Article

Prevalence of HPV infection by cervical cytologic status in Brazil

Department of Microbiology and Parasitology, Universidade Federal do Rio Grande do Norte, Natal-RN, Brazil.
International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics (Impact Factor: 1.54). 02/2009; 105(1):21-4. DOI: 10.1016/j.ijgo.2008.12.004
Source: PubMed

ABSTRACT

To assess the prevalence of human papillomavirus (HPV) infection according to cervical cytologic status in northeastern Brazil; identify other risk factors for low- and high-grade squamous intraepithelial lesions (LSILs and HSILs); and identify the most prevalent HPV genotypes associated with the lesions.
Two cervical smears were collected from 250 women referred for cancer screening, one for cytologic examination and the other to test for the presence of HPV by PCR with genotyping by dot blot hybridization.
There were 110 healthy cervices, 82 LSILs, and 58 HSILs. The overall HPV prevalence was 48%, with higher rates for HSILs, and HPV-16 was the most prevalent type. Age, multiple sexual partners, type of HPV present, smoking, and early onset of sexual activity were risk factors for cervical lesions.
Age, multiple sexual partners, and infection with HPV-16 increased the risk of having LSILs or HSILs. Early onset of sexual activity and smoking only increased the risk of having HSILs.

Full-text

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CLINICAL ARTICLE
Prevalence of HPV infection by cervical cytologic status in Brazil
José Veríssimo Fernandes
a,
, Rosely de Vasconcellos Meissner
a
, Maria Goretti Freire de Carvalho
b
,
Thales Allyrio Araújo de Medeiros Fernandes
c
, Paulo Roberto Medeiros de Azevedo
d
, Luisa Lina Villa
e
a
Department of Microbiology and Parasitology, Universidade Federal do Rio Grande do Norte, Natal - RN, Brazil
b
Department of Pathology, Universidade Federal do Rio Grande do Norte, Natal - RN, Brazil
c
Department of Biomedical Sciences, Universidade do Estado do Rio Grande do Norte, Mossoró - RN, Brazil
d
Departament of Statistics, Universidade Federal do Rio Grande do Norte, Natal - RN, Brazil
e
Ludwig Institute for Cancer Research, Hospital Alemão Oswaldo Cruz, São Paulo, SP, Brasil
abstractarticle info
Article history:
Received 9 September 2008
Received in revised form 12 November 2008
Accepted 1 December 2008
Keywords:
Cervical lesions
Human papillomavirus
Polymerase chain reaction
Risk factors
Objectives: To assess the prevalence of human papillomavirus (HPV) infection according to cervical cytologic
status in northeastern Brazil; identify other risk factors for low- and high-grade squamous intraepithelial
lesions (LSILs and HSILs); and identify the most prevalent HPV genotypes associated with the lesions.
Method: Two cervical smears were collected from 250 women referred for cancer screening, one for
cytologic examination and the other to test for the presence of HPV by PCR with genotyping by dot blot
hybridization. Result: There were 110 healthy cervices, 82 LSILs, and 58 HSILs. The overall HPV prevalence
was 48%, with higher rates for HSILs, and HPV-16 was the most prevalent type. Age, multiple sexual partners,
type of HPV present, smoking, and early onset of sexual activity were risk factors for cervical lesions.
Conclusion: Age, multiple sexual partners, and infection with HPV-16 increased the risk of having LSILs or
HSILs. Early onset of sexual activity and smoking only increased the risk of having HSILs.
© 2008 International Federa tion of Gynecology and Obstetri cs. Published by Elsevier Ireland Ltd. All rights reserved.
1. Introduction
Human papillomavirus (HPV) is a large group of epitheliotropic
viruses of more than 120 different types. Of the 40 HPV types infecting
the human body, more than a dozen are associated with probable or
denite oncogenic risk [1,2]. Infection of the cervix is initiated when
infectious particles reach and then bind to the basal layer of the
cervical epithelium, where they enter cells through small tears. It has
been suggested that for maintenance of the infection, the virus has to
infect an epithelial stem cell [3].
The infection occurs mainly in young, sexually active women in the
rst years following their rst sexual encounters [4,5]. The highest
HPV prevalence is among women younger than 25 years. It decreases
from age group to age group and is lowest among women aged
between 45 and 50 years, but increases in the postmenopausal years
[6]. Most HPV infections clear spontaneously, but cervical lesions can
develop in women who have persistent infection with high-risk types
of HPV [7]. A current epidemiologic challenge is to identify etiologic
cofactors that lead to HPV persistence and progression to neoplastic
lesions, and clarify how these cofactors contribute to carcinogenesis
[8]. The high-risk types of HPV have a higher tendency to cause
persistent infection and, in the presence of other environmental and
host factors, are associated with an increased risk of cervical lesions
that may progress to cervical cancer [8,9].
Various studies of screening testing for cervical cancer were
recently realized in the south and southeast regions of Brazil as part of
the Latin America Screening Study. These studies have analyzed the
relations between the cytologic and histologic abnormalities present
in cervical smears, and between HPV infection and the predictive
factors of these anomalies [1012], but so far have not included the
Northeast region of Brazil. Moreover, the method used for HPV de-
tection in these studies was Hybrid Capture 2, which does not identify
HPV type.
The present study was conducted to analyze prevalence of HPV
infection in women with healthy and abnormal uterine cervices in the
Northeast region of Brazil, and to identify the HPV types prevalent in
the local population, as well as risk factors for HPV infection.
2. Materials and methods
The cervical samples used were obtained between April 2001 and
June 2002 at Luis Antonio Hospital in Natal, Rio Grande do Norte State,
Northeastern Brazil, from 258 women referred for cancer screening
because of a history of cytologic alterations. The women's age ranged
from 15 to 65 years. All women were informed about the methods and
objectives of the research. All signed an informed consent form and
International Journal of Gynecology and Obstetrics 105 (2009) 2124
Corresponding author. Departamento de Microbiologia e Parasitologia, Centro de
Biociências, Universidade Federal do Rio Grande do Norte, Av. Sen. Salgado Filho, S/N,
Campus Universitário, Lagoa Nova, CEP: 59072-970, Natal, RN, Brazil. Fax: +55 84
32119210.
E-mail address: veris@cb.ufrn.br (J.V. Fernandes).
0020-7292/$ see front matter © 2008 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ijgo.2008.12.004
Contents lists available at ScienceDirect
International Journal of Gynecology and Obstetrics
journal homepage: www.elsevier.com/locate/ijgo
Page 1
answered a standardized questionnaire about their marital status,
ethnicity, sexual behavior and reproductive activities, oral contraceptive
use, smoking habits, and family history of cancer. The patients' ethnicity
was dened based on self-reports according to the criterion of the
Instituto Brasileiro de Geograa e Estatística (IBGE) that classies
ethnicity into 5 categories: white, black, mulatto, yellow, and native. In
this study, the black, mulatto, yellow, and native categories were
combined into a nonwhite category. The study was approved by the
Ethical Committee in Research of Federal University of Rio Grande do
Norte.
The cervical smears were obtained using a cytobrush for optimal
collection of exfoliated cells. A trained cytopathologist from the
Department of Pathology of Federal University of Rio Grande do
Norte stained the smears and analyzed them according to the
Bethesda classication (available at: h ttp://bethesda2001.cancer.
gov/te rminology.html). All ab normal smears were re-examined for
result conrmation. Sam ples with scant squamous cellularity were
considered unsatisfactory for evaluation and excluded from analysis.
The women with abnormal cytologic results we re followed up
according to the guidelines of the National Ca ncer Pro gram of Brazil.
Bas ed on the results of the cytologic evaluation, the 250 retained
participants were allocated to 1 of 3 groups: a normal cytology group
(n =110); a low-grade squamous intraepithelial lesions (LSIL) group
(n =82); and a high-grade squamous intraepithel ial lesions (HSIL)
grou p (n =58).
Another sample of exfoliated cervical cells was collected from each
participant and the collection brush was placed in a tube containing
PBS, vancomycin, and nystatin. The tube was kept at 4 °C until
processing for DNA extraction. The content was centrifuged at 3000 g
for 10 minutes following vigorous tube agitation and brush removal;
the supernatant was removed; and the remaining pellet was
processed for DNA extraction, using rapid isolation of DNA from
mammals, with proteinase K [13].
To check the quality of the obtained DNA, aliquots with about 30 ng
of DNA were submitted to polymerase chain reaction (PCR) using
the primers PCO3+/PCO4+, specic for the amplication of a 110 bp
fragment of the β-globin gene [14]. Only the 250 DNA samples positive
to β-globin were checked for HPV DNA.
Of the 250 good-quality DNA samples 110 were from participants
in the normal cytology group, 82 from participants in the L SIL group,
and 58 from participants in the HSIL group. The presence or absence of
HPV DNA was established using the degenerate primers MY09/M11,
specic for the L1 open reading frame (ORF) of the HPV genome [15].
The products of PCR were submitted to electrophoresis on 7%
polyacrilamide gel, followed by silver staining [16]. The specimens
were considered positive for HPV DNA if they presented a band of
450 bp. The amplicons were submitted to HPV genotyping by Dot blot
hybridization as described [17].
To check for associations between sociodemographic character-
istics and cervical lesions, and for differences in the prevalences of
HPV infection in the 3 groups, we used the Pearson χ
2
test for
comparison of pro portions. To identify variables that cou ld be
considered risk factors for cervical lesions we used all the considered
variables in a multivariate logistic regression analysis, with the
dependent variable assigned a value of 1 in the presence of low- or
high-grade intraepithelial cervical lesions and a value of 0 in the
absence of lesions. To check for associations between HPV type and
health status we used univariate logistic regression. All analyses were
performed using the software SPSS, version 13.0 (SPSS, Chicago,
Illinois, USA). P 0.05 was considered statistically signicant.
3. Results
Statistical analysis by the χ
2
test showed an association between
age and presence of HSIL (P =0.000) and between ethnicity and
presence of HSIL (P= 0.002). Considering separately married and
single women, we did not observe an association between marital
status and the presence of LSIL or HSIL (P= 0.09 and P= 0.62),
respectively (Table 1).
We observed that most (81.5%) of the women with both a normal
cytology result and HPV infection were younger than 34 years, with a
les ser prevalence of HPV infection in the older age groups. Among
women with LSILs, the prevalence of HPV infection increased as they
reached the age of 34 years, decreased as they aged from 35 to
44 years, and increased again after they were 4 5 years old. Most
(77.8%) of the women wi th HSILs were bet ween 25 and 54 years old
(Table 1). Differences in HPV prevalence between the normal
cytology group (24.5% of the participants) and the LSIL (58.5%) and
HSIL groups (77.6%) were statist ically signicant by comparison of
the proportions, revealing that HPV infection increased the risk of
developing both low-grade (P =0.000) and high-grade (P =0.000)
premalignant lesions. Age was associated with the occurrence of
HSIL (P = 0.000), as was nonwhite status (P =0.002). We observed
no associat ions between marital status a nd the presence of cervical
les ions (Table 1).
The women older than 34 years were at greater risk for LSILs and
those older than 45 years were at greater risk for HSILs. The women
who had their rst sexual intercourse between the ages of 14 and
17 years were at greater risk only for HSILs. Having had multiple
sexual partners and being a smoker also increased the risk of having
HSILs. There was no evidence that age at rst pregnancy, number of
pregnancies, use of oral contraceptives, and a family history of cancer
increased the risk of either LSIL or HSIL (Table 2).
Cervical HPV infection increased the risk of both LSIL and HSIL.
Fourteen different types of HPV were identied in the study
population, and most had a high oncogenic potential. Infection was
caused by 1 type of virus in 19.0% of the women in the normal cytology
group, 40.2% of the women in the LSIL group, and 67.2% of the women
in the HSIL group, and HPV-16 was the most prevalent type in all 3
groups. The second most common type was HPV-58 in the rst 2
groups and HPV-45 in the HSIL group. Infection with 2 HPV types were
detected in the 3 groups, the most frequent coinfection being with
HPV-56 and HPV-57 in the rst 2 groups, and with HPV-31 and HPV-33
or HPV-45 and HPV-59 in the HSIL group. With the probes we used, it
was not possible to identify the HPV types carried by 2 participants in
the normal cytology group, 1 participant in the LSIL group, and 1
participant in the HSIL group. Single infection by HPV-16 increased the
Table 1
Distribution of socio-demographic characteristics, according to health status
Variable Normal cytology group LSIL group HSIL group
No. of
patients
No. of
patients
with HPV (%)
No. of
patients
No. of
patients
with HPV (%)
No. of
patients
No. of
patients
with HPV (%)
Age at study entry
a
b 25 37 9 (24.3) 19 13 (68.4) 4 4 (100.0)
25-34 44 13 (29.5) 30 17 (56.7) 14 11 (78.6)
35-44 23 5 (21.7) 24 11 (45.8) 18 13 (72.2)
45-54 4 0 5 3 (60.0) 13 11 (84.6)
55 2 0 4 4 (100.0) 9 6 (66.7)
Total 110 27 (24.5) 82 48 (58.5) 58 45 (77.6)
Ethnicity
b
White 87 19 (21.8) 64 40 (62.5) 33 24 (72.7)
Nonwhite 23 8 (34.8) 18 8 (44.4) 25 21 (84.0)
Marital status
c
Single 32 11 (34.4) 15 12 (80.0) 14 10 (71.4)
Married 78 16 (20.5) 67 36 (53.7) 41 32 (78.0)
Widowed 0 0 0 0 3 3 (100.00)
a
Statistical analysis for age among the groups: Group I × Group II: χ
2
=5.262,=0.261;
Group I×Group III: χ
2
=39.606 P =0.000.
b
Statistical analysis for ethnicity among the groups: Group I×Group II: χ
2
=0.030,
P=0.862; Group I×Group III: χ
2
=9.166, P = 0.002.
c
Statist ical analysis for marital status among the groups: Group I × Group II:
χ
2
=2.963, P =0.085; Group I ×Group III: χ
2
=0.241, P=0.623.
22 J.V. Fernandes et al. / International Journal of Gynecology and Obstetrics 105 (2009) 2124
Page 2
risk of both LSIL and HSIL, whereas single infection by HPV-58 and
coinfection with HPV-56 and HPV-58 only increased the risk of LSIL
(Table 3).
4. Discussion
The prevalence of HPV infection in women with normal cytology
results was high in this study. Higher than in another study conducted in
Recife, also in Northeast Brazil [18], it was similar to that estimated for
Africa and higher than that estimated for South America in 2 large studies
of meta-analyses [19,20]. This high prevalen ce of HPV infection in
women with normal cyt ology results could be due to the high proportion
of women whose sexual activity began before they were 18 years old,
when they were biologicall y the most vulnerable to th is v irus. It could
also be attributed to false-negati ve results, which commonly occur in
cytologic studies [2,2 1]. Besides, most infections were caused by high-
risk HPV types, mainly by HPV-16, which has a greater capacity than the
other types to maintain infection without cytologic alterations.
The overall HPV prevalence among the participants with normal
cytology results was 24.5%. It was highest in the 25 to 34 years age group
and less in the 35 to 44 years age group, a nding similar to those
reported for other World Regions [20]. Among women with LSILs, the
Table 3
Distribution of HPV types according to health status and associated odds ratio obtained by univariate logistic regression model
Variable Normal cytology group(n=110) LSIL group(n = 82) HSIL group(n=56)
No. of patients No. of patients OR 95% CI No. of patients OR 95% CI
Only type
HPV 16 14 15 2.62 [1.146.0 0]
a
29 13.68 [5.7732.42]
a
HPV 18 1 2 4.88 [0.4355.65] 2 6.38 [0.38108.49]
HPV 58 3 7 5.70 [1.3923.33]
a
2 4.26 [0.6527.96]
HPV X 2 1 1.22 [0.1113.91] 1 3.19 [0.737.76]
Other 1 8 19.53 [2.35162.18]
a
5 31.92 [3.45295.46]
a
Double Infection
HPV 16+18 1 0 NA NA 0 NA NA
HPV 16+58 1 1 2.44 [0.1540.16] 1 6.38 [0.38108.49]
HPV 55+58 1 1 2.44 [0.1540.16] 0 NA NA
HPV 56+58 2 8 9.76 [1.9748.37]
a
0NANA
Other 1 5 12.21 [1.38108.39]
a
5 31.92 [3.4529.546]
a
HPV status
Positive 27 48 4.34 [2.348.05]
a
45 10.64 [5.0 022.63]
a
Negative 83 34 1 [Reference] 13 1 [Reference]
Abbreviations and note: See Table 2.
Table 2
Distribution of patients by cytological status according to the considered variables, and associated odds ratio (OR) obtained by multivariate logistic regression model
Variable Normal cytology group(n=110) LSIL group(n = 82) HSIL group(n=56)
No. of patients No. of patients OR 95% CI No. of patients OR 95% CI
Age at study entry, y
b 25 37 19 1 [Reference] 4 1 [Reference]
2534 44 30 2.27 [0.915.64] 14 1.72 [0.329.25]
3544 23 24 3.44 [1.1710.14]
a
18 5.49 [0.9432.04]
4554 4 5 9.66 [1.3071.56]
a
13 28.04 [2.24350.29]
a
N 54 2 4 30.18 [2.01453.90]
a
9 332.80 [7.5814621.26]
a
Age at 1st sexual intercourse, y
1417 49 52 2.34 [0.717.76] 49 26.09 [1.93352.05]
a
1821 38 20 1.19 [0.373.83] 8 9.68 [0.80117.00]
22 23 10 1 [Reference] 1 1 [Reference]
Age at 1st pregnancy, y
Never pregnant 17 11 NA NA 1 0.90 [0.0326.53]
1417 14 18 2.43 [0.708.43] 27 0.61 [0.113.50]
1821 43 36 1.69 [0.644.41] 21 0.50 [0.122.19]
22 36 17 1 [Reference] 9 1 [Reference]
No. of pregnancies
0 17 10 1 [Reference] 2 1 [Reference]
13 76 54 101.44 [0.0] 22 2.52 [0.2328.11]
46 11 12 53.42 [0.0] 22 6.32 [0.4784.25]
N 6 6 6 27.09 [0.0]12 NANA
Oral contraceptive use, y
0 37 32 1 [Reference] 28 1 [Reference]
13 43 27 0.65 [0.291.47] 9 0.56 [0.122.58]
46 20 13 0.56 [0.201.53] 15 0.68 [0.153.06]
79 5 6 1.01 [0.234.48] 1 0.47 [0.038.31]
9 5 4 0.75 [0.144.09] 5 1.74 [0.2313.41]
Multiple sexual partners
Yes 29 46 3.56 [1.807.04]
a
45 10.50 [3.0436.35]
a
No 81 36 1 [Reference] 13 1 [Reference]
Smoking
Yes 12 13 1.44 [0.524.02] 32 4.80 [1.3616.94]
a
No 98 69 1 [Reference] 26 1 [Reference]
Family history of cancer
Yes 21 26 1.33 [0.583.05] 18 0.74 [0.212.66]
No 89 56 1 [Reference] 40 1 [Reference]
Abbreviations: CI, condence interval; HSIL, High-grade lesion; LSIL, low-grade lesion; NA, not applicable; OR, odds ratio.
a
Denotes statistical signicance.
23J.V. Fernandes et al. / International Journal of Gynecology and Obstetrics 105 (2009) 2124
Page 3
prevalence was higher in this study than that reported for Porto Alegre,
in Southern Brazil [22]; it was similar to that estimated for Africa [23];
and it was less than that reported for Recife [18], Brasilia [24],or
estimated for Central and South America [23]. It was highest among
women younger than 34 years, less in the 35 to 44 years age group, and
higher again among women 45 years or older. Most of the women with
HSILs were between 25 and 54 years old, and there was no linear relation
between age group and HPV prevalence. The overall HPV prevalence in
this study for women with HSILs was higher than that reported for Porto
Alegre [22], but less than that reported for Recife or Brasilia [18,24].
These differences can be explained not only by variations usually
observed between populations of different geographic regions, but also
by differences in age and lesion grades among study populations and the
sensitivity of the HPV DNA assays used in different studies [2,25].
An association between ethnicity and cervical lesion was observed
only for HSILs, suggesting a trend for lesions to progress faster in
nonwhite women. Most of the women in the 3 groups were married or
had only 1 sexual partner. No associations were observed between
HPV prevalence or development of cervical lesions and marital status.
Compared with the participants with normal cytology results, HPV
prevalence was signicantly higher in participants with either lesion
grade. The overall prevalence of HPV-16 in this study was similar to
that estimated for Africa, but higher than that reported for Recife [18]
or estimated for South America [19,20]. We found an association
between HPV infection and the presence of LSILs among women
infected with HPV-16 and HPV-58 as single infections as well as
among those infected with both HPV-56 and HPV-58. We also found
an association between HPV-16 infection and presence of HSILs.
We found both LSILs and HSILs to be associated with age and
multiple sexual partners. On the other hand, we found only HSIL to be
associated with early age at rst sexual intercourse or with smoking,
even when all variables were considered simultaneously in a logistic
regression model. And we found no association between the presence of
premalignant lesions of either grade and oral contraceptive use or family
history of cancer. These results are concordant with those reported in
studies conducted in São Paulo, Porto Alegre, and Buenos Aires [12,22].
In the 3 study groups, the most of the women testing positive for HPV
were infect ed with 1 or 2 high-risk types. Among women with normal
cytology results, the HPV-16 preva lence w as very similar t o that estimated
for South America [19] , but higher than that estimated for Africa and twice
than that reported for Recife [1 8]. These results show that HPV-16 is
highly preva lent in the female population of Natal, Brazil. And since other
high-risk HPV types also infect the same population, these women in our
region are at high risk for HPV infection and, consequently , for cervica l
cancer. The distribution of the HPV types in this study was similar to that
described for w omen in Africa and in Central and South America.
The results of this study lead us to conclude that high-grade lesions
are associated with age and ethnic ity. Multiple lifetime sexual
partners, single infection with HPV-16 or HPV-58, and double infection
with HPV-56 and HPV-58 increased the risk of having LSILs. Early age at
rst sexual intercourse and multiple sexual partners, smoking, and
infection with HPV-16 all increased the risk of having HSILs. The most
prevalent virus type was HPV-16 in the 3 groups, followed by HPV-58
in the normal cytology and LSIL groups, and HPV-45 in the HSIL group.
Despite similarities in the order of prevalen ce of some HPV types
found for Natal in this study and other regions of Brazil in different studies,
there w ere importa nt differences in the prev ale nce of HPV types 3 1, 33, 45,
56, 5 7, and 59. By virtue of the existence of multiple HPV types and
variat ions in their distributions, even within the same geographic region,
more local studies should be conducted to ev alua te the cost-benetand
expect ed efcacy of a HPV v accination campaign, if found justied.
Acknowledgment
This study was supported by funds from the Conselho Nacional
de Desenvolvimento Cientíco e Tecnológico (National Council of
Scientic and Technological Development [CNPq]) and the Coorde-
nação de Aperfeiçoamento de Pessoal de Nível Superior (Coordination
of Improvement of Higher Education [CAPES]).
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    • "HPV16 was twice as common as any other genotype in all countries, except in Nigeria, where the prevalence of HPV35 was similar to that of HPV16 [21]. In countries in South America, such as Paraguay and Brazil, HPV16 and HPV18 have been reported to be the predominant types related to invasive cervical cancers, followed by HPV45, HPV33, HPV31, HPV52, HPV35, and HPV39 [10] [14]. "
    [Show abstract] [Hide abstract] ABSTRACT: Objective To determine the prevalence of atypical squamous cells of undetermined significance (ASCUS) and human papillomavirus (HPV) genotypes in a population in southern Brazil. Methods In a retrospective cross-sectional study, the prevalence of ASCUS was determined among women aged 20–60 years who were referred to a private medical center in Caxias do Sul by a gynecologist for assessment of a cervical condition between January 1, 2010, and September 30, 2011. Histologic and cytologic samples were tested for HPV, and polymerase chain reaction (PCR) was used to genotype any HPV DNA identified. Results Among the 250 included women, 25 (10.0%) had ASCUS. HPV DNA was found in 15 (60.0%) women with ASCUS and 115 (51.1%) of the 225 without ASCUS. Viral typing showed that 7 (46.7%) HPV-positive women with ASCUS had multiple infections with up to five different genotypes. Both low- and high-risk HPV genotypes were found in ASCUS samples; the most prevalent genotypes were HPV6/HPV11 (affecting 10 [66.7%] women), HPV51 (6 [40.0%]), and HPV16 (6 [40.0%]). Conclusion ASCUS is not an indication of HPV infection. HPV screening and genotyping would benefit women with ASCUS, because treatment can be planned according to risk of carcinogenesis.
    Preview · Article · Sep 2014 · International Journal of Gynecology & Obstetrics
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    • "A broader range of HPV prevalence (from 10.4% to 24.5%) has been described in Brazilian studies including women with normal cytology. Our result was similar to that described by the Latin America Screening Study (24.5%) [8] and to data related to Amazonas State (29.2%) [18]. However, it was lower than described in others Brazilian studies including women populations from Rio Grande do Sul (34%), São Paulo (58.4%), "
    [Show abstract] [Hide abstract] ABSTRACT: Background The main cause of cervical cancer in the world is high risks human papillomavirus infection (mainly represented by HPV-16 and HPV-18), that are associated to the development of malign transformation of the epithelium. HPV prevalence exhibits a wide geographical variability and HPV-16 variants have been related to an increased risk of developing cervical intraepithelial lesion. The aim of this study was to describe DNA-HPV prevalence and HPV-16 variants among a women population from Northern Brazil. Methods One hundred and forty three women, during routine cervical cancer screening, at Juruti Project, fulfilled an epidemiological inquiry and were screened through a molecular HPV test. HPV-16 variants were determined by sequencing the HPV-16 E6 open reading frame. Results Forty two samples were considered HPV positive (29.4%). None of those had abnormal cytology results. HPV prevalence varied between different age groups (Z(U) = 14.62; p = <0.0001) and high-risk HPVs were more frequent among younger ages. The most prevalent type was HPV-16 (14%) and it variants were classified, predominantly, as European (87.5%). Conclusions HPV prevalence in our population was higher than described by others and the most prevalent HPV types were high-risk HPVs. The European HPV-16 variant was the most prevalent among HPV-16 positive samples. Our study reinforces the fact that women with normal cytology and a positive molecular test for high-risk HPVs should be submitted to continuous follow up, in order to verify persistence of infection, promoting an early diagnosis of cervical cancer and/or its precursors.
    Full-text · Article · Aug 2014 · Infectious Agents and Cancer
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    • "Fifteen HPVs have been classified as high-risk types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82) that cause dysplasia and cancer, 12 have been classified as low-risk types (6, 11, 40, 42, 43, 44, 54, 61, 70, 72, 81, and CP6108) that usually cause low-grade mild dysplasia, genital warts, and respiratory papillomatosis, and three have been classified as probable high-risk types (26, 53, and 66) (Munoz et al., 2003). HPVs 31, 33, 35, 51, and 52 are sometimes regarded as 'intermediate-risk' viruses because they are more common in mild or severe dysplastic lesions than in carcinomas (Fernandes et al., 2009). Cutaneous HPVs constitute more than 75% of the HPVs described to date and are grouped into five different genera: alpha-PV, beta- PV, gamma-PV, mu-PV, and nu-PV (De Villiers et al., 2004) that are not generally associated with cancers. "
    [Show abstract] [Hide abstract] ABSTRACT: Human papillomavirus (HPV) infection is a central and necessary, although not sufficient, cause of cervical cancer. Besides HPV, the additional multiple risk factors related with the onset of cervical cancer are early-age sexual activities; high number of sexual partners, which is the most salient risk factor; suppression and alteration of the immune status; long-term use of oral contraceptives; and other hormonal influences. The tumor-suppressor proteins p53 and pRb are degraded and destabilized through ubiquitination by viral oncoproteins E6 and E7. Over 95% of cervical cancer cases worldwide test positive for oncogenic HPV DNA. Although cervical screening procedures have been successful in reducing the disease burden associated with HPV infection because of lack of resources or inadequate infrastructure many countries have failed to reduce cervical cancer mortality. Therefore, prevention may be a valuable strategy for reducing the economic and disease burden of HPV infection. At present, two successful prophylactic HPV vaccines are available, quadrivalent (HPV16/18/6/11) 'Gardasil' and bivalent (HPV16/18) 'Cervarix' for vaccinating young adolescent girls at or before the onset of puberty. Recent data indicate that vaccination prevents the development of cervical lesions in women who have not already acquired the vaccine-specific HPV types. Moreover, several therapeutic vaccines that are protein/peptide-based, DNA-based, or cell-based are in clinical trials but are yet to establish their efficacy; these vaccines are likely to provide important future health benefits. The therapeutic vaccination mode of prevention is a promising area of research, as revealed in preclinical trials; however, clinical trials based on large populations are warranted before reaching a valid conclusion. This review summarizes the studies on the epidemiology of HPV infection, the pathogenesis of viral oncoproteins in the oncogenesis of cervical cancer, the economic and health burden of HPV-related diseases, and, finally, focuses on the results of recent clinical vaccination trials.
    Full-text · Article · Oct 2013 · European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP)
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