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Abstract
Intratypic variations of HPV-18 are known to differ in the persistence of the infection, frequency of carcinogenesis and the progression of precursor lesions to advanced cervical cancer. This study was designed to analyze sequence variations of HPV-18 isolates in order to discover novel HPV-18 variants and to evaluate the variations among infected women in southwest China. Cervical biopsies from 56 HPV-18-positive women with cervical neoplasia were assayed by PCR amplification and sequencing of all eight genes (E1, E2, E4, E5, E6, E7, L1, L2) of the HPV-18 genome. The most frequently observed variation was a C to G transversion at nucleotide 287 of E6, which was found in 48.2% of samples. Analysis of E7 revealed only one specimen as having sequence variations. In addition, we have identified several novel variations: A551C in E6, G6906A in L1, and C4915T and C5147A in L2. The mutations in E6 and L2 are silent, while the E7 mutation results in a single amino acid change. This study complements and expands on previous descriptions of HPV-18 variants. The sequence variation data presented here provides a foundation for future research on HPV-induced oncogenesis and may prove valuable for developing diagnostic probes and in the design of HPV vaccines for targeted populations.
Highlights
Cervical cancer is the second leading cause of cancer-related deaths in women worldwide [1]
The present study examined a collection of 56 different isolates of human papillomavirus (HPV)-18 from cervical cancer patients in the southwest China and analyzed the sequence variations in the E1, E2, E4, E5, E6, E7, L1 and L2 viral genes
3.1 HPV-18 E1 Sequence Variations As shown in Fig. 1A, DNA sequence analysis of the HPV-18 E1 region revealed the following four variations: a T to G transversion at nt2856 and a G to C transversion at nt2857 leading to a L648C amino acid (AA) substitution (n = 18, 32.1%), and a C to G transversion at nt2858 and a G to T transversion at nt2859 leading to a R649V AA change (n = 18, 32.1%)
Summary
Cervical cancer is the second leading cause of cancer-related deaths in women worldwide [1]. Most cervical cancers are caused by human papillomavirus (HPV) infection [1]. Isolates with a L1 sequence more than 10% different than the nearest HPV type are a distinct ‘‘type’’, while isolates with differences of less than 2% are termed ‘‘variants.’’ There are 120 different HPV types identified to date [6,7], of which 15 have been termed ‘‘high-risk’’ types due to their significant association with cervical cancers [8]. There are 25 HPV types with strong, sufficient, or limited evidence of causing cervical cancer [9]. The HPV-16 was the most oncogenic HPV type, known to cause cancer at 7 sites. HPV-16 and HPV-18 represent the most commonly identified high-risk HPV genotypes, which cause 40– 60% and 10–20%, respectively, of all cervical cancers [11,12]
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