• HPV and cervical cancer
  • Fateme Shafikhani,1 Saman Hakimian,2,*
    1. Bachelor student of microbiology , Islamic Azad University of Shiraz , IR.IRAN
    2. M.sc student of Pathogenic Microbes Islamic Azad University Central Tehran Branch


  • Introduction: HPV is the most common sexually transmitted infection worldwide. The majority of sexually active people will contract HPV during their lifetime (approximately 75–80%). While most HPV infections (70–90%) are asymptomatic and will resolve on their own within 1–2 years, persistent infection (or multiple reinfections) can cause morbidity and mortality. There are around 200 different genotypes of HPV, of which more than 20 are known or probable carcinogens. Oncogenic strains of HPV (predominantly HPV 16/18, so-called “high-risk” strains) cause almost all cervical cancers.HPV also causes oropharyngeal (mouth, throat, tongue, and tonsils), vaginal,vulvar, penile, and anal cancers. Research suggests that HPV is also associated with sinonasal, conjunctiva, and lacrimal sac cancer. A rare but serious consequence of HPV infection is recurrent respiratory papillomatosis, whereby HPV infection can be transmitted by maternal HPV infection as well as individual sexual behaviours. HPV infection has also been associated with a higher risk of HIV acquisition. In addition, two strains of HPV (HPV 6/11, i.e., so-called “low risk” strains) are responsible for 96–100% of anogenital warts. While not deadly, anogenital warts can impact one’s quality of life and accrue substantial financial costs to health care systems.
  • Methods: HPV was the first virus that was recognized as the cause of cervical cancer and is widely distributed in mammals and about 40 of its genotypes can cause the infection of the mucous and skin epithelial cells of the anogenital area and other areas. In addition, endogenous hormonal factors have a relatively small effect on the growth of cervical and vaginal cancer and are one of the effective endogenous factors in the composition of vaginal microbiota. Because some of these microorganisms inhibit the growth of bacteria and viruses by producing bacteriocins and biosurfactants and regulate vaginal homeostasis. On the contrary, some of them produce substances that endanger the integrity of the vaginal epithelium and multiply pathogenic infections.
  • Results: Therefore, microbiota It is the first line of defense against infections. Also, according to scientific data, in female patients over 40 years of age, it is possible that persistent high-risk HPV infections play an important role in the risk of cervical cancer due to the reduction of estrogen and progesterone hormones.and an average adult has an 80% risk of contracting the HPV infection by the age of fifty. Every year, 570,000 cases among females and 60,000 cases among males can be attributed to HPV infection among cancer cases. This uncoated virus is one of the DNA viruses whose genome contains double-stranded DNA. Another structure of this virus can be mentioned its specific proteins such as E1 and E2 proteins as factors identifying the origin of replication, E4 and E5,which play a role in the life cycle of the virus, and most importantly, oncogenic proteins E6 and E7, which target cell cycle regulators, including P53 and retinoblastoma proteins. Also, L1 proteins create species diversity.
  • Conclusion: High-risk HPV viruses can integrate inside infected cells and coordinate the expression program of a gene for the transcription of its oncogenic proteins (E6 and E7) and spread cancer. Persistent infection with high-risk human papillomavirus (HPV) is the cause of most cervical cancers . Over the past deca- des, there has been significant progress in primary and second- ary prevention of cervical cancer through HPV vaccination and screening.
  • Keywords: cancer; HPV; Uterus; Human papilloma virus