American Association for Cancer Research
201783_2_supp_5088772_pgq57l.doc (202 kB)

Supplementary Data from Interaction Between Susceptibility Loci in MAVS and TRAF3 Genes, and High-risk HPV Infection on the Risk of Cervical Precancerous Lesions in Chinese Population

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journal contribution
posted on 2023-04-03, 22:07 authored by Di Xiao, Dandan Liu, Zihao Wen, Xiuxia Huang, Chengli Zeng, Zixing Zhou, Yajing Han, Xiaohong Ye, Jing Wu, Yao Wang, Congcong Guo, Meiling Ou, Shiqi Huang, Chuican Huang, Xiangcai Wei, Guang Yang, Chunxia Jing

Table S1. The distribution of demographic characteristics. Table S2. Primer sequences and amplified length of 8 SNPs in MAVS and TRAF3 gene. Table S3. Distribution of SNPs in MAVS and TRAF3 genes. Table S4. The haplotype frequencies of MAVS and TRAF3 polymorphisms and cervical precancerous lesions. Figure S1. AIC values of five genetic models in relating each SNP loci to the SIL cases and control groups.


National Natural Science Foundation of China

Guangdong Natural Science Foundation

Guangdong Province Medical Research Foundation

Project from Jinan University



Persistent high-risk HPV infection is considered as a major cause of cervical cancer. Nevertheless, only some infected individuals actually develop cervical cancer. The RIG-I pathway in innate immunity plays an important role in antivirus response. Here, we hypothesized that altered function of mitochondrial antiviral signaling protein (MAVS) and mitochondrial TNF receptor–associated factor 3(TRAF3), key molecules downstream of the viral sensors RIG-I, may impair their ability of clearing HPV and thereby influence the risk for cervical precancerous lesions. To investigate the effects of MAVS and TRAF3 polymorphisms on susceptibility to cervical precancerous lesions, 8 SNPs were analyzed in 164 cervical precancerous lesion cases and 428 controls. Gene–environment interactions were also calculated. We found that CA genotype of rs6052130 in MAVS gene were at 1.48 times higher risk of developing cervical precancerous lesion than individuals with CC genotype (CA vs. CC: ORadjusted = 1.48, 95% CI, 1.02–2.16). In addition, a significant synergetic interaction between high-risk HPV infection and rs6052130 was found on an additive scale. A significantly decreased risk of cervical precancerous lesions for the TC genotype of rs12435483 in the TRAF3 gene (ORadjusted = 0.67, 95% CI, 0.45–0.98) was also found. Moreover, MDR analysis identified a significant three-locus interaction model, involving high-risk HPV infection, TRAF3 rs12435483 and number of full-term pregnancies. Our results indicate that the MAVS rs6052130 and TRAF3 rs12435483 confer genetic susceptibility to cervical precancerous lesions. Moreover, MAVS rs6052130–mutant individuals have an increased vulnerability to high-risk HPV-induced cervical precancerous lesions.