Setayesh Bahramifar,1,*Hoda Sabati,2
1. Bachelor`s student ,Microbiology group,Faculty of Advanced Science and Technology,TehranMedical Science,Islamic Azad University,Tehean,Iran 2. Biotechnology and Biological Science Research Center, Faculty of Science, Shahid Chamran University of Ahvaz, Iran
Introduction: Introduction:
Human papillomavirus (HPV) is a circular, non-enveloped, double-stranded DNA virus belonging to the Papillomaviridae family. HPV infection is usually cleared naturally by the immune system. However, it can cause cancer when the immune system is weak or has a latent infection, especially genotypes 16 and 18. Types of human papillomavirus are divided into two high-risk groups based on their carcinogenicity, including strains (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, 65) and low-risk strains (6, 11, 42. 43,44) are divided. The HPV virus can remain in the skin and cause genital warts. Genital warts that appear on the genitals increase the risk of cervical cancer. Chronic infections with high-risk HPV strains like HPV-16, HPV-18, HPV-31, and HPV-33, can cause malignancy. In all papillomaviruses, a single genome encodes approximately eight open-reading frames (ORF). The ORF has three functions: early viral function (E1-E7) and late viral function (L1, L2)and long Control Region (LCR) segment. LCR genes are necessary for viral DNA replication and transcription. E6 and E7 are the two main proteins in the viral carcinogenesis pathway. L1andL2encode structural capsid proteins. HPV is usually transmitted through sexual activity through contact with infected epithelium of the cervix, vagina, vulva, penis, or anus, possibly through microscopic scratches in the mucosa or skin. Papillomaviruses infect mucosal and skin epithelial membranes and cause cell proliferation. The viral life cycle begins with the differentiation of infected epithelial cells and the infection of basal epithelial cells, possibly at the sites of injury. Where the viral genome is created, the nuclear plasmid and early genes are expressed. In immunosuppressed patients, the incidence of warts and cervical cancer is higher. Also, all cancers related to HPV are prevalent in people with HIV.
Methods: Methods:
By reviewing various data and articles published in Google Scholar, PubMed, and Scopus, based on this information, we realized that preventive vaccines could activate humoral immunity and, with the production of virus-neutralizing antibodies, inhibit viruses. Vaccines to prevent high-risk HPV infection Available in most countries, the vaccines are Gardasil and Cervarix. These vaccines use HPV L1 capsid proteins that are non-infectious, called virus-like particles(VLP).
Results: Result:
The three different approved vaccines are designed to protect against infection from various numbers of HPV types. Cervarix: It is a bivalent vaccine that Protects against HPV types 16 and 18. 4vHPV: It is a quadrivalent vaccine that Protects against HPV types 6, 11, 16, and 18. 9vHPV: It is a nine-valent vaccine that Protects against HPV types 6, 11, 16, 18, 31, 33, 45, 52, and 58. The 9vHPV vaccine is usually recommended for men and women aged 9-45 years to prevent dysplastic and diseases caused by HPV. The vaccine is injected intramuscularly. People under the age of 15 can inject two doses at an interval of 6 to 12 months or three doses at 2 and 6 months. People over 15 should inject three doses in 2 to 6 months.
Conclusion: Conclusion:
HPV is a common virus that can be transmitted from person to person, and this virus is venturesome because it is carcinogenic. Knowing how to prevent HPV infection or HPV-related cancers is essential. HPV vaccination, like most vaccinations, is an effective and safe way of preventing vaccination-specific HPV infection as well as reducing HPV-related neoplasms. As we learn more about the immunity mechanisms against HPV infection, we will have better insights and strategies for designing effective vaccines. Although somewhat difficult, every effort should be made to publicize the efficacy and safety of HPV vaccination.