Clinical overview
HIV does not just produce immunodeficiency in the abstract — in the gynaecology clinic it produces patterned, predictable changes in the prevalence, presentation, severity, and natural history of common conditions. A registrar in South Africa needs to know these patterns because they shift screening thresholds, treatment regimens, and follow-up frequency for HIV-positive patients. This chapter complements HIV counselling by focusing on what HIV does to gynaecological organs, the diseases it amplifies, and how clinical management must adapt.
The guideline behind everything below is the NDoH National Consolidated Guidelines for the Management of HIV (published January 2026, updated May 2026 as version 2), which supersede the 2023 ART guidelines and the 2019 PMTCT guideline. Three of its changes run through this whole chapter. Viral suppression now means a viral load below 50 copies/mL, and that one number decides who is safe for elective surgery, who can conceive naturally, and whose infant needs extended prophylaxis. The first viral load is taken after three dispensing cycles, not at six months, so a woman recently started or restarted on ART has a result due sooner than the older documents implied. And the vocabulary has moved with the programme: Prevention of Vertical Transmission (PVT) replaces PMTCT, TLD 1 and TLD 2 replace first-line and second-line, and the dispensing cycle replaces the month as the unit of supply and monitoring.
Core knowledge
Cervical disease
HIV-related HPV persistence drives CIN at the cervical transformation zone.
- HPV acquisition and persistence: HIV-positive women acquire HPV more frequently, clear it less, and harbour multiple high-risk types simultaneously. The interaction between HIV and HPV is bidirectional — HIV impairs HPV clearance; HPV (particularly high-risk types) and the associated inflammation may modestly increase HIV shedding.
- CIN incidence and progression: 2–4× higher than HIV-negative; faster progression CIN1 → CIN2/3 → invasive carcinoma.
- Cervical cancer: AIDS-defining illness; in SA accounts for a substantial fraction of cervical cancer presentations. Younger age at diagnosis, more advanced stage at diagnosis.
- Screening adjustment: two current national documents disagree here, so name the one you are following. The NDoH Elimination of Cervical Cancer in South Africa framework (May 2026) brings all women into screening at age 25 whatever their HIV status, and a woman living with HIV (WLWH) then returns every 5 years for life, against 10-yearly if she is HIV-negative, with exit at 60 (or at 50 after three negative screens). The HIV Consolidated Guidelines (version 2, May 2026) still print the older line, screen at HIV diagnosis then 3-yearly, but they explicitly defer to the current National Cervical Cancer Prevention and Control Policy, so the elimination framework is the operative schedule. The point to hold is that HIV no longer moves the start; it halves the interval. Screen sooner than that if a result is abnormal. See Cervical screening SA.
- Treatment: LEEP and other excisional treatments are effective; recurrence higher in HIV-positive women, especially with low CD4 and uncontrolled viral load. See CIN management.
Vulval and vaginal disease
- Genital warts (condyloma): more numerous, larger, more refractory to treatment.
- VIN and vulval cancer: increased risk, similar HPV mechanisms. See Vulvar epithelial hyperplasia and Vulval carcinoma.
- Recurrent vulvovaginal candidiasis: more common; long-term suppressive antifungal therapy may be needed. See Candidiasis.
- Herpes simplex: more frequent recurrences, severe and atypical lesions, slower healing, sometimes resistant to standard aciclovir doses → escalate.
- Molluscum contagiosum: larger, more numerous, persistent.
- Bacterial vaginosis: more common; may contribute to PID and vertical-transmission risk.