Table of Contents

2.1 CERVICAL CYTOLOGY: AN OVERVIEW..............................................................................................2

2.1.1 A Brief History:.........................................................................................................................2
2.1.2 Visual Testing With Acetic Acid:...............................................................................................3
2.1.3 Purposes:.................................................................................................................................4
2.2 CERVICAL CANCER:..........................................................................................................................5
2.2.1 Causes and Risk Factors:..........................................................................................................5
2.2.2 HPV and Cervical Cancer:.........................................................................................................5
2.2.2.1 Immunology of HPV Induced Cervical Cancer:.....................................................................6
2.2.3 Treatment:...............................................................................................................................8
2.2.4 Statistics and Incidence:...........................................................................................................9
2.2.5 Access to Health Care and Socio-Political Factors:.................................................................10
2.3 CONCLUSION.................................................................................................................................11
REFERENCES..............................................................................................................................................13
2.1 CERVICAL CYTOLOGY: AN OVERVIEW..............................................................................................2
2.1.1 A Brief History:.........................................................................................................................2
2.1.2 Purposes:.................................................................................................................................3
2.2 CERVICAL CANCER:..........................................................................................................................4
2.2.1 Causes and Risk Factors:..........................................................................................................4
2.2.2 HPV and Cervical Cancer:.........................................................................................................4
2.2.2.1 Immunology of HPV Induced Cervical Cancer:.....................................................................5
2.2.3 Treatment:...............................................................................................................................7
2.2.4 Statistics and Incidence:...........................................................................................................8
2.2.5 Access to Health Care and Socio-Political Factors:...................................................................9
2.3 CONCLUSION:................................................................................................................................10
REFERENCES..............................................................................................................................................12
 2.1 CERVICAL CYTOLOGY: AN OVERVIEW

The cervix is a fibrous and bulbous organ with which lies between the upper and lower
reproductive tract and serves important structural and functional purposes for the uterus
specifically and the female reproductive system generally with regards to gestation, and as a
selective buffer between the “sterile endometrial cavity and the bacteria-laden vagina by
preventing the passage of bacteria yet allowing the optimal passage of spermatozoa into the
upper genital tract” for reproductive purposes. [CITATION Jua \l 1033 ].By reason of this peculiar
situation and relevance to sexual and reproductive activities, most pathologies that affect the
cervix arise as a result of sexually transmitted diseases. The detection of these diseases and
pathologies of the cervix which involve inspection of smears (specimens) of mucosal and/or
histological matter under a microscope to check for abnormalities in the normal cellular
composition of the squamous epithelia or the mucosal lining of the cervix is called cervical
cytology.

2.1.1 A Brief History:

After years of a systematic study of vaginal smears from volunteers in New York Women’s
Hospital on the effects of ovarian hormones on the epithelial lining of the female genital tract, in
1928, Dr George Papanicolaou, a Greek anatomist, reported the existence of cancer cells in the
vaginal secretions of women with cervical cancer. He described a non-invasive technique of
gathering cellular matter from the linings of the vagina and placing them on a slide for
microscopic inspection as a way to identify incidences of cervical cancer – a technique he had
been carrying out in the hospital since 1925[ CITATION Vil98 \l 1033 ]. This was a low-cost and
relatively easy screening test for the early cytological detection of cervical cancer that would
come to be known as the Pap smear test. Clinical trials in collaboration with Herbert Traut would
show that through this technique, a significant number of asymptomatic and unsuspicious cases
of cervical cancer could be identified in their very early stages [ CITATION Pap41 \l 1033 ].

The conventional Pap smear approach to cervical cytology which involves directly smearing
samples onto a microscope slide and then fixing them using alcohol, or a spray fixative proved to
be an effective method and was established as the standard screening test for cervical cancer and
premalignant lesions in 1941 and endorsed by the American Cancer Society in 1957 [CITATION
Bre79 \l 1033 ]. The widespread use of the test resulted in dramatic reduction in cancer incidence
and mortality in different countries. [ CITATION Joh78 \l 1033 ] reported a 50% reduction in
Finland, Sweden and Iceland in two decades, while according to [ CITATION Har02 \l 1033 ] and
[ CITATION Ame21 \l 1033 ], the US has seen more than a 100% reduction since the 1950s. More
recently, the pap smear has been shown to reduce the incidence of deaths from cervical cancer by
as much as 80% when it is combined with regular screening and medical follow-up [CITATION a10
\l 1033 ]. In 1988, relevant terminologies for reporting on premalignant cervical cytology was
codified as the Bethesda system for Reporting Cervical and Vaginal Cytologic Diagnoses
[ CITATION Nay17 \l 1033 ]. This system has proven relevant in facilitating smooth communication
between laboratories and the providers of healthcare services, research into the science of
cervical pathologies, and data homogenization. Over the years, the resulting increase in
understanding of the molecular pathogenesis of cervical squamous carcinoma has provided a
standardized biomarker of risk that has proven relevant in defining effective therapeutic
approaches.

Despite the effectiveness of the Pap smear, there were certain limitations to its technology. It
reported false negatives of about 14 – 33% most of which were due to problems with sampling
[ CITATION Har02 \l 1033 ] , had unsatisfactory smears of up to 7.1% [ CITATION Pan18 \l 1033 ], and
showed lower sensitivity and specificity. In addition to this, increased awareness of “lax lab
practices” in the conduction of pap smears [CITATION Bod87 \l 1033 ], resulted in calls for
improvements which prompted research into the automation of cytological screening. According
to [ CITATION Bib08 \l 1033 ], due to its requirement of a screening method which would depend on
representative samplings of a monolayer of well-stained and well preserved cells on standardized
slides. The automation of cytological screening led to the development of liquid based cytology
with its attendant benefits such as greater fixation, better preservation of specimens for further
research, greater specimen adequacy, removal of obscurant substances from the specimen and
better HSIL detection. Liquid Based Cytology involves the suspension of sample in a fixative by
stirring the spatula used in specimen collection in the fixative solution [ CITATION Har02 \l 1033 ].
According to [CITATION McI \l 1033 ] the existence of High-Grade Squamous Intraepithelial
Lesions (HSIL), which are indicative of Cervical Intraepithelial Neoplasia (CIN) or Carcinoma
in situ, increases the probability of cervical cancer by 20%, it follows that increased detection of
HSIL would see significant reduction in the incidence of female cancer [ CITATION Gib11 \l 1033 ].
2.1.2 Visual Testing With Acetic Acid:
While the Pap Smear Test happens to be the more popular approach to testing for cervical
cancer, one major criticism of it is the fact of its expensiveness both by itself and in its corollary
infrastructural requirements such as: laboratory facilities, transportation and tracking systems for
specimens, trained cytopathologists, trained cytotechnologists, costs, the multiple follow-up
visits required, and the necessary oversight and synergistic efforts required for a national
healthcare system to provide the efficient services and tracking of women with abnormal
cytology [ CITATION Bis95 \l 1033 ], [CITATION Flo \l 1033 ]. All these combined make the Pap smear
test a “non-ideal screening tool.” [ CITATION Bea14 \l 1033 ] . Its cost ineffectiveness makes it
difficult to establish as a standard approach to cervical cancer screening in low-income countries.
This prompted research into alternative screening methods for cervical cancer, and one of the
consequences of this has been the emergence of the Visual Inspection with Acetic Acid test
among others. The Visual Inspection with Acid Test (VIA) has shown great promise in cross-
sectional studies into its efficacy.
VIA is the simplest and the least expensive screening test of all the available Cervical screening
tests. Its functionality is dependent on observations of Cervical Intraepithelial Neoplasia under
laboratory conditions. When vinegar or 5% acetic acid is applied to the cervical epithelium, any
pre-cancerous lesions that are present on it turn white. In other words, they are acetowhite. The
normal cervical epithelium is pink in colour, so the presence of CIN lesions will be prominent
upon the application of acetic acid.
The procedure for VIA goes thus: a speculum examination is conducted to visualise the cervix,
and then vinegar is applied to the cervix. Women that exhibit acetowhitening (the presence of
lesions) are classed as screen positive, women without acetowhite lesions are classed either as
screen negative or as suspicious for invasive cancer (if it happens that ulcerated, necrotic or
exophytic lesions are observed on the epithelial lining of the cervix).
Its performance has been evaluated in many studies across localities and some promising results
have been made. A meta-analysis of VIA studies conducted by [ CITATION Sau11 \l 1033 ] assessed
the efficacy of VIA on the basis of different factors including patient population. It reported VIA
sensitivity for CIN2+ at 80%, 92% specificity a PPV of 10% and NPV of 99%. Sauvaget, et al,
concluded that “…VIA is a simple, low-cost, and efficient alternative to cytologic testing in low-
resource areas.”

2.1.3 Purposes:

Cervical cytology is primarily aimed at preventing the development of invasive cancer of the
cervix through early detection of HSIL indicative of precancerous lesions known as cervical
intraepithelial Neoplasia (CIN) or carcinoma in situ in the cervix, which is usually asymptomatic
and only discovered through screening. The discovery of precancerous lesions is usually
followed with a conservative treatment by local ablation or surgical excision of the identified
lesions thereby significantly reducing the risk of progression of CIN to invasive cancer.

The results of cervical cytology tests should not be relied on to justify definitive diagnoses or
initiation of treatment. Instead, observations from cervical screening only serve to assess vaginal
specimens for cellular abnormalities that are indicative of an increased risk for the development
of cancer. It helps clinicians to select those women who should be eligible for further evaluation
such as colposcopy and/or biopsy. Approximately 7 to 10 percent of women who are screened
require additional evaluation [ CITATION Jon00 \l 1033 ] and then treatment decisions are made
dependent on diagnostic results of a histological examination, usually from biopsies and/or
colposcopy.

2.2 CERVICAL CANCER:

Cervical cancer (also called invasive cervical carcinoma) is a cancer that arises from the cervix
due to the abnormal growth of cells that have the ability to invade or spread to other parts of the
body. It progresses from its asymptomatic early stages [ CITATION Kum07 \l 1033 ] to latter stages
that may be expressed through symptoms such as vaginal discharges, abnormal vaginal bleeding
(especially after sexual intercourse), pain during sexual intercourse and/or pelvic pain, loss of
appetite, fatigue, back pain, swollen legs, leakage of urine (or faeces) from the vagina. In its
advanced stages, the cancer may also have metastasised to other different organs like the
abdomen, lungs or elsewhere[ CITATION Che16 \l 1033 ]. It is one of the few tumours that develop
from well-defined precancerous, premalignant lesions that can be treated in early stages
[CITATION Pia \l 1033 ]. Cervical screening using either Liquid-Based Cytology or the Pap Smear
Test (and high-risk HPV co-testing as appropriate) is the standard screening test for cervical
cancer and precancerous cervical lesions. These tests enable early detection, thereby increasing
chances of survival by as much as 91%.

2.2.1 Causes and Risk Factors:

A number of studies have adduced and proven the influence of certain risk factors in the
development of cervical cancer or its precursor lesions, such as age at first sexual activity,
multiple sexual partners, lower socioeconomic status, multiparity, cigarette smoking, oral
contraceptive use, and immunosuppression [CITATION SLa \l 1033 ][CITATION Kie99 \l 1033 ]
[CITATION Kie38 \l 1033 ]. Their effect has been to push forward the idea of cervical cancer as a
sexually transmitted disease. In addition to this, [ CITATION Cam85 \l 1033 ], [ CITATION Bri92 \l
1033 ] and [CITATION Cas03 \l 1033 ] showed that the sexual history of the male sexual partner is
relevant in determining the woman’s risk levels for the development of cervical cancer thereby
implying the existence of a transmissible agent as responsible (at least partly) for the
development of cervical cancer or its precursor lesions. In two large PCR based studies, it was
demonstrated that when adjusted for the effect of HPV, none of the standard sexual risk factors
were independently responsible for cervical cancer [ CITATION Pen91 \l 1033 ] , [CITATION Bos92 \l
1033 ]. The inference from this being that, the influence of these sexual risk factors in this regard
can only be said to be only to the extent that they increase the risk of or facilitate the
transmission of HPV.

2.2.2 HPV and Cervical Cancer:

HPV is a double-stranded, free DNA virus and member of the Papovaviridae family. To date,
about 170 HPV genotypes have been identified and numbered sequentially although, due to
different classification standards, some researchers put this number at 200 [ CITATION deV13 \l
1033 ]. More than 40 types are spread through sexual contact [ CITATION Mar08 \l 1033 ],
[ CITATION CDC15 \l 1033 ], and of these, there are 15 recognised as high-risk (cancer causing)
genital serotypes viz.: types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73 and 82
[ CITATION Ghi15 \l 1033 ]. According to [ CITATION CDC15 \l 1033 ] , any sexually active person is at
risk of a HPV infection. These cancer causing types have also been strongly associated with
anogenital cancers (especially invasive cervical carcinoma) and their related precursor lesions
(also known by other names such as: (dyskaryosis, dysplasia, intraepithelial neoplasia,
squamous intraepithelial lesion)) [ CITATION Hae13 \l 1033 ] [ CITATION Sch09 \l 1033 ], and the
available evidence strongly supports the proposition that invasive cervical cancer is usually
preceded by a pre-invasive phase[ CITATION Jua \l 1033 ]. Cancerous HPV infects the cervix by
entering basal cells, or immature squamous metaplastic cells at the Squamocolumnar Junction
(SCJ), integrating itself with the host cell genome by a covalent binding of viral genome with
host DNA at fragile sites in the human DNA where the strand is prone to breakage [ CITATION
Ara19 \l 1033 ] resulting in an expression of viral genes in the cells [ CITATION Par21 \l 1033 ] .
These are expressed both as atypical cellular matter in the cervix observable under a microscope,
and as resulting observable histological lesions identifiable through clinical colposcopy.
The majority of HPV infections are usually benign and show no symptoms; and retrospective
studies indicate that more than more than 90% of infections are resolved spontaneously and
without further consequences within 12 to 24 months post infection [ CITATION deS18 \l 1033 ] .
However, persistent infection with HPV types 16 or 18 carry a 40% risk of progression to pre-
cancer [ CITATION Sch01 \l 1033 ] and if left untreated, invasive cervical cancer [ CITATION Doo12 \l
1033 ]. According to a meta-analysis of records on 30,848 invasive cervical cancers worldwide
conducted by [ CITATION LiN11 \l 1033 ](Li, et al., 2011), HPV type 16 is the most prevalent type
detected in HPV-associated cancers (56%), followed by HPV type 18 (16%). It was concluded
that HPV 16 and 18 cause about 70% of cervical cancers worldwide confirming an initial study
by ([ CITATION Bos08 \l 1033 ]. In addition to these, the body of evidence from multiple studies
show that HPV infection is the primary cause of 90 – 100% of all cases of cervical cancer
[ CITATION Bos95 \l 1033 ], [CITATION Wal99 \l 1033 ], [ CITATION Bos02 \l 1033 ]. Anogenital HPV
are also associated with cancers of the anus, penis, vagina and vulva, as well as a growing
number of head and neck cancers.

2.2.2.1 Immunology of HPV Induced Cervical Cancer:

Available body of evidence reveals the role of the immune system in preventing cancer by,
among other ways, fighting the infections that cause cancer. Viruses are responsible for a
significant portion of the global cancer burden, causing an estimated 15% of all human cancers
worldwide [ CITATION zur91 \l 1033 ]. Viruses contribute to the aetiology of human tumours in
different ways, such as: by inducing immunosuppression, by inducing increased expression of
oncoproteins, etc. [ CITATION zur91 \l 1033 ] . Both DNA and RNA viruses share this
responsibility. Developments in the study of cancer immunology show the important role of the
body’s immune system in preventing cancer or eliminating cancer cells by a process called
immunosurveillance.
As has already been observed, due to the workings of the immune system, a vast majority of
HPV infections are resolved without complications within two years of infection. Effective
immunity from HPV consists of a Cell Mediated Response at the early stages of infection.
However, virological assessments of the Human Papillomavirus reveal it to be a “poor natural
immunogen” (i.e. very successful infectious agents) for many reasons. First, it is a double
stranded DNA virus which lacks an RNA intermediate. This enables it to avoid the body’s innate
immune response against foreign RNA. Secondly, the major instances of viral replication occurs
in superficial epithelial cells where the body’s immune system has limited reach. In the words of
[ CITATION Fra04 \l 1033 ], “there is little to no systemic viremia” because viral activity occurs in
mucosal cells, far from vascular and lymphoid channels; most encoded nucleoproteins are not
expressed or secreted; and HPV is non-cytolitic. This means that a failure to mount an effective
Cell Mediated Immune (CMI) response to clear or restrict infection results in persistent infection,
and for oncogenic HPVs, higher chances of cervical cancer. This prolonged duration of infection
has been associated with successive evasion of the immune system thus facilitating viral
persistence and increasing the probability of progression to cancer.
From the aforementioned, an inference may be drawn that a person who is immunocompromised
would be less able to mount an effective cell mediated immune responses against an HPV
infection. As is known, prolonged infection with HIV/AIDS interferes with the body’s immune
system and severely truncates its ability to effectively ward off diseases and infections. HIV
specifically targets and destroys certain cells of the immune system, such as the CD4+ T cells,
macrophages, and dendritic cells [ CITATION Cun10 \l 1033 ]. The consequent reduction of CD4+ T
cells below a critical level (immunosuppression) results in loss of cell-mediated immunity, thus
making the body more susceptible to opportunistic infections that could result in AIDS.

Data from multiple studies of adult HIV-positive men and women reveal a relationship between
immunosuppression (as measured by CD4+ levels less than 500/mm3) and increased prevalence
of cervical and anal HPV infections with many others showing even higher risks for those with
CD4+ levels ,200/mm3. The relationship between CD4+ counts and the amount of HPV DNA
found in their anogenital areas have been shown to be inverse such that the lower the CD4+
levels, the higher the DNA quantity [ CITATION Sun97 \l 1033 ] [ CITATION Pal01 \l 1033 ]. Not only
that, lower CD4+ levels also accounted for multiple infection with a wider spectrum of different
HPV types. [ CITATION Pal03 \l 1033 ] analysed different studies into the interactions between
introduction of Highly Active Anti-Retroviral Therapy (HAART) in HIV-positive patients and
the progression of high-grade HPV infections, they conclude that, according to the data, HAART
neither induces a regression of a high-grade infection, nor prevents the progression from high-
grade disease to cancer. The interpretation offered was that immunocompromise was only
relevant to initial stages of high-risk HPV infection, and that “once a particular level of disease
has been reached, ‘reconstitution’ of immune response may be of little value”. But this however
somewhat contradicts previous findings of [ CITATION Pet94 \l 1033 ] whose study examining 48
HIV-infected women and 52 allograft recipients over a 3 year period resulted in findings of a
significant positive correlation between the grade of the lesions and the amount of HPV DNA,
and of progressive lesions in all patients with CD4+ less than 400/mm 3. They concluded that
“malfunction of the cellular immune response following either HIV induced depletion or
iatrogenic inhibition of CD4-lymphocyte activation enhances the progression of HPV-induced
cervical lesions to malignancy.) Petry’s findings are supported by two latter studies with even
larger samples. The first is a study by, Frisch, et al., with a larger sample of 309,365 US patients
with HIV infection/AIDS over a period of 10 years (5 years before the date of AIDs onset to 5
years after). Frisch reported findings that “all HPV-associated cancers in AIDS patients occurred
in statistically significant excess compared with expected numbers of cancers” for the general
population. The findings supported a conclusion that “HPV-associated malignancies occur at
increased rates in persons with HIV/AIDS” with the most significantly increased risks for
precancerous lesions and invasive cancers in the cervix [ CITATION Fri00 \l 1033 ]. Another study
relying on data from an even bigger sample of 499,230 individuals diagnosed with AIDS over an
even longer period of time (from January 1, 1980 through December 31, 2004) was conducted by
[CITATION Cha \l 1033 ]. An evaluation of the connection between immunosuppression (by
measure of CD4+ count) and the risk of invasive HPV related cancers compared with that of the
general population yielded an observation of “statistically significantly elevated risk of all HPV
in situ…and invasive…cancers”. The authors concluded that “risk of HPV associated cancers
was elevated among persons with AIDS and increased with increasing immunosuppression”.

2.2.3 Treatment:
Given the already established links between anogenital HPV infections and the development of
HSIL, Low-grade squamous intraepithelial lesions (LSIL), squamous cell carcinoma, and
adenocarcinoma in women, therapeutic and prophylactic actions against these situations would
necessarily be mostly directed towards addressing and preventing HPV infections as root causes.
One such treatment option has been the development and introduction of vaccines in order to
activate and improve the body’s immunity against HPV.
The Human Papillomavirus has evolved an assortment of mechanisms (active and passive) to
evade the immune system and confound attempts by the body to generate a sufficient HPV
directed immune response. The host becomes HPV antigen tolerant, and defences become
compromised thereby facilitating viral persistence and progression towards cancer [ CITATION
del15 \l 1033 ]. The function of vaccines is to trigger adaptive immune resistance by triggering
seroconversion. The very high antibody titre that results is then transuded to the epithelial lining
thereby offering protection from the infections present there [ CITATION Mar08 \l 1033 ] . The
development of HPV vaccines build on the work of Shope, the founding father of papillomavirus
research. He conducted experiments with rabbits which were systemically infected with the
cotton tail rabbit papillomavirus (CPRV) by direct injection into the bloodstream. The rabbits
generated neutralising antibodies, and papillomas did not arise on their skins. They were also
totally resistant to viral infections of the epithelium [ CITATION Sho37 \l 1033 ]. This research
showed that vaccines which induce high concentrations of antibodies would be effective
protection against HPV. Different analysis and of infection induced immunity versus vaccine
induced immunity show significantly higher antibody levels for vaccinated persons and “modest
protection against subsequent cervical HPV infection in female subjects” through natural
infection [ CITATION Bea16 \l 1033 ] while some other studies suggest that natural infection
induced antibodies may not provide complete or sufficient protection against HPV over time.
[ CITATION Wan04 \l 1033 ] show that recurring HPV type specific natural infections occur equally
in in women after a period of 5-7 years, notwithstanding their type specific serostatus. A
subsequent study by [ CITATION Fer08 \l 1033 ] into the effectiveness of vaccine showed that the
placebo group (women with natural immunity against HPV) developed new infections despite
having naturally induced antibodies to the infecting HPV types”. This study was subsequently
confirmed by the WHO which stared that host antibodies “…do not necessarily protect against
subsequent infection by the same HPV genotype”[ CITATION WHO09 \l 1033 ].

2.2.4 Statistics and Incidence:

Lower income countries account for almost 85% of the world’s 570,000 yearly cases of cervical
cancer and almost 90% of the 311,000 annual deaths [ CITATION Arb20 \l 1033 ]. Cervical Cancer
is the second most occurring cancer among women in Nigeria and in West Africa. In 2018, there
was an observed 31,995 new cases of cervical cancer in West Africa with almost 50% (14,943)
of these cases occurring in Nigeria [CITATION Bru \l 1033 ] . In the same year, Nigeria also saw
10,403 deaths from cervical cancer, of the 23,529 deaths in West Africa. In spite of these dismal
statistics and the dangerous forecasts regarding incidences and mortalities for cervical cancer,
only 8.7% of Nigerian women had a pap smear in 2018. Due to a combination of factors such as
absence of information, poor access to healthcare services, the financial barriers, shortage of
health facilities and workers, poor management and planning, and inequities in resource
distribution, most cases are diagnosed at their advanced stages with the result that treatment
options are limited, and the odds of survival severely truncated [CITATION Mor13 \l 1033 ]. A
descriptive cross-sectional study of women of reproductive age in a slum area of Lagos state,
Nigeria revealed a widespread ignorance of cervical cancer and related concepts amongst
women, not due to unwillingness (89% reported a willingness to undergo screening while 93%
were willing to take HPV vaccines and recommend to a friend or relative), but due to
socioeconomic factors beyond their control [CITATION k \l 1033 ]. In Mexico [ CITATION Kna09 \l
1033 ] and Zambia [ CITATION Mwa11 \l 1033 ] programs for the integration of cervical cancer
educational and screening services into pre-existing delivery platforms for sexual and
reproductive health services showed great success in improving access to screening services
thereby dramatically reducing the morbidity and mortality.
Since its discovery in the 1980s, HIV/AIDS has posed a serious public health challenge to
persons and societies across the globe. The speedy spread of infection has also served to make it
an epidemic that should not be taken too lightly for its implications on the public health situation
in any country. [ CITATION UNA20 \l 1033 ] estimates that there are over 37.7 million people living
with HIV in the world. Women constitute approximately half of all people living with HIV, but
in sub-Saharan Africa, which bears a disproportionately high burden of people living with HIV
(67% of global HIV population) and of global new infections at 75.4% of estimated 1.5 million
global new infections, adolescent girls and young women aged 15 to 24 years have HIV
prevalence rates at up to eight times more than men in similar age group [ CITATION Del15 \l
1033 ]. Per [ CITATION UNA20 \l 1033 ], six in seven new HIV infections among adolescents in sub-
Saharan Africa are among girls, young women aged 15-24 years are twice as likely to be living
with HIV than men and women and girls accounted for 63% of all new infections in the region in
2020. A similar trend holds sway in Nigeria wherein the prevalence of HIV infection in the
country is higher for females than males across all age groups. HIV prevalence among women in
Nigeria aged 15 to 64 is 1.9% and 1.1% for men aged 15-64 and 0.9% for men aged 15-49 years
[ CITATION UNA21 \l 1033 ] . In Nigeria, an estimated 1.8 million people are living with HIV/AIDS
with a prevalence rate of 1.4% in 2021, down from 3.8% in 2015 [ CITATION UNA21 \l 1033 ]. In
Nigeria, the south-south region has the highest HIV prevalence rate at 3.1% and Rivers state has
a prevalence rate of 3.8% with over 200,000 people living with HIV. For women in Rivers state,
the figures are even direr as the prevalence rate is 4.7% [CITATION Fed19 \l 1033 ]. The implication
is that a large number of these women are at high risk of HPV infections and then cancer.

Right from the start of the AIDS pandemic, the United States Centre for Disease Control (CDC)
has classified cervical cancer as an AIDS-defining illness[ CITATION Mbu11 \l 1033 ]. The
reasons are not far-fetched. While HPV infections are very common in the general population,
and most women with healthy immune systems will clear these infections over time, the
repression of the immune system as a result of a HIV infection makes it far less likely or even
impossible for infected persons to clear an HPV infection. Women living with HIV therefore
have an increased chance of developing pre-invasive lesions (up to five times) that can, if left
untreated, progress rapidly to invasive and life-threatening cervical cancer [ CITATION
UNA16 \l 1033 ]. [ CITATION Aka13 \l 1033 ] showed that women living with HIV in Nigeria
had higher rates of HPV infection and were more likely to be not only infected with high-risk
HPV, but also with multiple HPV strains and significantly higher viral loads than the general
population of HPV infected patients. [ CITATION van14 \l 1033 ] confirmed similar findings
with a wider population sample of both men and women living with HIV. In two large
prospective studies, reviewed by [ CITATION Sil02 \l 1033 ] – HIV Epidemiology Research
Study (HERS) and the Women’s Interagency HIV Study (WIHS) – the prevalence of a HPV
infection, particularly with types 6 or 11 was 3.6 times (HERS) or 5.6 times (WIHS) higher than
among the control groups of HIV-negative women.

2.2.5 Access to Health Care and Socio-Political Factors:

While it is true that the incidence of HPV, HIV and associated issues like viral suppression are
quite improved from their dire situations years before, the distorted statistics show that women
and young girls still bear a disproportionate burden in this regard. The benefits of improved
access to testing and treatment do not have as much effects as would be intended especially for
women. A combination of factors – social, cultural and political – pose a clog in the wheel of
progress towards adequate responses to these problems [ CITATION UNA16 \l 1033 ]. If there
must be advancements in this regard, then comprehensive approaches to addressing the problems
must be undertaken. WHO recommends certain programs such as: Health education
(encompassing comprehensive education on sex and sexuality as are age appropriate) and
effective social awareness programs regarding HPV, HIV and Cervical Cancer; wide reaching
HPV vaccination programs for adolescent girls with information and counseling as required and
appropriate; mass screening programs for cervical cancer offered at cheap or at relatively
affordable rates considering social and economic situations of the population; integrating HIV
counselling, testing and treatment agenda, HPV vaccination and cervical cancer screening
programs with other sexual & reproductive health services as has been done in places like India
[CITATION Par14 \l 1033 ] and Zambia [ CITATION Bin13 \l 1033 ]; ensuring access to
therapy when required and making them free or affordable; facilitating research into both the
science of health issues and social studies into peculiar social influences and factors affecting
disease transmission within the country in order to enable policy makers to put forth informed,
evidence-based policies; developing national programs dedicated to planning, monitoring and
delivering on the healthcare requirements of citizens [ CITATION Din07 \l 1033 ], [ CITATION
Bin13 \l 1033 ].

2.3 CONCLUSION:

Since the introduction of cytologic screening for cervical cancer using the Papanicolaou (Pap)
test in the 1950s, and subsequent developments in the realm of women sexual and reproductive
health, the incidence of invasive cervical cancer across the world has fallen significantly. And
this reduction has occurred despite an increase in the risk factors for cervical cancer, such as
younger age at initiation of sexual intercourse, increased number of sexual partners in a lifetime,
and the consequent greater prevalence of human papilloma virus (HPV) infection and cigarette
smoking. Initial exposure to HPV is marked by sexual debut. Even a singular engagement in
sexual intercourse increases a person’s risks for infection by significant degrees, with per-coital
transmission rates appraised at 40% [ CITATION Bur06 \l 1033 ] . Approximately half of all men and
women who are sexually active will be infected with HPV at least once during the course of their
lives, some even repeatedly. HPV is one of the most common venereal diseases transmitted
sexually. Testing for HPV DNA has been found to be more sensitive than cytologic screening for
detecting HSIL, but it is less specific than conventional and liquid-based cytology [ CITATION
May07 \l 1033 ](Mayrand, et al., 2007), [ CITATION Ron10 \l 1033 ] (Ronco, et al., 2010). So current
intimations of cervical screening procedure usually incorporates both cervical cytology and HPV
testing on initial examination as a way to determine risks for CIN. The success of prevention
efforts can be relied on to justify three inferences: (a) that the progression from early cellular
abnormalities (low-grade dysplasia), to more severe and dangerous HSIL, to carcinoma in situ
and then invasive cancer is generally slow, and therefore allows sufficient time for detection; (b)
relevant cellular abnormalities can be identified with high level of confidence; (c) that effective
treatment is available for premalignant lesions. From these, it is to be concluded that invasive
squamous cell carcinoma of the uterine cervix is a highly preventable disease

Most people who get infected with HPV will have the disease cleared by the workings of their
immune systems within 12-24 months post infection. However, an infection with HIV makes it
difficult for the immune system to clear infections. Coupled with the poor immunogenic
properties of HPV, the prospects for natural immune resolution of the infections become
extremely unlikely. Young women and girls, who are both more likely to be infected with HPV
and have higher HIV prevalence rates than their male counterparts. In the words of Michel
Sidibe, former executive director of UNAIDS, “this [HIV] epidemic unfortunately remains an
epidemic of women”. This disparity is also reflected in Nigeria’s HIV statistics, thus marking
women and girls out as being at seriously high risks for cervical cancer. A complex interplay of
biology, gender disparities and social, political and economic factors contribute to the heightened
vulnerability of young women. Such problems as lack of access to healthcare services, especially
reproductive health services for women; discrimination, as studies show that social factors
preclude young unmarried women from accessing needed contraception thus exposing them to
higher risks of STDs [ CITATION And13 \l 1033 ]; lack of legal rights to make decisions for their
own health, as evidence from sub-Saharan Africa shows that 52% of women in rural areas, and
47% in urban areas are not legally or socially allowed to make decisions about their own health
[CITATION UNA19 \l 1033 ]; poor education, whether general or specific healthcare education.
Studies show a positive correlation between higher educational achievement among women and
girls and better sexual reproductive health results [CITATION UNA19 \l 1033 ] [ CITATION DeN15 \l
1033 ]; poverty; sex trafficking and exploitation; and gender based violence;
The solutions to these problems are not only medical, but will require a holistic combination of
social, economic and political programmes and cooperation between the institutions, public and
private, geared towards improving the wellbeing of women and girls in society.
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