Molecular Genotyping of Human Papillomavirus among HIV-infected and HIV-uninfected Women in Ouagadougou, Burkina Faso

Abstract

This study particularly focused on the human papillomavirus (HPV) that causes cervical cancer. The objective was to study the profile and genotypic prevalence of HPV among HIV infected and HIV uninfected women. Method: The study was conducted in Ouagadougou, from February 2009 to January 2013 and involved 421 women: 183 HIV positive women (HIV+) and 238 HIV-negative women (HIV-). PCR/hybridization and real-time PCR were performed for the detection of high and low-risk HPV genotypes.
Results: The two populations of women differed in socio-economic, behavioral and sexual characteristics. HPV prevalence was 24.8% and 63.9%, respectively, among HIV- and HIV+ women. Except for HPV16, HPV52,HPV58 and HPV6, which were higher in HIV- women compared to HIV+ women, it's the opposite effect that was found for the other genotypes. We found many more cases of co-infection with three or more genotypes in HIV- women compared to HIV+ women. Contraceptive use and low CD4 count were associated with HPV infection in HIV+ women (p < 0.05). Parameters such as age group, marital status, occupation, level of education, history of gynecological infection, and condom use differed according to HIV status (p < 0.05). Conclusion: Through this study, we found that HPV are highly prevalent among HIV positive women in Burkina Faso. However, given the high prevalence of other HPV types than 16 and 18, in our study, another type of vaccine should be considered to cover them. In the meantime, the results of this study could be a springboard for the introduction of vaccines against HPV already existing in Burkina Faso.

Full text

Journal of Medical Biomedical and Applied Sciences
J Med Biomed App Sci 8 (1), 324–333 (2020) ISSN (O) 2349-0748
Molecular Genotyping of Human Papillomavirus among HIV-infected and HIV-
uninfected Women in Ouagadougou, Burkina Faso
Florencia Wendkuuni DJIGMA1,2, Théodora Mahoukèdè ZOHONCON2,3,4, Zoénabo DOUAMBA5,
Pegdwendé Abel SORGHO1,2, Dorcas Obiri-Yeboah6, Abdoul Karim OUATTARA1, Tani SAGNA7,
Lassina TRAORE1,2, Nadine W. GHILAT-AVOID-BELEM3, Korotomi SANOGO3, Jedida SEMPORE3,
Albert Théophane YONLI1,2, Virginio PIETRA3, Cyrille BISSEYE8, Charlemagne OUEDRAOGO1,9 and
Jacques SIMPORE1,2,3*
1. Molecular Biology and Genetics Laboratory (LABIOGENE), Department of Biochemistry and
Microbiology; University JOSEPH KI-ZERBO, P.O. Box 7021, Ouagadougou 03, Burkina Faso;
2. Pietro Annigoni Biomolecular Research Center (CERBA), P.O. Box 364, Ouagadougou 01, Burkina Faso;
3. Saint Camille Hospital of Ouagadougou (HOSCO) P.O. Box 444 Ouagadougou 09 Burkina Faso;
4. University Saint Thomas d’Aquin, Faculty of Medicine, 06 BP 10212 Ouagadougou 06, Burkina Faso;
5. Research Institute in Applied Sciences and Technologies (IRSAT); P.O. Box 7047 Ouagadougou 03, Burkina
Faso;
6. Department of Microbiology and Immunology, School of Medical Sciences, University of Cape Coast, PMB,
Cape Coast, Ghana;
7. Institut de Recherche en Sciences de la Sante (IRSS), Biomedical and Public health Department, P.O Box
7047 Ouagadougou 03 ;
8. Laboratory of Molecular and Cellular Biology, University of Science and Technology of Masuku (USTM),
BP 943, Franceville, Gabon;
9. Department de Medicine, University JOSEPH KI-ZERBO, P.O. Box 7021, Ouagadougou 03, Burkina Faso.
Corresponding author:
*Prof. Jacques SIMPORE; Molecular Biology and Genetics Laboratory (LABIOGENE), Department of
Biochemistry and Microbiology; University JOSEPH KI-ZERBO, P.O. Box 7021, Ouagadougou 03, Burkina
Faso.
DOI: 10.15520/jmbas.v8i1.207
Accepted 9 January 2020; Received 29 December 2019; Publish Online 18 January 2020
Reviewed By: Dr. Daniel V.
Abstract
This study particularly focused on the human papillomavirus (HPV) that causes cervical cancer. The objective
was to study the profile and genotypic prevalence of HPV among HIV infected and HIV uninfected women.
Method: The study was conducted in Ouagadougou, from February 2009 to January 2013 and involved 421
women: 183 HIV positive women (HIV+) and 238 HIV-negative women (HIV-). PCR/hybridization and real-
time PCR were performed for the detection of high and low-risk HPV genotypes.
Results: The two populations of women differed in socio-economic, behavioral and sexual characteristics. HPV
prevalence was 24.8% and 63.9%, respectively, among HIV- and HIV+ women. Except for HPV16, HPV52,
Journal of Medical Biomedical and Applied Sciences, Vol 8 Iss 1, 324–333 (2020)

HPV58 and HPV6, which were higher in HIV- women compared to HIV+ women, it's the opposite effect that
was found for the other genotypes. We found many more cases of co-infection with three or more genotypes in
HIV- women compared to HIV+ women. Contraceptive use and low CD4 count were associated with HPV
infection in HIV+ women (p < 0.05). Parameters such as age group, marital status, occupation, level of
education, history of gynecological infection, and condom use differed according to HIV status (p < 0.05).
Conclusion: Through this study, we found that HPV are highly prevalent among HIV positive women in
Burkina Faso. However, given the high prevalence of other HPV types than 16 and 18, in our study, another
type of vaccine should be considered to cover them. In the meantime, the results of this study could be a
springboard for the introduction of vaccines against HPV already existing in Burkina Faso.
Key words: HPV; HIV; Genotypes; Women; Burkina Faso.
1. Introduction
Since the onset of Human Immunodeficiency Virus
(HIV) infection, an increase in the frequency of
cervical lesions (dysplasia and invasive cervical
cancer) has been described [1]. From 1997, the
Center of Disease Control and prevention of Atlanta
recommended regular gynaecological monitoring of
women infected with HIV [2] . It is now certified
that high-risk HPV (HR-HPV) cause approximately
95% of precancerous and cancerous lesions of the
cervix. Currently, there are 3 prophylactic vaccines
on the market: Cervarix (GlaxoSmithKline,
Brentford, UK) which is bivalent and target
HPV16/18; Gardasil (Merck Inc, NY, USA), which
is quadrivalent and target HPV6/11/16/18 and
Gardasil-9 (Merck Inc., NY, USA), which is
nonavalent and target HPV
6/11/16/18/31/33/45/52/58. This means that
prevention against cervical cancer is a possibility
especially for developing countries like Burkina
Faso where prevalence of HPV is high. The
relationship between the frequency, severity of
cervical dysplasia and the degree of immune
deficiency was quickly established. The
transmission of HPV is mainly through sex. Indeed,
HPV infection is the commonest STI in the world.
Seventy-five percent of women are infected with
HPV at least once during their sex life [3, 4] . At the
ages of greatest sexual activity, the prevalence of
infection by subclinical HPV can reach more than
40% of the female population [5]. However, it
varies according to the different regions of the
world with the highest in Africa [6]. In general,
HPV16 is the most widespread with a prevalence of
26.3% in the world population [7]
Burkina Faso is no exception in terms of the
prevalence of HPV. For the past ten years, fairly
regular studies have been carried out in several
regions of the country and they are all unanimous
regarding the prevalence of HPV, which is between
24 to 41% for women in the general population and
around 60% for women infected with HIV [8-16].
Most comparative studies in Africa have found very
high prevalence of HPV in HIV positive women
compared to HIV negative women [17-23].
The objective of this study was to compare the
frequencies and genotypes of HPV in HIV positive
and HIV negative women in Ouagadougou, Burkina
Faso.
2. Methods
2.1 Study design and population, sample
collection
The samples were taken from May 2009 to January
2010 in three reference and much frequented health
centres in the capital of the country, Ouagadougou:
Saint Camille hospital of Ouagadougou (HOSCO),
the teaching hospital centre of Bogodogo and the
Pietro Annigoni Biomolecular Research Centre
(CERBA). These three centres are located on the
outskirts of the city and are accessible to all strata of
the population. The real-time PCR analysis was
performed.
The Saint Camille Hospital of Ouagadougou
(HOSCO) and the Biomolecular Research Centre
Pietro Annigoni (CERBA) are reference centres in
Burkina Faso for the management of people living
with HIV/AIDS (PLHIV). The samples were taken
by three gynaecologists on site and the samples
were stored at -80 ° C pending further handling.
We included in the study 183 women screened
positive for the carriage of anti-HIV antibodies
(HIV positive), at the asymptomatic stage of
infection and 238 HIV negative women came in
gynaecological consultation without distinction of
age. HIV-positive women were selected from those
monitored at HOSCO and CERBA and who must
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Molecular Genotyping of Human Papillomavirus among HIV-infected and HIV-uninfected Women in Ouagadougou, Burkina Faso 325

be screened annually for cervical cancer. The
consent of these two groups of women was obtained
by the doctor after detailed explanation of the type
of examination to be performed, the possible results
expected as well as the possible management from
which they will benefit. Each woman answered a
questionnaire in order to determine socio-economic,
professional status and certain behavioural habits.
2.2 Ethical Aspects
The Ethics Committee of the Saint Camille Medical
Center and the Pietro Annigoni Biomolecular
Research Center has given its formal agreement for
this study (n°2009-009/CR/135 of 22 April 2009)
and each woman gave her informed consent before
the samples were taken.
2.3 Sampling
Samples were collected with sterile cotton swabs
from the endocervix. The collected samples were
then allowed in sterile and dry extraction tube and
stored at −80 ◦C prior to DNA extraction.
2.4 DNA Extraction
The DNA extraction was assayed from swabs using
“INSTANT Virus DNA Kit” Analytkjena® (Italy)
bio solutions following the protocol provided by the
manufacturer. We used extraction columns in which
we placed the DNA extract obtained after the lysis
of membranes and hydrolysis of the proteins. The
DNA extract was then washed and eluted.
2.5 Research and genotyping of HPV
For this step, we used two different techniques: a
first one called PCR/Hybridization for the diagnosis
of high risk HPV 16, 18, 45, 30’S, 50’S and low
risk HPV 6 and 11. This technique does not allow
us to specify the 30'S and 50'S genotypes. We
completed our genotyping with a second technique
using the Sacace biotechnologies® kit which
allowed us to specify the following high-risk
genotypes: 16, 18, 31, 39, 45, 59, 33, 35, 56, 51, 52,
58. The use of these two techniques allowed us at
the same time to verify the concordance of the
results between the two methods.
PCR / Hybridization
The PCR/hybridization was performed using a kit
“HPV Blot STAR” of Diatech® (Italy). This assay
enables the detection of HPV and the differentiation
of high-risk and low-risk HPV strains by in vitro
amplification of the gene L1 with biotinylated
primers and subsequent reverse dot blot
hybridization with sequence-specific
oligonucleotides probes. The kit can detect the
following HPV genotypes: 16, 18, 30’S, 45, 50’S, 6,
and 11. The PCR program was previously described
[8].
Detection of HPV genotypes with the kit « HPV
High Risk Typing Real-TM» (SACACE
biotechnologies®, Italie)
The High Risk HPV Typing Real-TM kit is based
on two major processes: isolation of DNA from
specimens, and multiplex Real Time amplification
of 4 tubes for each sample. Each tube contains
primers directed against regions of three HPV types
and the β-globin gene used as Internal Control. PCR
conditions were as follows : 1 cycle of 95°C for 15
minutes ; 5 cycles of 95°C for 05s, 60°C for 20s and
72°C for 15s; and 40 cycles of 95°C for 05s,
60°Cfor 30s and 72°C for 15s.
2.6 Statistical analysis
Data were analysed using SPSS 20.0 and Epi Info
3.5.1 softwares. The Chi-square test was used for
comparisons. Statistical difference was calculated
with Epi Info 6 and was significant for p ≤ 0.05.
3. Results
3.1 Socio-economic, behavioral and sexual
characteristics of women in this study based on
HIV status
We enrolled a total of 421 women in our study: 238
HIV negative women constituting the control group
and 183 other HIV positive women considered as
cases. The average age of our study population was
33.91 ± 6.18 years (Minimum = 20; Maximum =
53) and 30.67 ± 8.03 years (Minimum = 15 years;
Maximum = 63 years) respectively for HIV + and
HIV- women. By comparing the socio-economic,
behavioural and sexual characteristics of these two
groups of women, we notice that there are
statistically significant differences between them
regarding all characteristics except the number of
visits to the gynaecologist by year and the use of
contraceptives. (Table 1). In HIV positive women,
the average CD4 count was 401.67 ± 211.03 cells /
uL (Minimum = 6 and Maximum = 1382).
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326 Jacques SIMPORE Etal.

Table 1: Socio-economic, behavioural and sexual characteristics of women in our study based on HIV status
HIV- n(%)
HIV+ n(%)
P value
Average age (years)
30.67±8.03
33.91±6.18
< 0.001
Average age at first intercourse
(years)
18.90±2.66
18.18±2.36
< 0.001
Marital status
Married
178 (74.8%)
107 (58.5%)
< 0.0001
Divorced
5 (2.1%)
18 (9.8%)
Widow
2 (0.8%)
34 (18.6%)
Single
53 (22.2%)
24 (13.1%)
Profession
Unemployed
90 (37.8%)
116 (63.4%)
< 0.0001
Merchant
21 (8.8%)
9 (4.9%)
Salaried
24 (10.1%)
23 (12.6%)
Informal sector
69 (29.0%)
31 (16.9%)
Students
34 (14.3%)
4 (2.2%)
Study level
No formal
education
76 (31.9%)
53 (29.0%)
< 0.0001
Primary school
47 (19.7%)
62 (33.9%)
Secondary school
87 (36.6%)
65 (35.5%)
University
28 (11.8%)
3 (1.6%)
Number of visits to the
gynaecologist by year
Never
174 (73.1%)
133 (72.6%)
0.994
1<X≤2
37(15.6%)
29 (15.9%)
X˃2
27 (11.3%)
21 (11.5%)
History of gynecological
infection
Yes
97 (40.8%)
116 (63.4%)
< 0.0001
No
141 (59.2%)
67 (36.6%)
Contraceptive use
Yes
70 (29.4%)
41 (22.4%)
0.106
No
168 (70.6%)
142 (77.6%)
HPV frequency
HPV+
59 (24.8%)
117 (63.9%)
< 0.0001
HPV-
179 (75.2%)
66 (36.1%)
3.2 Different genotypes of HPV found among
HIV positive and HIV negative women
Overall, 41.81% of the women in this study were
diagnosed with HPV, with 24.8% (59/238) of HPV
in HIV uninfected women and 63.9% (117/183) in
HIV infected women (p < 0.001). Genotyping of
different HPV found in our sample shows quite
different prevalence of HPV strains based on HIV
status. The HPVs 16, 18, 31, 33, 35, 39, 45, 51, 52,
56, 58, 59 and 6 are found in the two groups. We
obtained respectively in HIV+ and HIV- women the
following proportions (Table 2): HPV18 (18.8%
versus 15.2%), HPV35 (13.3% versus 8.1%),
HPV31 (10.7% versus 7.1%), HPV52 (8.8% versus
12.1%), HPV58 (8.1% versus 11.1%), HPV56
(7.8% versus 7.1%), HPV45 (6.2% versus 6.1%),
HPV59 (5.8% versus 5.1%), HPV33 (5.8% versus
1, 9%), HPV51 (5.2% versus 5.1%), HPV16 (4.9%
versus 7.1%), HPV39 (2.6% versus 1.9%), HPV6
(2.0% versus 12.1%).
Multiple HPV infections were found for 53.4%
(94/176) of all HPV infections. These types of
infections concerned 62.4% of all infections in HIV
negative women and 35.6% of all infections in HIV
positive women. In 46.6% (82/176) remaining, only
one type of HPV was present. The maximum
number of genotypes found in HIV negative women
was 5 and 7 in HIV positive women. (Table 3)
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Molecular Genotyping of Human Papillomavirus among HIV-infected and HIV-uninfected Women in Ouagadougou, Burkina Faso 327

Table 2: Different genotypes of HPV found among HIV positive and HIV negative women
HPV Genotypes
HIV+
HIV-
P value
HPV16
15 (4.9%)
7 (7.1%)
0.400
HPV18
58 (18.8%)
15 (15.2%)
0.406
HPV31
33 (10.7%)
7 (7.1%)
0.289
HPV33
18 (5.8%)
2 (1.9%)
0.206
HPV35
41 (13.3%)
8 (8.1%)
0.164
HPV39
8 (2.6%)
2 (1.9%)
0.960
HPV45
19 (6.2%)
6 (6.1%)
0.968
HPV51
16 (5.2%)
5 (5.1%)
0.955
HPV52
27 (8.8%)
12 (12.1%)
0.324
HPV56
24 (7.8%)
7 (7.1%)
0.813
HPV58
25 (8.1%)
11 (11.1%)
0.361
HPV59
18 (5.8%)
5 (5.1%)
0.766
HPV6
6 (2.0%)
12 (12.1%)
< 0.0001
Total
308 (100%)
99 (100%)
Table 3: Co-infections with one or more genotypes depending on HIV status
Co-infections
HIV+
HIV-
P value
1 genotype
38 (64.4%)
44 (37.6%)
0.0007
2 genotypes
9 (15.3%)
14 (12.0%)
0.541
3 genotypes
7 (11.9%)
23 (19.6%)
0.194
4 genotypes
3 (5.0%)
14 (12.0%)
0.144
5 genotypes and
more
2 (3.4%)
22 (18.8%)
0.005
Total
59 (100%)
117 (100%)
3.3 HPV prevalence in relation to HIV status and
socio-economic, behavioural and sexual
characteristics
In HIV negative women, no characteristic was
correlated with HPV infection. In contrast, among
HIV+ women, taking contraceptives and low CD4
counts were statistically associated with HPV
infection. However, when we compare HIV-/HPV+
women to HIV+/HPV+ women, we found that age
classes, marital status, profession, education, history
of gynaecological infections and use of condoms
were significantly associated with HPV infection
and HIV status. (Table 4)
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328 Jacques SIMPORE Etal.

p* : comparison HIV-/HPV- and HIV-/HPV+ ; p** : comparison HIV+/HPV- and HIV+/HPV+ ; p*** : comparison HIV-/HPV+ and HIV+/HPV+
HIV negative N= 238
HIV positive N=183
Total (HIV+/HIV-) N=421
P***
HPV-
N= 179
HPV+
N= 59
p*
HPV-
N= 66
HPV+
N= 117
p**
HPV-
N= 245
HPV+
N= 176
Age group (years)
X< 29
92 (51.4%)
31 (52.5%)
0.364
19 (28.8%)
26 (22.2%)
0.468
111 (45.3%)
57 (32.4%)
< 0.0001
30≤X<39
65 (36.3%)
17 (28.8%)
34 (51.5%)
71 (60.7%)
99 (40.4%)
88 (50.0%)
X ≥ 40
22 (12.3%)
11 (18.6%)
13 (19.7%)
20 (17.1%)
35 (14.3%)
31 (17.6%)
Marital statut
Married
139 (78.1%)
39 (66.1%)
-
42 (63.6%)
65 (55.6%)
0.441
181 (73.8%)
104 (59.1%)
< 0.0001
Divorced
2 (1.1%)
3 (5.1%)
5 (7.6%)
13 (11.1%)
7 (2.9%)
16 (9.1%)
Widow
2 (1.1%)
-
9 (13.6%)
25 (21.4%)
11 (4.5%)
25 (14.2%)
Single
36 (19.7%)
17 (28.8%)
10 (15.2%)
14 (12.0%)
46 (18.8%)
31 (17.6%)
Profession
Unemployed
72 (40.2%)
18(30.5%)
0.384
45 (68.2%)
71 (60.7%)
-
117 (47.8%)
89 (50.6%)
< 0.0001
Merchant
16 (8.9%)
5 (8.5%)
3 (4.5%)
6 (5.1%)
19 (7.8%)
11 (6.3%)
Salaried
16 (8.9%)
8 (13.6%)
4 (6.1%)
19 (16.2%)
20 (8.2%)
27 (15.3%)
Informal sector
53 (29.7%)
16 (27.1%)
14 (21.2%)
17 (14.5%)
67 (27.3%)
33 (18.7%)
Students
22 (12.3%)
12 (20.3%)
-
4 (3.4%)
22 (8.9%)
16 (9.1%)
Study level
No formal education
61 (34.1%)
15 (25.4%)
0.519
17 (25.7%)
36 (30.8%)
-
78 (31.8%)
51 (29.0%)
0.005
Primary school
36 (20.1%)
11 (18.6%)
24 (36.4%)
38 (32.5%)
60 (24.5%)
49 (27.8%)
Secondary school
63 (35.2%)
24 (40.7%)
25 (37.9%)
40 (34.2%)
88 (35.9%)
64 (36.4%)
University
19 (10.6%)
9 (15.3%)
-
3 (2.5%)
19 (7.8%)
12 (6.8%)
Number of visits to
the gynaecologist
by year
Never
129 (72.1%)
45 (76.2%)
0.667
51 (77.3%)
82 (70.1%)
0.345
180 (73.5%)
127 (72.1%)
0.503
1<X≤2
30 (16.8%)
7 (11.9%)
7 (10.6%)
22 (18.8%)
37 (15.1%)
29 (16.5%)
X˃2
20 (11.1%)
7 (11.9%)
8 (12.1%)
13 (11.1%)
28 (11.4%)
20 (11.4%)
History of
gyneacological
infection
Yes
75 (41.9%)
22 (37.3%)
0.532
41 (62.1%)
75 (64.1%)
0.789
116 (47.3%)
97 (55.1%)
0.0007
No
104 (58.1%)
37 (62.7%)
25 (37.9%)
42 (35.9%)
129 (52.7%)
79 (44.9%)
Contraceptive use
Yes
53 (29.6%)
17 (28.8%)
0.907
22 (33.3%)
19 (16.2%)
0.008
75 (30.6%)
36 (20.5%)
0.051
No
126 (70.4%)
42 (71.2%)
44 (66.7%)
98 (83.8%)
170 (69.4%)
140 (79.5%)
Condom use
No
127 (70.9%)
32 (54.2%)
0.075
11 (16.7%)
25 (21.4%)
-
138 (56.3%)
57 (32.4%)
< 0.0001
Rarely
5 (2.8%)
4 (6.8%)
-
2 (1.7%)
5 (2.0%)
6 (3.4%)
Sometimes
21 (11.7%)
11 (18.6%)
11 (16.7%)
19 (16.2%)
32 (13.1%)
30 (17.1%)
Every time
15 (8.4%)
4 (6.8%)
28 (42.4%)
39 (33.3%)
43 (17.6%))
43 (24.4%)
No answer
11 (6.2%)
8 (13.6%)
16 (24.2%)
32 (27.4%)
27 (11.0%)
40 (22.7%)
Number of
pregnancies
0
36 (20.1%)
13 (22.0%)
0.591
3 (4.5%)
8 (6.8%)
0.900
39 (15.9%)
21 (11.9%)
0.203
1
41 (22.9%)
15 (25.4%)
8 (12.1%)
12 (10.3%)
49 (20.0%)
27 (15.3%)
2
29 (16.2%)
10 (16.9%)
10 (15.2%)
20 (17.1%)
39 (15.9%)
30 (17.1%)
3
33 (18.4%)
6 (10.2%)
9 (13.6%)
11 (9.4%)
42 (17.4%)
17 (9.7%)
4
22 (12.3%)
5 (8.5%)
5 (7.6%)
11 (9.4%)
27 (11.0%)
16 (9.1%)
5 et plus
18 (10.1%)
9 (15.3%)
6 (9.1%)
13 (11.1%)
24 (9.8%)
22 (12.5%)
Non répondant
-
1 (1.7%)
25 (37.9%)
42 (35.9%)
25 (10.2%)
43 (24.4%)
CD4 count
X≤ 350 cells/uL
-
-
-
21 (31.8%)
58 (49.6%)
0.019
-
-
-
X˃ 350 cells/uL
-
-
45 (68.2%)
59 (50.4%)
-
-
Table 4: HPV prevalence in relation to HIV status and socio-economic, behavioural and sexual characteristics
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Molecular Genotyping of Human Papillomavirus among HIV-infected and HIV-uninfected Women in Ouagadougou, Burkina Faso 329

Discussion
The average age of our two study populations is
around 30 years, reflecting screening for HPV in
predominantly young women, and in an age group
where they are sexually active. HIV uninfected
women had their first sexual intercourse on average
later than HIV positive women. This information,
added to the fact that they more often live alone
than HIV uninfected women (over 74% are
married) could help to explain why there are more
of gynaecological infections history in HIV+
women than HIV- women (p < 0.0001). In terms of
occupation as well as level of education, HIV+
women were less represented in the workforce than
HIV- women. This is complementary to the high
level of study (higher and secondary) which was
much more common among HIV- women.
Although we have not investigated the
discrimination of positive HIV status, there is no
longer any evidence that people living with HIV
experience discrimination that is even more
pronounced among women. And this fact, in
addition to the disease could help explain why in
our population of women infected with HIV we
have fewer working women. We find through our
results that women infected with HIV attend health
centres because of their status but this did not
influence their number of visits to the gynaecologist
per year. Generally, a woman goes to the
gynaecologist when she is referred by a health
worker. And health workers only refer patients to
specialists when indicated as per the working
guidelines. Precisely through regular medical
consultations enjoyed by women living with HIV,
this promotes fast and fairly effective management
of diseases that otherwise could have developed
negatively. We also note that contraceptives usage
rate is low for both HIV+ and HIV- women. This
reflects the national reality of the use of
contraceptive methods.
The prevalence of HPV was 24.8% and 63.9%
respectively among HIV negative and HIV positive
women (p < 0.0001). This confirms that HIV+
status has a negative influence on the prevalence of
HPV, especially because these two viruses have in
common the sexual route as the main route of
transmission. Other studies have come to a similar
conclusion [24, 25]. Knowing that HIV-induced
immunosuppression can also play an important role
in the persistence of HPV infection and the
onset/persistence of precancerous and cancerous
lesions, it seems important to us that the population
of HIV positive women has very early burden of
precancerous lesions. We also recommend the
implementation of systematic vaccination of all
young girls infected with HIV (from the age of 9)
who have contracted their infection vertically
(young girls born to HIV positive mothers). After
an initial infection and a latency of around three
weeks, active viral replication of HPV follows and
continues for a variable duration. When HPV DNA
can no longer be detected by available technology,
it is "clearance", but the virus can be latent and
reactivate when conditions are favourable. Among
HIV-negative populations with normal immunity,
approximately 10-20% of infections become
persistent. It is suspected that in PLHIV, this
prevalence is higher. Host factors are therefore
important in determining viral suppression via
cellular immunity [26, 27].
A total of 13 different HPV genotypes were found
in this study. This is mainly due to the limit of our
genotyping kits that did not allow us to look for
more. In women infected with HIV, the genotypes
found in decreasing order were: HPV18 (18.8%),
HPV35 (13.3%), HPV31 (10.7%), HPV52 (8.8%),
HPV58 (8.1%), HPV56 (7.8%), HPV45 (6.2%),
HPV59 (5.8%), HPV33 (5.8%), HPV51 (5.2%),
HPV16 (4.9%), HPV39 (2.6%) and HPV6 (2.0%).
In HIV infected women, the genotypes found in
decreasing order were: HPV18 (15.2%), HPV52
(12.1%), HPV6 (12.1%), HPV58 (11.1 %), HPV35
(8.1%), HPV56 (7.1%), HPV31 (7.1%), HPV16
(7.1%), HPV45 (6.1%), HPV51 (5.1%), HPV59
(5.1%), HPV33 (1.9%), HPV39 (1.9%). HPV18, 35,
52 and 58 are among those who are leading in
prevalence in women infected with HIV or not.
These are high-risk HPV and therefore may cause
damage that may change later to cervical cancer. In
women not infected with HIV, HPV6 is still one of
the top 5 genotypes found in terms of prevalence.
HPV6 is relatively uncommon in women infected
with HIV, as confirmed by a study carried out in
Burkina in 2012 [28]. The authors of this study had
found 1.5% of HPV11, which is not the case in our
study. We assume that with a larger population, we
would have had roughly the same frequencies. The
most prevalent high-risk genotypes in our study
differ from those found in other countries, like
Kenya where the top 4 in women infected with HIV
was HPV16, 53, 66 and 58 and in women not
infected, we had HPV58, 45, 52 and 53 [29]. In
Kenya, a meta-analysis found that HPV52 and 35
were the most common genotypes found in women
Journal of Medical Biomedical and Applied Sciences, Vol 8 Iss 1, 324–333 (2020)
330 Jacques SIMPORE Etal.

with HIV infection [30]. In Ghana, Obiri-Yeboah et
al., found HPV35, 52, 58 and 18 as the most
prevalent genotypes in HIV infected women and
HPV35, 33, 18 and 56 as the most prevalent
genotypes in HIV uninfected women [25].
However, we do keep in mind that we have been
looking for HPV genotypes in women who did not
necessarily have cervical lesions. It would be
interesting to repeat the same study but in women
with cancerous lesions. This will allow us to better
specify the genotypes responsible for cancer in
Burkina.
By comparing the socio-economic, behavioural and
sexual parameters of our study population with HIV
status and HPV infection, we find that only
contraceptive use and low CD4 count appear to be
associated with HPV infection in women infected
with HIV. However when we compare these same
parameters between HIV+/HPV+ women and HIV-
/HPV+ women, we have a p < 0.05 for some of the
parameters such as age group, marital status,
profession, level of education, history of
gynaecological infections and condom use.
Regarding age groups, HPV was more found among
women not infected with HIV under 29 and for
those aged 30-39 infected with HIV. These two age
groups roughly correspond to the active period of
sexual life, therefore an increased risk of
contracting HPV infection in women. Our results
are similar to those of Obiri-Yeboah et al., 2017
[25]. For marital status, married women were more
affected by HPV in the two study populations. This
means that the status of a married woman does not
protect against acquiring HPV infection in our
study. Perhaps also the number of sexual partners
could explain it. Especially that men play a key role
in the virus transmission chain.
When we look at the profession, we notice that
housewives/unemployed women were more
affected by HPV in women infected with HIV
compared to uninfected women. This could be
partly due to the fact that this study has find many
more housewives in women infected with HIV
compared to uninfected women. And this may be
the result of the discrimination that people have
against PLHIV. This last explanation is consistent
with the results we obtained in relation to the level
of study: women with a secondary and higher
school level were more infected with HPV in HIV-
women (56.0%) compared to HIV+ women (36,
7%). Clearly, in HIV+ women, the history of
gynaecological infection was associated with HPV
infection (62.1%) while in HIV- women it was quite
the opposite (37.3%).
Conclusion
Women infected with HIV are much more infected
with HPV than women who are not infected with
HIV. As a special population, these women are at
increased risk of cervical cancer. The overall risk of
co-morbidities will increase with the aging of the
HIV positive population favoured by the
effectiveness of treatment. Prevention of cervical
cancer, therefore, include the implementation of an
effective vaccine against HPV in HIV positive
children, extending the screening program for
cervical cancer, early diagnosis and treatment of
precancerous and cancerous cervix lesions.
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