Clinical overview
Cervical cancer is the second commonest cancer in South African women and the leading cause of cancer death among them. This is not a problem of biology alone but of access: cervical cancer is almost entirely preventable, the natural history is slow (a decade or more from infection to invasion), and we possess effective tools to interrupt that history at three separate points — vaccination, screening, and treatment of pre-invasive disease. The reason South Africa still loses so many women is that those tools are unevenly delivered. Layered on top is the highest HIV burden of any country: HIV-driven immunosuppression accelerates HPV persistence, multiplies the risk of high-grade lesions, and shortens the runway from CIN to cancer. A registrar who understands screening must therefore hold two things together — the international evidence on which test, how often, in whom — and the specific South African policy that governs what actually happens in a Pretoria clinic or a rural Eastern Cape primary-care site.
Screening rests on two things: the tests themselves and the SA policy that governs them. That means the performance characteristics of cytology, HPV-DNA testing and visual inspection; the screen–triage–treat logic; and a working command of the National Department of Health (NDoH) screening policy and the SASOG/BetterGyn 2024 guideline that is steering South Africa towards HPV-based primary screening. Screening is best understood as a population programme, not a clinic test, and it connects to HPV pathology, Cervical carcinogenesis and CIN management.
Core knowledge
Why screening works: the natural history it exploits
Persistent infection with a high-risk human papillomavirus (HPV) — chiefly types 16 and 18, which cause roughly 70% of cervical cancers — is necessary for almost all cervical squamous and most glandular carcinomas. The viral oncoproteins E6 and E7 inactivate p53 and Rb respectively, driving the squamocolumnar junction through progressive intraepithelial change. In WHO 2020 (LAST-aligned) pathology terminology, transient productive infection produces a low-grade squamous intraepithelial lesion (LSIL, ≈ CIN 1), which usually regresses, whereas transforming infection produces a high-grade squamous intraepithelial lesion (HSIL, ≈ CIN 2–3), the true cancer precursor. Because progression from HSIL to invasion typically takes years, there is a long, detectable, treatable pre-invasive window — this is the entire rationale for screening. The screen identifies women carrying the virus or harbouring HSIL so that the lesion is ablated or excised before it becomes cancer.
The three screening tests
Figure D5.1 — The three screening tests compared: cytology vs HPV-DNA vs VIA (sensitivity, specificity, setting and self-sampling).
1. Cervical cytology (the Pap smear). A sample of the transformation zone is examined for dyskaryosis, reported using the Bethesda system (ASC-US, LSIL, ASC-H, HSIL, AGC). Its great strength is specificity and a long track record; its weakness is moderate, single-test sensitivity for HSIL (around 50–70%), which is why it must be repeated at intervals to be effective. It is operator- and laboratory-dependent and requires a functioning cytopathology service — in South Africa, the National Health Laboratory Service (NHLS).
2. High-risk HPV-DNA testing. A molecular assay detecting the DNA of oncogenic HPV types, often with partial genotyping that separately flags HPV 16 and 18. Its sensitivity for HSIL+ is high (>90%) and its negative predictive value is excellent, which is what allows long screening intervals and confident reassurance after a negative result. Its trade-off is lower specificity — many positives reflect transient infection that will clear — so a positive HPV test must be triaged (by genotyping, reflex cytology, or visual inspection) rather than taken straight to treatment. HPV testing can be done on a clinician-taken or self-collected vaginal sample, a feature with profound implications for reach in a country where pelvic examination is a major access barrier.
3. Visual inspection with acetic acid (VIA). The cervix is painted with dilute acetic acid; aceto-white areas suggest dysplasia. It is cheap, requires no laboratory, and gives an immediate result, enabling same-visit "screen-and-treat" with thermal ablation. Its sensitivity and specificity are operator-dependent and modest, and it performs poorly when the squamocolumnar junction is not fully visible (post-menopausal women). It remains valuable as a triage step or in resource-constrained, single-visit settings.