South African HPV Advisory Board

back »

New in South Africa:
Roche Diagnostics announces the formation of a
Woman’s Health Advisory Board

for the advancement of women's health by assessing information and issuing guidelines through its

South African HPV Advisory Board

that was formed as a partnership between SASOG and Roche Diagnostics with input from other interested parties.

Woman's Health Advisory Board

South African HPV Advisory Board

Report of a meeting held at Kloofzicht on 12-14 August 2005

 

The Board

This Board was convened by Roche Diagnostics, in partnership with the South African Society of Obstetricians and Gynaecologists (SASOG), as part of the Roche Women's Health Project. The Board consists of senior members of SASOG with a special interest in gynaecological oncology and who are considered to be opinion leaders in the field, a senior clinical pathologist and a senior microbiologist who is an expert in the field of sexually transmitted infections.

 

The Board is an independent body and is separate from the sponsoring company. No company employee is a members of the Board or has influenced the recommendations made by the Board. No members of the Board declared any conflict of interest or are employed by the company.

 

The objectives of the Board are:

 

To develop recommendations for the use of human papilloma virus (HPV) testing and to revise these on an ongoing basis

To stimulate and support research on HPV and cervical cancer in South Africa
To enter and participate in discussion forums on the policy and implementation of national cervical screening, and
To develop and implement educational strategies on HPV and cervical cancer.
The opinions and recommendations of the Board expressed in this document do not reflect the policy of the company or the opinion of any individual board member. It is the result of a critical assessment and discussion of literature by the Board members. In the development of the recommendations and the “Patient Information Leaflet” the Board used published research data including conference proceedings and recommendations from the website of the Association of Reproductive Health Practitioners (www.arhp.org).
This report is intended and presented as summarized information and advice for health care providers and managers, interpreted with South African conditions in mind, on which to base clinical decision making without it being prescriptive or a legally binding document. These opinions and recommendations are not intended to be final and will be revised on a continuous basis.

Members of the health profession and health care managers are invited to comment on the contents of this document. All feedback on these recommendations will be appreciated and will be used during the process of revision. Comments can be addressed to:

The Chairperson
South African HPV Advisory Board
C/o Dept Obstetrics and Gynaecology
PO Box 667
Pretoria
0001
e-mail : glindequ@medic.up.ac.za

CERVICAL CANCER AND HUMAN PAPILLOMA VIRUS:

Introduction

Cervical carcinoma is still the most common cancer of women on the African continent. Mortality remains high - worldwide at 50% - mainly because of late presentation, advanced stage of disease and absence of a functioning screening process. The aetiological link between human papilloma virus (HPV) infection and cervical cancer has been well established and a number of high-risk HPV genotypes have been identified. HPV infection is the most common sexually transmitted infection (STI) in the world today – up to 80% of sexually active females will harbour HPV at some point in their lives. The majority of women will experience natural elimination of HPV infection because of an intact immune system. Persistent infection with a high risk type HPV puts women at high risk to develop precursors of cervical cancer or carcinoma itself. As part of a public health response to this serious problem several HPV vaccines are under development. Use of vaccines still poses unanswered questions in many respects.

 

The precursors of cervical cancer can be detected and treated. The most important aspect of detection is screening of asymptomatic women. The Pap smear is generally used for this purpose. If this is used with wide coverage in a population Pap smear screening has been shown to lead to a drastic reduction in the occurrence of cervical cancer in that population.

 

As more information becomes available about HPV and as tests for accurate detection of HPV have been developed much of current discussion on cervical cancer and its precursors should centre on HPV, the role of HPV testing and the clinical use of these tests in South Africa .

 

Screening for cervical cancer

1. Objectives of screening

    

   Screening programmes aim to reduce mortality and morbidity from cervical cancer and to decrease the number of patients suffering from cervical cancer. Through screening the existence of precursor lesions of the cervix can be detected and managed. Basic screening programmes can lead to downstaging of cervical cancer which offers benefit for patients in its own right.

    

2. Current status of cervical screening in South Africa

    

   The National Policy on cervical screening allows for 3 smears in a woman's lifetime taken at 10 year intervals from 30 years of age. This policy has been implemented in some areas but not throughout the country. The National Health Laboratory Service where cytology laboratories in the public sector are to be found has not fully rolled out a programme to become a part of the process. Several initiatives for screening are starting or are in the planning stage: this includes initiatives from the National Department of Health, its Directorate of Maternal and Child Health and some provincial Health Departments. Over the years several proposals for screening made by academics and professional societies were rejected by policy making authorities, frequently on the basis of perceived high cost. The result is that currently there is no population wide screening programme in South Africa . In several areas partial screening does take place. In the private sector opportunistic screening is commonly practiced.

    

3. Current status of cervical screening internationally

    

   In populations where coverage is wide enough to reach more than 70% of women the maximum impact of decreasing the incidence of cervical cancer and cervical cancer deaths becomes apparent and plateaus out at 84% coverage. It is expected that the occurrence of cervical cancer can be reduced by 70% or more under such circumstances. In such programmes the frequent recall of women led to huge cost increases that in turn resulted in curtailment of the programmes in many areas. Current recommendations include that the first Pap smear should be taken at age 21 years or within 3 years of onset of sexual activity. Thereafter smears should be taken annually until age 30 after which smears should be taken every three years, concluding the screening at age 65-70 years for those women who have had persistent normal smears.

    

   In developing countries the objectives are very different. The WHO advocates one smear (at age 30-35 years) in a woman's lifetime as the least to be performed. Never having had a Pap smear remains one of the highest risk factors for the development of cervical cancer.

    

4. Obstacles and ideals

   The Pap smear has a lower than expected sensitivity of only 54%. This is improved when liquid based cytology is used. Cost of a national population based screening programme is a serious obstacle. Lack of capacity, lack of treating facilities and lack of knowledge in the patient population all prove to be huge obstacles. The HIV pandemic is a massive obstacle in several respects.

    

   Ideals for cervical screening in South Africa include the achievement of wide enough coverage of the female population to impact on the health of the women of South Africa, the empowerment of women to expect and indeed demand proper screening programmes to be in place, and improved popular education and awareness. Better knowledge may lead to increased acceptance of screening requirements by women, including acceptance of the need for follow-up visits. The highest ideal is improved sexual health for the population. Other ways of screening should be developed and assessed to overcome the problems and impasse of the current programmes. Capacity for diagnosis and treatment must be increased.

    

HPV and cervical cancer

HPV are mucosotropic DNA viruses that cause most of the malignancies of the anogenital tract. More than 100 HPV genotypes can be defined of which more than 40 infect the anogenital tract.

 

HPV infections are the most common sexually transmitted infections today. Based on research findings of the last two decades the firm conclusion has been reached that infection with a high risk HPV genotype is regarded as the primary cause of cervical cancer. Cervical carcinogenesis involves several cofactors – not all well understood or of equal importance – including cigarette smoking, poor nutrition, folate deficiency, HIV infection, genetic predisposition and the possibility of other genital infections such as with herpes simplex virus.

 

Certain high risk HPV types have been identified relating strongly to cervical carcinogenesis. Types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73 and 82 have been linked to cervical cancer. The virulence of these types differ. Some genotypes have been identified as of intermediate risk namely 23, 53 and 66. The low risk HPV types cause genital warts but not cancer.

 

HPV is easily transmitted but requires entry into the basal layer of the cervical epthelium at sites of micro- or macro-trauma. Most HPV infections are transient and persistent infection with a high-risk type of HPV poses a carcinogenic risk. When the cervix is infected with HPV mild cytological abnormalities are frequently present. Persistence of high risk HPV over time contributes to occurrence of random mutations leading to cervical cancer. Once HPV is integrated into the host genome severe cytological abnormalities are found and the histological diagnosis of cervical intraepithelial neoplasia (CIN) and eventually cervical carcinoma can be expected.

 

The different HPV types have been shown to have different viral persistence, different potential for viral integration and also different carcinogenic potential. The proportions of viral types in cervical cancer specimens therefore do not reflect the incidence of these viruses in the population, but rather their nature. Its is known that HPV type 16 alone causes about two-thirds of all cervical cancers worldwide and it is therefore the main pathogen.

 

Testing for high risk HPV

New assays able to detect high risk HPV DNA have recently been approved and are available for screening and diagnostic use.

1. Different tests

    

   Currently available tests will detect the most common high-risk HPV viruses present in the sample. The different tests have subtle differences regarding the viral types included in the test battery. Commercially available tests in South Africa reflect active infection of the cells with HPV but do not test for viral integration into the genome, which is the carcinogenic event. The presence of HPV is therefore accurately established but not the state of the disease process.

    

   Test results can be reported as either positive or negative for the presence of high risk HPV. Alternatively the list of high- and intermediate risk HPV types found in the sample can be reported. The clinical significance of presence of multiple HPV types or changes in the HPV types over time is not currently known. The list of viruses-type of result does not have any clinical importance or superiority above a simple positive or negative answer but may have useful research implications.

    

2. Sampling methods

    

   HPV-DNA can be isolated from various samples. Physician sampling has been performed over years. Recently patient self-sampling was developed.

   Physician sampling with cervical swab or brush or spatula has been found adequate. It is not imperative to obtain take the sample from the transformation zone and a sample taken from the posterior vaginal fornix or vaginal walls is adequate. Sampling in different areas of the vagina and cervix may render different results and different HPV–types can be found. The prognostic importance and clinical impact of these differences are not currently known.

   Self-collection obviates the need for speculums, examination rooms and trained personnel and will have an important impact on the cost of screening. It has been found to be more acceptable to women than traditional Pap smear testing and the expectation is that this method will improve uptake. This has to be seen as a significant potential advantage. Self-collected samples for cervical cytology markedly decrease the sensitivity of the test unless the device is left inside the vagina for 10 minutes or longer. Some tampons need to be inserted for at least an hour. Vaginal swabs tipped with Dacron can be used with ease and collection with two consecutive brushes render better results than using a single one. Self-collected samples will render good results when DNA based testing is used.

    

   Physician sampling and patient self-sampling have been extensively tested and both have been found to produce satisfactory and comparable results. The reason for this is that PCR (polymerase chain reaction) amplification of DNA makes the test method highly sensitive.

    

3. Transporting samples

    

   Samples can be transported dry or in an essential buffer solution, depending on the sampling method and device used. When liquid based cytology is used, the same liquid used for cytology can be used for HPV testing.

    

4. Costs

    

   The cost elements of HPV testing include the sampling device and transport method, the laboratory and personnel costs and the cost of the test kit used for DNA extraction, PCR and costs to read and report the result. The cost elements of screening also include the cost of the facilities and personnel to do initial sample collection, management of women with abnormal results and all communication between the provider and the patient. It is complicated to calculate the cost of different screening programmes and to compare these, as large differences in collection methods and call back rates exist.

    

   Various authors have calculated cost of HPV based screening and compared it with existing cytology testing. HPV testing as a primary screening method may be cost effective when compared with existing protocols but these analyses are highly situation and protocol specific.

    

   An attempt will be made by the Board to do cost analysis on the three recommended screening protocols (see annexures) and the results will be communicated at a later stage.

    

Clinical uses of HPV testing:

1 Primary screening of a low risk population

High risk HPV testing offers several potential advantages over conventional cervical cytology in the setting of primary screening but also has many limitations.

 

1. High sensitivity

   HPV testing is significantly more sensitive than cytology to predict cervical cancer and its precursors. The sensitivity of the test approaches 100% due to the ability of PCR to detect HPV DNA even when present in minute quantities. This high sensitivity and the long interval between infection and invasive cancer mean that HPV negative woman can safely have a considerably longer screening interval than when using a cytology-based screening programme. The recommended screening interval will differ between countries and will depend to a large extent on available resources. In many countries even a once-in-a-lifetime screening with the much less sensitive cytology test is still to be reached! Most cytology based screening programmes compensate for the low sensitivity of a single test by repeating cytology every three to five years. This strategy leads to a high sensitivity of the screening programme but is expensive to implement.

    

   It is apparent that HPV testing seems to be a much better test to use in any programme with once-in-a-lifetime testing or with long screening intervals (> 5 years). Longer screening intervals are more cost-effective overall.

    

2. Technical aspects HPV testing is a more automated test than cytology. The margin for human error is much smaller as is the need for trained personnel.
3. When is HPV testing not indicated?
   

   Certain subgroups of the population are NOT suited to HPV screening due to a very high prevalence of HPV. This includes women under the age of 30-35 years where HPV has been reported to be present in up to 80% of women and where its presence is mostly transient. In immune compromised women the incidence of HPV is also high but the high negative predictive value can be useful as a triage method.

4. Cost and availability
   
   HPV testing is currently more expensive than cytology and is only available in certain specialized laboratories.
5. Need for education

   A large proportion of women already know about Pap testing, while HPV testing is new. The diagnosis of HPV infection may have a negative psychological impact on the woman. There is also a potential for confusion with HIV in the mind of the patient.

6. Recommendations for HPV testing in primary screening:
   
   The following options for HPV testing as a primary screening test may include:
   Alone as a once-in-a-lifetime test between the age of 35 and 65 years in low resource settings (see Flow diagram A)
   Alone or in combination with cytology in women over the age of 30 years to safely increase screening interval in negative women (see Flow diagram B).

    

2 HPV testing as a management tool

HPV testing is a very good indicator of prognosis in several clinical situations and can therefore successfully be used to triage patients. The absence of high risk HPV accurately predicts a very low risk for cervical carcinoma and absence of this disease for many years to come. This finding can be used to discharge patients from strict follow-up in various clinical circumstances. In a patient after the age of 30 years a finding of negative HPV plus negative cytology is regarded as highly predictive of no CIN lesions or cervical cancer and this patient needs very few screening episodes in her life (the “Super test”).

On the other hand HPV positivity can predict future disease with some accuracy even in patients who are cytologically negative. Persistent HPV strongly correlates with future disease and is an indication for strict follow up or even for treatment.

1. The current role of HPV testing in triage

    

   A Ambiguous or low risk abnormal cervical cytology

   If a patient had a low risk abnormal cytology result, HPV testing can identify those who test HPV negative who can be followed up with a relatively long interval of up to 10 years, and those who test HPV positive who can be offered treatment or close follow-up (see Flow diagram C).

   B Follow-up after treatment for pre-invasive and invasive cervical disease
   

   Women who test positive for HPV during follow-up after LLETZ or similar treatment for CIN lesions have a much increased risk for recurrent disease. Specific follow-up protocols have not been evaluated and most reports refer to the first follow-up visit. The most likely implication is a recommendation for a tight follow-up schedule for HPV positive patients.

2. Immune compromised women

   Women found to be HPV negative can be screened with normal screening intervals, while HPV positive woman must have increased surveillance or treatment.

   The next steps

   1. This Report should be widely circulated to elicit comments
   2. The Board should construct models of costing and then consult with Health Policy experts including persons in the National Department of Health and other governmental structures
   3. The Board will review the report on a continuous basis
   4. The Board will also examine other topics: This may include vulvovaginal condylomata especially in HIV infected women, screening after hysterectomy for precursor disease or after treatment for cervical cancer.
   5. The Board has formed a Research Subcommittee to manage its research efforts. The subcommittee of the Board consists of Prof Greta Dreyer (convenor), Dr Hennie Botha, Dr Mani Moodley and Dr Trudy Smith. This committee will advise on research priorities. National studies with study centres throughout South Africa will be planned. Alternative screening options, HIV and HPV, epidemiological differences in a multiracial South Africa and other meritorious aspects will be addressed.

   Roche Diagnostics may sponsor a visit of a key international opinion leader to South Africa .

   The final report will be widely distributed including communications with family physicians and medical officers.

   Signed on behalf of the Board

   Prof BG Lindeque

   Chair

   
   List of members of the Board

   • Dr Hennie Botha MMed (O&G) FCOG(SD).

   Head: Unit for Gynaecological Oncology, Tygerberg Hospital and Stellenbosch University .
   PO Box 19063 , Tygerberg 7505.
   e-mail: mhbotha@sun.ac.za
   tel: +27 21 938 5696
   fax: +27 21 938 4648

   • Prof Bruno Cooreman MD

   Senior Consultant, Dept Obstetrics and Gynaecology, University of the Free State , Bloemfontein , SA
   e-mail: cooreman@mweb.co.za

   • Prof Greta Dreyer MBChB, MMed(O&G) MCOG(SA)

   Principal specialist, Pretoria Academic Hospital and Adjunct Professor, Dept Obstetrics and Gyanecology, University of Pretoria

   Head of Gynaecologic Oncology Unit
   e-mail: greta.dreyer@mweb.co.za
   tel: +27 12 354 2366/8/9
   fax: +27 12 325 0302
   

   • Prof Franco Guidozzi FCOG(SA) MRCOG

   Chief Specialist and Academic Head: Dept Obstetrics and Gynaecology, University of the Witwatersrand
   e-mail: niewenhuysa@medicine.wits.ac.za
   tel: +27 11 488 4853
   fax: +27 11 643 2572
   

   • Prof Anwar Hoosen MSc, MBChB, MMed (Microbiological Pathology) FCPath(SA)

   Head; Department of Microbiological Pathology, Faculty of Medicine, MEDUNSA Campus, University of Limpopo
   PO Box 211 , MEDUNSA 0204
   e-mail: hoosen@medunsa.ac.za
   tel: +27 12 521 5667
   fax: +27 12 521 5727
   

   • Prof Tony Koller MBBCh, DipMid COG(SA), FRCOG, FOG(SA)

   Adjunct Professor: Department of Obstetrics and Gynaecology, Johannesburg Hospital , School of Clinical Medicine, University of the Witwatersrand, Johannesburg . Consultant Gynaecologist in private practice.
   e-mail: koller@mweb.co.za
   tel: +27 11 485 2210
   fax: +27 11 485 4905
   

   • Prof Gerhard Lindeque MBChB, MMed(O&G), FCOG(SA), MD

   Professor and Head: Dept Obstetrics and Gynaecology, University of Pretoria . President of SASOG
   PO Box 667 , Pretoria 0001
   e-mail: glindequ@medic.up.ac.za
   tel: +27 12 354 2366
   fax: +27 12 329 6258
   

   • Dr Louis Marcus MBChB MMed (ClinPath) DTM&H

   Clinical Pathologist.
   Vermaak Pathcare Laboratories
   Lifestyle building 1
   Clifton Avenue
   Centurion.
   
   

   • Dr Manivasan Moodley MBChB MMed(O&G) FCOG(SA)

   Principal Specialist/senior lecturer and Head: Gynaecologic Oncology, Nelson R Mandela School of Medicine and Inkosi Albert Luthuli Central Hospital , University of KwaZulu-Natal
   719 Umbilo Road , Congella, Durban 4000
   e-mail: moodleym29@ukzn.a.za
   tel: +27 31 260 4428
   

   • Dr Arrie Mouton MBChB M Fam Med MMed (O&G) FCOG(SA)

   Senior Specialist, Dept Obstetrics and Gynaecology, University of pretoria , PO Box 667 , Pretoria 0001
   e-mail:
   tel: +27 12 354 2368
   fax: +27 12 329 6258
   

   • Dr Trudy Smith MBBCh, FCOG(SA)

   Principal Specialist, Johannesburg Hospital , Senior Lecturer, Dept Obstetrics and Gyanecology and Gyanecologic Oncology Unit, University of the Witwatersrand
   e-mail: thsmith@mweb.co.za
   tel: +27 11 4883179
   fax: +27 11 643 2572
   

   • Dr Robbie Soeters MD PhD

   Head: Gynaecologic Oncology Unit: Groote Schuur Hospital , University of Cape Town
   Private Gynaecology Practice
   at Vincent Palotti Hospital , Pinelands
   e-mail: rsoeters@uctgsh1.uct.ac.za
   tel: +27 21 531 9311 / +27 21 404 4480
   fax: +27 21 531 4626
   
   Resources and recommended reading:
   
   ACOG/FIGO Statement of Policy: Cervical cancer prevention in low-resource settings. Int J Gynecol Obstet 2005;90:86-7
   
   Anhang R, Goodman A, Goldie SJ. HPV communication: Review of existing research and recommendations for patient education. CA 2004;54:248-59
   
   Anhang R, Stryker JE, Wright TC Jr., Goldie SJ. News media coverage of human papillomavirus. Cancer 2004;100:308-14
   
   Anhang R, Wright TC Jr., Smock L, Goldie SJ. Women's desired information about human papillomavirus. Cancer 2004;100:315-20
   
   Association of Reproductive Health Professionals. Health and Sexuality: Cervical cancer prevention and HPV DNA testing. 2005;10:1-22
   
   Brigham and Women's Hospital: Cervical cancer screening recommendations. 2004.
   
   Cooper D, Morroni C, Orner P et al. Ten years of democracy in South Africa : Documenting transformation in reproductive health policy and status. Reprod Health matters 2004;12:70-85
   
   Cronje HS. Screening for cervical cancer in developing xountries. Int J Gynecol Obstet 2004;84:101-8
   
   Dannecker C, Siebert U, Thaler CJ et al. Primary cervical cancer screening by self-sampling of human papillomavirus DNA in internal medicine outpatient clinics. Ann Oncol 2004;15:863-9
   
   Denny LA, Wright TC Jr. HPV testing and screening. Best Practice and Research: Obstet Gynaecol 2005; August: in press.
   
   Fowler JR, Sayegh R. Cervical cancer prevention: more than just a Pap in a diverse urban community. Curr Wom Health Rev 2005;1:79-83
   
   Henderson JW. Cost-effectiveness of cervical cancer screening strategies. Expert Rev Pharmacoeconomics Outcomes Res 2004;4:287-296
   Jin XW, Zanotti K, Yen-Lieberman B. New cervical cancer screening strategy: Combined Pap and HPV testing. Clevel Clin J Med 2005;72:141-8
   
   Koliopoulos G, Martin-Hirsch P, paraskevaides E, Arbyn M. HPV testing versus cervical cytology for screening for ancer of the uterine cervix (Protocol). Cochrane Collaboration 2005 Issue 2
   
   Malloy C, Sherris J, Herdman C. HPV DNA testing: Technical and programmatic issues for cervical cancer prevention in low-resource settings. PATH 2000.
   
   Mandelblatt JS, Lawrence WF, Gaffikin L et al. Costs and benefits of different strategies to screen for cervical cancer in less-developed countries. J Natl Cancer Inst 2002;94:1469-83
   
   Van Doorn L-J, Kleter B, Quint WGV. Molecular detection and genotyping of human papliiomavirus. Expert Rev Mol Diagn 2001;1:394-402
   
   Wagner PD, Maruvada P, Srivastata S. Molecular diagnostics: a new frontier in cancer prevention. Expert Rev Mol Diagn 2004;4:503-510
   
   Yu T, Ferber MJ, Cheung TH et al. The role of viral integration in the development of cervical cancer. Cancer Genetics and Cytogenetics 2005;158:27-34
   
   

   Frequently asked questions 

   What is Cervical cancer?
   

   Cervical cancer affects the mouth or the part of the womb that opens to the vagina. It is still common in Africa and many other countries and it occurs worldwide. Less women than before get cervical caner if a Pap smear or other screening strategy is followed in a country. Early detection of cervical cancer contributes much to an improved outcome.

   What is a CIN lesion?

   A CIN lesion means “cervical intraepithelial neoplasia”. This means that the skin of the cervix has become abnormal and that if this condition is left untreated over time this abnormality will become worse and even develop into cervical cancer. In this sense CIN is a precursor or early warning lesion. It can be detected on Pap smears and can be treated effectively. This will prevent the development of cervical cancer in most instances.

   What is HPV infection?

   HPV stands for “human papillomavirus”. HPV infection is common in sexually active persons. It is mostly harmless and tends to disappear on its own as the body eliminates the virus. There are many types of HPV but only a few types can lead to cervical cancer. These are called “high-risk types” and spread through sexual contact. If a high risk HPV type does not disappear on its own it can lead to the formation of abnormal cells in the skin of the cervix leading to a CIN lesion or later to the development of cervical cancer. In such cases treatment must be offered. Low-risk HPV types cause genital warts and do not cause cancer. How common is HPV?

   HPV can be found in the genitalia of the large majority of sexually active persons at some stage in their lives. As the infection is mostly temporary most women will not have any HPV by the age of 30 to 35 years.

   Who is at risk and can get HPV and CIN?

   All persons, male and female, who have been sexually active can get HPV infection. About three out of every four persons are estimated to have HPV infection at some stage in their lives, usually when quite young (late teens and twenties). Women who start with sexual activity at a young age, who have several sex partners or whose partners have or had several partners are at increased risk for having HPV infection.

   It is now known that almost all cervical cancers are caused by HPV. Women who are at risk for HPV infection are therefore also at risk for cervical cancer if the HPV infection is of a high-risk type. The cervical cancer risk is increased by other factors such as smoking and HIV infection. As Pap smear and other screening tests for CIN and cervical cancer are very important in the early detection of abnormality women who have had no such screening tests are at the highest risk of all.

   How is HPV diagnosed?

   HPV infection rarely causes symptoms. Infection with a high-risk HPV type will lead to abnormalities in the cells covering the cervix that can be detected on special HPV tests and on Pap smear testing. Only a small number of women with HPV will develop cell changes.

   Can HPV infection be treated?

   There is no treatment against the HPV itself. If the cervical cells have undergone changes and have become abnormal those areas on the cervix can be treated.

   Who should be tested for HPV infection?

   The HPV tests are used to detect high-risk types of HPV. It can be used with most success in women over the age of 30 in many cases together with Pap smears. In women younger than 30 years HPV is quite commonly present and in the large majority it will be eliminated. To do HPV testing on young women does not contribute much to her gynaecologic management.

   Where did I get this HPV infection?

   HPV is spread through sexual activity. The HPV can be dormant or resting for a short to very long period before causing cellular abnormalities. It is not possible to link HPV infection to a specific episode or time.

   Can HPV infection go away on its own?

   In the majority of women HPV infection is transient and will be eliminated by the immune system of the body. HPV infection may persist especially after age 30 years or older.

   Can I do other things to help HPV disappear?

   Yes: stop smoking as this can increase the risk for development of cellular abnormalities on the cervix. Maintain good sexual health and take care of your relationships.

   What is the difference or relationship between HPV and HIV?

   HIV is also a virus: the human immune deficiency virus. This is currently a massive health care problem especially in developing countries but also worldwide. It is linked to the development of AIDS. It is very different from HPV. Persons who get HPV infected and who are also HIV infected may have a more serious outcome of the HPV infection. Like HPV, HIV is transmitted sexually.

   Does my partner need to be tested for HPV?

   If you have a positive HPV test showing that you have infection with HPV it is absolutely likely that your partner will also have HPV infection. As most HPV infections are transient and tend to disappear it will not always be the case that both partners test positive. As there is no treatment against HPV testing the partner does not contribute to management. As condom use offers incomplete protection partner HPV testing will not influence this practice either.

   Do we have to use condoms now, and for how long?

   As HPV infection is common condom use will not be total prevention. If you had treatment it is not certain (but possible) that condom use may decrease the risk of recurrent infection.

   After treatment can I be re-infected by my partner?

   If a couple only has sexual relations with each other HPV will not be passed back and forth. Further contact with the same virus will not make it more difficult for either the HPV infection to go away or for cellular changes to be treated. Once a person has formed immune reaction to a specific HPV type a next exposure may be eliminated. There are however many HPV types and a person can get re-infected with another HPV type.

   Can I still get pregnant if I am infected with HPV?

   HPV does not cause infertility. There are many reasons for infertility and this may include other sexually transmitted infections.

   How will it affect my baby and my pregnancy if I am infected with HPV?

   HPV infection does not influence the course of the pregnancy. If a person has genital warts (low-risk HPV infection) these may increase in size during pregnancy. If a baby is born from a mother with extensive genital warts there is a possibility of infection of the newborn.

   Does it affect other organs and can it spread?

   HPV infection can also have effects on the vulva and the vagina and it is possible that HOPV infection can spread from the cervix to these organs. It can be detected during clinical examination.