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Human pappilomavirusus (HPV) infection is an sexual transmitted disease, which can lead to cervical cancer in women (Koutsky et al., 2002). Most infected persons with HPV will not have any symptoms and eliminate the virus on their own. Infection with HPV is very common, in the United States 20 million women are currently infected with HPV and every year 6,2 million new cases are diagnosed. Sexual active person have even 75 to 80 percent change to get a HPV infection at some point in their life (Weaver, 2006).
There are nearly 100 types of HPV identified, 40 types can infect the genital mucosa through sexual transmission and 16 types are highly carcinogenic (Pagliusi and Teresa Aguado, 2004). Cervical cancer is mostly related to the HPV type 16 and 18, which are together responsible for 70 percent of the cervical cancers. In 60 percent of the cervical cancers the person is infected with HPV type 16 and in 10 percent of the cases HPV type 18 is responsible for the cancer. Other HPV types that play a important role in developing cervical cancer are HPV types 31, 33, 35, 45, 52 and 58, which are together responsible for another 18 percent (Pagliusi and Teresa Aguado, 2004).
Cervical cancer is after breast cancer, the second common cancer of women worldwide (Pagliusi and Teresa Aguado, 2004). There are 470 000 new cases and 230 000 deaths every year as the result of cervical cancer worldwide (Harper et al., 2004). HPV infects keratinocytes at the basal epithelial layer of the squamous epithelium through micro-abrasions in the skin or mucosa. (Carrillo-Infante et al., 2007). It integrates randomly into the host genome and encodes for both non-structural viral regulatory proteins (E1, E2, E4, E5, E6 and E7) from the early region of the viral genome and structural viral capsid proteins (L1 and L2) from the late region. The DNA integration leads to a deletion of the E2 region, resulting in activation of the E6 and E7 promoter. After viral DNA replication, in which 50 to 100 copies of the virus are produced, only the genes in the early region are transcribed. E6 inactivates the tumor suppressors p53 and retinoblastoma suppressor protein (Rb), leading to a increased cell growth and the inability of apoptosis, which causes an accumulation of mutations (Carrillo-Infante et al., 2007). The enhance cell growth and the absent of apoptosis can lead to histological changes of the cervical squamous epithelium. Cervical intraepithelialneoplasia (CIN) is a histologic abnormality of the cervicalsquamous epithelium andis assumed to be a precursor of cervical cancer.CIN is classified into three grades. The CIN grade 1 (CIN1) is amild dysplasia with abnormal cells in the lowest layers of the cervical epithelium and is the most benign grade of the three grades. In 70 to 90 percent of a CIN 1 stage, the lesions regressed spontaneously. In CIN grade 2 (CIN2) the dysplasia is moderate with abnormal cells present in the lower two thirds of the epithelial layer. A CIN 2 stage leads in 57 percent of the cases to invasive cancer. CIN grade 3(CIN3) is characterized by a severe dysplasia, with abnormal cells in the total layer, or nearly in the total layer, of the cervicalepithelium. 70 Percent of the persons with a CIN 3 stage develop invasive cancer (Kahn, 2009).
Nowadays there is al lot of interest in protecting women against cervical cancer using a HPV vaccine. Many countries have already started a HPV vaccination campaign. The HPV vaccine which is used against the most common HPV types 16 and 18 is based on L1 virus-like particles and have shown promising results in protecting against HPV 16/18 infection and the development of lesions after HPV infection. Many studies showed a positive effect, especially if vaccination occurs at a young age, on the prevention against cervical cancer. Harper et al. showed a vaccine efficacy of 91,6 percent against incident infection and 100 percent against persistent infection with HPV type 16 and type 18. In the intention-to-treat analyses, vaccine efficacy was 95,1 percent against persistent cervical infection with HPV 16/18 and 92,9 percent against cytological abnormalities associated with HPV 16/18 infection (Harper et al., 2004). Another study showed a vaccine efficacy of 90,4 percent against CIN2+ containing HPV 16/18 DNA (Paavonen et al., 2007). Both Harper and Paavonen showed the HPV 16/18 vaccine is safe. A study of Harper et al., which is published 2 years later, also tested the efficacy and safety of the vaccine, at this time for a period of 4,5 years. This study suggest the vaccine is effective and safe using for a longer period, at least for 4,5 years (Harper et al., 2006).
The last published article of Paavonen et al. also showed, according to many studies, a preventing effect of the HPV16/18 vaccine against cervical cancer. Paavonen et al. investigate the efficacy of the vaccine in both young women (15-25 years) with evidence of current or previous HPV infection and young women with no evidence of current or pervious HPV infection. Participants were from 14 different countries, the HPV vaccine was adjuvanted with AS04 and the trails were double-blinded. The control group were injected with a hepatitis A vaccine. The article suggest HPV 16/18 AS04-adjuvanted vaccine provide protection against CIN2+ lesions, which were associated with HPV 16 and HPV 18, as well as lesions that were associated with HPV 31, HPV 33 and HPV 45. This suggest the HPV 16/18 vaccine also attend crossprotection against the non-vaccine HPV types 31, 33 and 45. These five HPV types (16, 18, 31, 33, 45) are together responsible for about 82 percent of all cervical cancers. The article conclude HPV 16/18 vaccine has a substantial overall effect in cohort that are relevant to universal mass vaccination and catch-up programs. But is the HPV 16/18 in reality a good vaccine for universal mass vaccination? The article showed the vaccine works much better in young women, who did not have any sexual contact than in women who have. But the article do not shows any difference in vaccine efficacy between the 15 years old young women and 25 year old women. The vaccine may be very different in efficacy or in safety. Furthermore, the girls who are vaccinated right now in The Netherlands are 12 to 15 years old. It is possible that girls at the age of 12 react different at the vaccine than young women from 15 to 25 years old. The vaccine may not be efficient and/or safe at this age. A lot of vaccination programs are focusing on vaccination of very young girls, but in all studies investigating the efficacy and safety of the vaccine, the participant were older than 15 years old. You cannot assume 12 year old girl react the same on a vaccine than 15 to 25 year old young women. So the vaccine is may not as good as the article is suggesting for a universal mass vaccination, because it is not (yet) certain if it is safe.
Also the long term safety and efficacy is not known. The article suggest the vaccine is effective and safety for at least a period of 3 years. But it is not known if the vaccine protects someone lifelong, or if there is a booster necessary to stay protected after a couple of years after vaccination. Furthermore, there is not any knowledge about the long term effects of the vaccine. Is it still safe 10 years after vaccination and is a booster, if those are necessary, safe over the long term? Is it ethical to vaccinate young girls if the long term effects of the vaccine are uncertain? It may be better to investigate first the effect on very young girls (12 to 15 years) to see if the vaccine is efficient and safe at this age, before starting a vaccination campaign.
There is still many unknown about the efficacy and safety of the HPV16/18 vaccine. This article contributes in the knowledge about the efficacy and safety of vaccination, but is not very important if you want to vaccinated very young girls (12 to 15 years old). Much more research is necessary to investigate if the vaccine is effective and safe for girls under 15 years old, who are already vaccinated right now.
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