes of human papillomavirus 52 from Central China.
Result: A378C and A379G together led to the amino acid substitution of K93R.
Result: G108C and A379G, leading to the amino acids substitution of E3Q and K93R, respectively.
Result: Due to K93R, the score of epitopes 89-104EERVKKPLSEITIRCI and 81-96YSLYGKTLEERVKKPL changed from 0.87 to 0.90 and 0.81 to 0.84, respectively; due to E3Q, the score of epitope 3-18EDPATRPRTLHELCEV changed from 0.68 to 0.74.
Result: Due to K93R, there was a potentially affected on the epitope HLA-DPA1*02:01/DPB1*01:01.
Discussion: The two non-synonymous mutations of E6, E3Q and <
Oncogenicitiy Comparison of Human Papillomavirus Type 52 E6 Variants.
PMID: 30676312
2019
The Journal of general virology
Abstract: In the present study, we compared the oncogenicity of E6 derived from the HPV-52 prototype and three commonly found variants, V1 (K93R), V2 (E14D/V92L) and V3 (K93R/N122K), through molecular and phenotypic approaches.
Analysis of Sequence Variation and Risk Association of Human Papillomavirus 52 Variants Circulating in Korea.
Abstract: We also found that a lineage B-specific mutation K93R (A379G) was associated with an increased risk of cervical neoplasia.
Discussion: K93R (A379G) is a nonsynonymous mutation located in the E6 oncogene, which may have a specific role in carcinogenesis: it is not only the most frequently detected variation, but is also independently associated with high-grade lesions.
Discussion: Lineage B-specific mutations included the most frequently detected nonsynonymous mutation K93R (A379G) in E6, while lineage C-specific mutations included an E6 nonsynonymous mutation (L83V, concurrent
Human papillomavirus type 52 polymorphism and high-grade lesions of the uterine cervix.
PMID: 23015309
2013
International journal of cancer
Abstract: CIN2,3 risk was significantly associated with a deletion at nucleotide position 7695 in the LCR (OR 4.9, 95% CI 1.2-20.8), the T7744C variation in the LCR (OR 5.7, 95% CI 1.1-32.0), and the K93R variation in E6 (OR 6.9, 95% CI 1.3-36.8), after adjusting for age, detection of HPV16 or 18 and study site.
Genomic polymorphism of human papillomavirus type 52 in women from Northeast China.
PMID: 23203106
2012
International journal of molecular sciences
Result: Compared to the reference sequence, all the obtained sequences harbored the nucleotide variation of G350A and 65 had the nonsynonymous mutation of A379G (K93R) in the E6 gene (Table 2).
Result: The A379G (K93R) mutation was located in the strand H1 and the third predicted zinc finger of Discussion: Among the four mutations, only A379G (K93R) was nonsynonymous.
Discussion: In accordance with Xin's report, the unique A379G (K93R) variation was located in the strand H1 and the third predicted zinc finger of E6 protein and occurred in almost all of the HPV 52 positive samples.
HPV mutation literature information.
PMID: 
2022
Virology journal
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