***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: ABSTRACT Carriers of certain human leukocyte antigen class I alleles show favorable prognosis of human immunodeficiency virus type 1 ( HIV-1 ) infection  , presumably due to effective CD8 + cytotoxic T-lymphocyte responses , but close relationships between class I variants mediating such responses to natural and to vaccine HIV-1 antigen have not been established . During 6 to 30 months of administration and follow-up in trials of ALVAC-HIV recombinant canarypox vaccines , cells from 42 % of 291 HIV-1-negative vaccinated subjects typed at class I loci responded to an HIV-1 protein in a lytic bulk CD8 + cytotoxic T-lymphocyte assay . By 2 weeks after the second dose , higher proportions of vaccinees carrying one of two alleles consistently associated with slower progression of natural HIV-1 infection reacted at least once : B∗27 carriers reacted to Gag ( 64 % ; odds ratio [ OR ] = 10.3 , P = 0.001 ) and Env ( 36 % ; OR = 4.6 , P = 0.04 ) , and B∗57 carriers reacted to Env ( 44 % ; OR = 6.6 , P < 0.05 ) . By 2 weeks after the third or fourth dose , B∗27 carriers had responded ( two or more reactions ) to Gag ( 33 % ; OR = 4.4 , P < 0.05 ) and B∗57 carriers had responded to both Gag ( 39 % ; OR = 5.3 , P = 0.013 ) and Env ( 39 % ; OR = 9.5,P = 0.002 ) . Homozygosity at class I loci , although conferring an unfavorable prognosis following natural infection , showed no such disadvantage for vaccine response . Individual class I alleles have not previously demonstrated such clear and consistent relationship with both the clinical course of an infection and cellular immunity to a vaccine against the infectious agent . This proof of principle that class I an alleles modulate both processes has implication s for development of HIV-1 and presumably other vaccines Human papillomaviruses ( HPVs , most notably types 16 and 18 ) cause cervical carcinoma , the second most common cancer among women . Vaccination of adolescents against HPV16/18 might prevent large proportion of cervical and other anogenital cancers . However , because of ethical reasons this can not be proven by clinical studies . To determine the long-term vaccine efficacy ( VE ) of HPV16/18 virus-like-particle ( VLP ) vaccine against cervical carcinoma in situ ( CIS+ ) and invasive cervical carcinoma , the following three population -based cohorts of adolescent women have been enrolled : ( 1 ) women vaccinated with the HPV vaccine ; ( 2 ) women vaccinated with hepatitis A control vaccine ; and ( 3 ) unvaccinated control women . These cohorts will be passively followed for cumulative incidence of CIS+ endpoints by population -based cancer registry . Overall 24,046 16- to 17-year-old adolescent women from 18 cities in Finl and were invited between May 2004 and June 2005 to participate in a phase III trial with bivalent  HPV16/18 VLP vaccine . A total of 58,996 18- to 19-year-old women were invited in May 2005 to participate as unvaccinated controls . Women who reported their willingness to participate in an HPV vaccination trial had they been 1–2 years younger were eligible .  Cumulative incidence ( CI ) of CIS+ in our cohorts over 15 years is approximately 0.45 % . VE of 70 % against CIS+ with 80 % power requires 3357–3189 HPV16/18 vaccine recipients , 3357–3189 other vaccine recipients , and 6714–9567 unvaccinated controls . We have now enrolled 2404 HPV16/18 vaccine recipients , 2404 hepatitis A-vaccine recipients , and 5130 unvaccinated controls . This enrolment in addition to our earlier enrolment in another phase III trial guarantees enough power so that by 2020 we can ultimately provide data on the efficacy of HPV16/18 vaccination against CIS+ Human papillomavirus ( HPV ) type 16 is the major cause of cervical carcinoma , the incidence of which is decreasing in western countries . In Finl and the incidence is , however , increasing in women aged < 40 years , but possible underlying changes in HPV-16 epidemiology are unknown . To assess incidence trends of HPV infections , paired sera from a r and om sample of 8000 women with two pregnancies/sera within 5 years , taken from the serum bank of the Finnish Maternity Cohort ( 1983 - 98 ) , were analysed for HPV-6 , -11 and -16 antibodies . For 23 - 31-year-old women , HPV-16 incidence increased over the period 1983 - 97 . HPV-16 seroprevalence increased from 17 % in 1983 - 85 to 24 % in 1995 - 97 , but HPV-6 and HPV-11 prevalence was stable at 9 - 12 % throughout the study period . Epidemic spread of the oncogenic HPV-16 , but not the non-oncogenic HPV-types , throughout the 1980s and 1990s preceded an increase in the incidence of cervical carcinoma in fertile-aged Finnish women To examine Senegalese women to confirm and extend associations between HLA class II types and  cervical cancer  previously observed among African-American , Caucasian , Hispanic , and Japanese ethnic population s , 55 Senegalese women with invasive cervical carcinoma were compared with age-matched ( human papillomavirus ) HPV-positive ( n = 83 ) and HPV-negative ( n = 107 ) control women .  PCR-based HPV and HLA typing methods were used . Data were analyzed using a global r and omization test and conditional logistic regression . Although this study failed to confirm a previously reported association between cervical cancer and DQB1 * 03 alleles , the DRB1 * 1101-DQB1 * 0301 haplotype was detected more frequently among cervical carcinoma cases than among controls ( adjusted odds ratio , 2.6 ; 95 % confidence interval , 1.0 - 7.1 ) . Furthermore , as reported by others , we observed a negative association of borderline statistical significance between DRB1 * 13 and cervical carcinoma ( adjusted odds ratio , 0.5 ; 95 % confidence interval , 0.2 - 1.1 ) . Observations from this study confirm earlier findings of a negative association between DRB1 * 13 and cervical cancer and suggest that specific DRB1-DQB1 haplotype combinations , rather than individual DQB1 * 03 alleles , increase the risk for cervical cancer The association between cervical neoplasia and certain HLA phenotypes observed in different studies has not been consistent . By serological typing , the association between HLA antigens , cervical carcinoma and cervical intraepithelial neoplasia ( CIN ) was studied in a group of 172 and 116 patients , respectively . We demonstrated an increased frequency of B63 in patients with HPV types other than HPV 16 or 18 , and B55 in patients that were negative for all HPV types . The association between cervical carcinoma and DQ3 , described in various population s , was not observed in the present study . However , we confirmed other previously observed associations between cervical cancer and class II antigens , i.e. , a positive correlation with DR15 irrespective of the HPV status , with DR3 in patients harboring HPV types other than HPV 16 or 18 , and with DR11 among HPV 16 positive patients . In contrast , a negative correlation between DR13 and HPV positive cervical cancer was observed which suggests protection of this antigen against HPV-associated cervical cancer . A slight increase of DR15 and DQ4 antigens was observed in CIN patients , suggesting that these specific HLA antigens may be important in determining the risk of CIN Vaccines against high‐risk ( hr ) human papillomaviruses ( HPVs ) causing cervical cancer may soon be licensed . Thus , nature of HPV epidemics needs to be studied now . R and om sampling for studies on HPV epidemiology was done from all 230,998 women belonging to the population ‐based Finnish Maternity Cohort and having a minimum of 2 pregnancies between 1983 and 1994 . First pregnancy serum specimens were retrieved for 7,805 subjects , and were analyzed for antibodies to HPV6/11 , 16 and 18 with st and ard ELISAs . HPV16 seroprevalence almost doubled from the 1980s to the 1990s , and the epidemic spread to new areas in 23–31 year olds , i.e. the bulk of pregnant female population in the southwest part of the country . The HPV16 epidemic in the 14–22 year olds in 1983–1988 ( 1961–1974 birth cohorts ) and in the 23–31 year olds in 1989–1994 ( 1958–1971 birth cohorts ) overlapped with strong clustering of HPV16 and HPV18 infections in the latter ( odds ratio 8.0 , 95 % confidence interval 6.6–9.7 ) . Similar clustering of HPV16 and HPV6/11 infections was not found . The epidemic and the clustering may be due to high transmission probability of the hrHPV types and increase in sexual activity of the index birth cohorts . © 2006 Wiley‐Liss , 
    Output:
    
Increased incidence of CxCa was found in a region of western coastal Finl and , where frequency of two CxCa susceptibility genes ( HLA-DR2 and B7 ) was increased , and frequency of one CxCa resistance gene ( HLA-B15 ) was decreased .