Persistent human papillomavirus after thermal ablation in Malawian women with and without HIV: Implications for risk-based cervical cancer prevention in low- and middle-income countries

Abstract

Background:

Persistent high-risk human papillomavirus (hrHPV) infection can lead to cervical precancer, with women living with HIV (WLWH) at increased risk due to impaired immune clearance. Thermal ablation (TA) is a low-cost treatment for precancerous lesions, but data on hrHPV persistence after TA among WLWH are limited.

Objectives:

To evaluate overall and channel-specific hrHPV persistence 12 months after TA among women in Lilongwe, Malawi.

Design:

Cross-sectional analysis of Malawian women who received TA during and after the PEER trial (prevention of cervical cancer through two HPV-based screen-and-treat implementation models in Malawi).

Methods:

We analyzed 495 hrHPV-positive women (113 WLWH, 382 without HIV) treated with TA. Self-collected cervicovaginal samples were obtained before treatment and at 12 months post-treatment and tested with the GeneXpert HPV assay, which detects hrHPV across five high-risk genotype channels (P1–P5). Channels P3–P5 were grouped as non-16/18/45 hrHPV types (HPV 31, 33, 35, 39, 51, 52, 56, 58, 59, 66, 68). Persistence was defined as the detection of the same channel at both time points. Differences in persistence rates were assessed using Fisher’s exact and Welch’s t-tests.

Results:

At 12 months post-TA, 35.6% of women were persistently hrHPV-positive. Persistence was higher among WLWH (46.0%) than women without HIV (32.0%, p = 0.01). By genotype, persistence was most common for non-16/18/45 types (37.7%), followed by HPV16 (28.9%) and HPV18/45 (18.0%). WLWH had higher persistence of non-16/18/45 types (51.8% versus 33.7% in HIV-negatives, p = 0.003), while persistence of HPV16 (35.0% versus 27.1%, p = 0.58) and HPV18/45 (26.3% versus 14.9%, p = 0.14) did not differ significantly.

Conclusions:

Over one-third of women had persistent hrHPV 12 months after TA, with higher rates among WLWH, primarily for non-16/18/45 genotypes. Findings highlight the need for enhanced follow-up and adjunct therapies to improve post-treatment clearance and advance cervical cancer prevention in low-resource settings.

Keywords

screen-and-treat programs papillomavirus infections virus persistence thermal ablation sub-Saharan Africa early detection of cancer

Introduction

Persistent infection with high-risk human papillomavirus (hrHPV) is the primary driver of high-grade cervical lesions that may progress to invasive cervical cancer.^1,2 hrHPV persistence is more common among individuals with compromised immune systems, which impairs the body’s ability to mount an effective antiviral response.^1,2 Women living with HIV (WLWH) are particularly vulnerable, as chronic immune dysregulation promotes the reactivation or persistence of latent virus.^3,4 Although antiretroviral therapy (ART) improves immune function, WLWH remain disproportionately affected – developing cervical cancer at nearly six times the rate of women without HIV.⁵ This burden is concentrated in low- and middle-income countries (LMICs), which are home to approximately 70% of WLWH and account for 85% of new cervical cancer cases and 95% of cervical cancer-related deaths worldwide.⁶

To address this, the World Health Organization (WHO) launched a global cervical cancer elimination strategy targeting 90% HPV vaccination coverage, 70% screening coverage, and 90% treatment of precancerous lesions by 2030.⁷ In Malawi, where HIV prevalence among women aged 15–49 is estimated at 10.4%, cervical cancer mortality remains among the highest globally, with an age-standardized mortality rate of 54.1 and a crude mortality rate of 32.7 per 100,000 women (cumulative risk to age 75: 5.8%).^8,9 Prevention efforts focused on WLWH are therefore a national priority. However, widespread health system constraints, particularly in rural communities, continue to hinder early detection and delay treatment, reflecting structural barriers common to many LMICs.

In this context, non-excisional approaches such as thermal ablation (TA) have re-emerged as safe, effective, and scalable treatment options.^10,11 In contrast to the loop electrosurgical excision procedure and cryotherapy – which require advanced surgical infrastructure and a continuous supply of gas cylinders, respectively – TA is portable, affordable, and can be performed by nurses and clinical officers in areas with limited physician availability.¹² These features make TA particularly well-suited for under-resourced health systems, as in Malawi, where access to standard excisional therapies remains inconsistent.^13,14 However, treatment success among WLWH continues to be significantly lower than among those without HIV, with higher rates of hrHPV persistence, visual inspection with acetic acid (VIA) positivity, and CIN2⁺ recurrence observed across treatment modalities.^10,11,15

Progress toward understanding this disparity has been slowed by limited cervical cancer screening coverage and challenges in ensuring post-treatment follow-up across LMICs. The introduction of rapid hrHPV testing – such as the GeneXpert assay, which groups genotypes by oncogenic risk – has supported the expansion of same-day screen-and-treat programs, improving timely access to care for high-risk populations. If these screening approaches are to achieve population-level impact through national adoption, evaluating whether grouped hrHPV persistence predicts outcomes after treatment will be essential to guiding risk-adapted follow-up strategies for WLWH. Emerging evidence from South Africa¹⁶ suggests that grouped genotype persistence may carry prognostic value for CIN2⁺ recurrence following treatment with TA; however, to our knowledge, few studies have evaluated this metric as an independent predictor of post-treatment outcomes.¹⁷

This study seeks to address that gap by evaluating overall and channel-specific hrHPV persistence 12 months after TA among women with and without HIV in Lilongwe, Malawi. By characterizing HPV persistence patterns stratified by HIV status, we aim to inform risk-based treatment pathways and strengthen cervical cancer prevention strategies in high-burden LMICs.

Materials and methods

Study design and parent trial overview

This cross-sectional analysis evaluated patterns of hrHPV persistence among Malawian women who underwent TA during and after the PEER trial—Prevention of cervical cancer through two HPV-based screen-and-treat implementation models in Malawi.¹⁸ PEER was a cluster-randomized trial that tested the integration of self-collected hrHPV screening into family planning services, using either a clinic-only model or a combined clinic-plus-community model. The study protocol has been published previously,¹⁸ and the trial is registered at ClinicalTrials.gov Identifier: NCT04286243. Participants for this analysis of HPV persistence were identified during two distinct periods:

PEER trial period: Comprehensive clinic register data were available, including the number of hrHPV tests performed, the number of positive HPV results, and the number of TA treatments performed.

Post-implementation period: After the trial concluded, UNC Project – Malawi continued to support hrHPV screen-and-treat services using the same clinical workflow and supplies. However, systematic participant-level data abstraction was no longer conducted, and detailed study register data were not maintained. Only limited follow-up information, specifically 12-month post-ablation hrHPV testing results, was available for inclusion in this analysis.

Setting and participants

Participant data were abstracted between June 2022 and December 2023 by trained staff from the University of North Carolina Project – Malawi (UNC Project – Malawi), based at the Tidziwe Center within Kamuzu Central Hospital in Lilongwe. Data were collected from eight affiliated health clinics in Lilongwe District: Area 18, Bwaila, Chileka, Chiwamba, Kabudula, Kawale, Lumbadzi, and Nkhoma.

We abstracted data from 564 women aged 25–65 years who screened hrHPV-positive, received same-day TA, and returned for 12-month follow-up hrHPV testing. Participants with unknown HIV status (n = 68) and those with invalid follow-up HPV results (n = 1) were excluded from our analyses, resulting in 495 participants in the final analytic cohort (113 WLWH, 382 women without HIV). Figure 1 summarizes participant flow through study stages.

Figure 1.

Participant flowchart: hrHPV persistence analytic cohort.

Participant data were abstracted from the Ministry of Health cervical cancer and laboratory registers of the eight participating clinics. These registers include information on patient age, HIV status (positive, negative, or unknown), ART use (if HIV-positive), and HPV test results. Two trained research assistants independently abstracted and cross-verified all data against source documents. All records were securely entered into a study-specific electronic database.

The study was approved by the University of North Carolina at Chapel Hill Institutional Review Board (IRB # 21-3266) and the Malawi National Health Sciences Research Committee (NHSRC Protocol # 21/11/2831). Informed consent was waived, as the analysis relied solely on retrospective abstraction of de-identified information from routine clinical and laboratory registers, for which individual consent was not required under institutional and national ethical guidelines.

Cervical cancer screening and treatment

In the PEER study, hrHPV screening was performed using self-collected cervicovaginal specimens. Women who tested hrHPV-positive were offered same-day VIA whenever possible, provided they could receive their HPV results that day.

Eligibility for TA was determined based on VIA findings. Women were considered eligible if they had no visible lesions or if lesions met all of the following criteria:

Not suspicious for invasive cancer,

Did not extend into the endocervical canal, and

Covered ⩽75% of the cervical surface.

Eligible participants were offered immediate TA. Those who underwent TA were counseled to repeat hrHPV testing approximately 12 months after treatment as a WHO-recommended test-of-cure to evaluate treatment effectiveness and assess for hrHPV persistence.¹⁹

Laboratory testing

Self-collected cervico-vaginal specimens were obtained using the Evalyn^® Brush (Rovers Medical Devices, Oss, Netherlands) and preserved in ThinPrep Pap Test PreservCyt^® Solution (Hologic, Marlborough, MA, USA), consistent with the PEER trial protocol.¹⁸ hrHPV testing was conducted using the Xpert HPV assay (Cepheid, Sunnyvale, CA, USA), a cartridge-based real-time polymerase chain reaction platform that detects 14 high-risk HPV types by amplifying the E6/E7 viral DNA regions.

Results were reported in five pooled genotype channels: P1 (HPV16), P2 (HPV18/45), P3 (HPV31/33/35/52/58), P4 (HPV51/59), and P5 (HPV39/56/66/68). Invalid or unsatisfactory samples were retested once; persistently invalid tests were excluded. In the PEER study, channels P3–P5 were grouped to represent non-16/18/45 hrHPV types. Each assay included internal quality controls to confirm specimen adequacy and test validity.

Statistical analysis

The primary outcome was overall hrHPV persistence, defined as detection of hrHPV in at least one GeneXpert channel at both baseline and 12-month follow-up. The secondary outcome was channel-specific persistence, defined as repeated detection of the same GeneXpert channel at both time points. Because channels P2–P5 represent pooled genotype groups, single-channel persistence was used as a proxy for genotype group persistence.

Persistence, treated as a binary outcome, was compared between women with and without HIV using Fisher’s exact test. Odds ratios (ORs) with exact conditional 95% confidence intervals (CI) were calculated. For continuous variables, between-group differences were assessed using Welch’s t-test to account for unequal variances. Categorical variables were summarized as n (%) and continuous variables as mean (standard deviation (SD)).

Statistical significance was defined as a two-sided p-value <0.05. All analyses were conducted in R version 4.3.1 (R Foundation for Statistical Computing, Vienna, Austria).

Sensitivity analyses were performed to estimate the minimum detectable effect (MDE) at 80% power (two-sided α = 0.05) based on observed sample size and event rates. This cross-sectional analysis included only complete cases; participants without available hrHPV testing results at baseline or follow-up were not included.

The reporting of this study conforms to the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement for cross-sectional studies.²⁰ The completed STROBE checklist is provided in Supplemental Material.

Results

Table 1 summarizes the baseline demographic and clinical characteristics of the 495 participants, overall and stratified by HIV status. Of the 495 participants, 113 (22.8%) were WLWH, and 382 (77.2%) were without HIV. The mean age of participants was 35.2 years (SD = 6.3), with no significant difference between WLWH (35.9 years, SD = 6.6) and women without HIV (35.0 years, SD = 6.2; p = 0.21).

Table 1.

Baseline characteristics of participants with high-risk HPV infection who underwent thermal ablation and 12-month follow-up, stratified by HIV status (N = 495).

Characteristic	Overall ( N = 495), n (%)	Women with HIV(n = 113), n (%)	Women without HIV ( n = 382), n (%)	p -value^a
Age, mean (SD), years	35.2 (6.3)	35.Th (6.6)	35.0 (6.2)	0.21^b
25–34	239 (48.3)	48 (42.5)	191 (50.0)
35–44	211 (42.6)	53 (46.9)	158 (41.4)
45–54	45 (9.1)	12 (10.6)	33 (8.6)
Channel positivity^c				0.60
Single-channel	394 (79.6)	88 (77.9)	306 (80.1)
Multi-channel	101 (20.4)	25 (22.1)	76 (19.9)
Channel-specific HPV high-risk positivity^d
HPV 16 (P1)	90 (18.2)	20 (17.7)	70 (18.3)	>0.99
HPV 18/45 (P2)	139 (28.1)	38 (33.6)	101 (26.4)	0.15
HPV P3–P5 pooled	371 (74.9)	83 (73.5)	288 (75.4)	0.71

hrHPV: high-risk human papillomavirus; SD: standard deviation.

p-values calculated using Fisher’s exact test unless otherwise specified.

Welch’s t-test used for continuous variables.

Channel positivity refers to whether a participant tested positive for hrHPV DNA in one versus multiple GeneXpert assay channels at baseline.

Channel-specific positivity refers to the detection of hrHPV DNA in individual GeneXpert channels at baseline, whether present in single- or multi-channel infections. P1 detects HPV16; P2 detects HPV18/45; P3–P5 represent pooled high-risk genotype groups: P3 (HPV31/33/35/52/58), P4 (HPV51/59), and P5 (HPV39/56/66/68). Totals may exceed N due to multi-channel infections.

At baseline, 394 (79.6%) participants tested positive for a single GeneXpert channel, while 101 (20.4%) had multi-channel hrHPV infections. Pooled high-risk genotypes detected in channels P3–P5 were most prevalent (74.9%), followed by P2 (HPV 18/45; 28.1%) and P1 (HPV16; 18.2%). Genotype group distributions were similar across HIV status (p > 0.99).

Table 2 presents hrHPV persistence outcomes at 12-month follow-up, stratified by HIV status. The average time to follow-up was 13.3 months (SD = 2.1), with no significant difference between groups (p = 0.19). Overall, 176 of 495 participants (35.6%) had persistent hrHPV infection, defined as detection of the same GeneXpert channel(s) at both baseline and follow-up. Persistence was higher in WLWH compared to women without HIV (46.0% versus 32.0%; OR: 1.77, 95% CI 1.13–2.78; p = 0.01). Based on the observed sample sizes and control group event rate, the MDE for overall persistence corresponded to an OR of 1.90. Given the observed OR of 1.77, the estimated post-hoc power was 73.7%, suggesting a modest sensitivity to detect the observed association.

Table 2.

High-risk HPV persistence at 12-month follow-up among participants treated with thermal ablation, stratified by HIV status, with odds of persistence (N = 495) and odds of single or multi-channel detection among the persisted subgroup (n = 176).

Outcome	Overall ( N = 495)	Women with HIV ( n = 113)	Women without HIV ( n = 382)	OR (HIV⁺ vs HIV⁻) (95% CI)	p-value^a
Time to follow-up, average (SD), months	13.3 (2.1)	13.5 (2.1)	13.2 (2.1)	—	0.19^b
Overall persistence, n (%)	176 (35.6)	52 (46.0)	124 (32.0)	1.77 (1.13–2.78)	0.01
Detection pattern^c – subset with persistence ( n = 176)				—
Single-channel	152 (86.4)	34 (82.7)	109 (87.9)	0.52^d (0.19–1.48)	0.21
Multi-channel	24 (13.6)	9 (17.3)	15 (12.1)	1.92^e (0.68–5.18)	0.21
Channel-specific persistence^f – based on baseline genotype positivity
HPV 16 (P1), n = 90	26 (28.9)	7 (35.0)	19 (27.1)	1.44 (0.42–4.62)	0.58
HPV 18/45 (P2), n = 139	25 (18.0)	10 (26.3)	15 (14.9)	2.04 (0.73–5.51)	0.14
HPV P3–P5 pooled, n = 371	140 (37.7)	43 (51.8)	97 (33.7)	2.11 (1.25–3.58)	0.003

hrHPV: high-risk human papillomavirus; OR: odds ratio; SD: standard deviation; CI: confidence interval.

p-values calculated using Fisher’s exact test unless otherwise specified.

Welch’s t-test used for continuous variables.

Detection pattern refers to whether hrHPV DNA was detected in one versus multiple GeneXpert channels at 12-month follow-up.

This OR quantifies the odds of single-channel positivity at follow-up between women with and without HIV among those with persistent infection.

This OR quantifies the odds of multi-channel positivity at follow-up between women with and without HIV among those with persistent infection.

Channel-specific persistence refers to continued detection of hrHPV DNA in the same GeneXpert channel(s) that tested positive at baseline. The “n” reflects the number of participants who were positive for that genotype group at baseline and were thus eligible for follow-up persistence assessment.

Among those with persistent infections, 86.4% had single-channel persistence, and 13.6% had multiple-channel persistence, with comparable proportions across groups. Channel-specific persistence was most frequent in pooled P3–P5 channels (37.7%), with significantly higher rates of persistence among WLWH than participants without HIV (51.8% versus 33.7%; OR: 2.11, 95% CI 1.25–3.58; p = 0.003). No statistically significant differences were observed for P1 (28.9%; p = 0.58) or P2 (18.0%; p = 0.14) persistence by HIV status.

Figure 2 illustrates changes in multi-channel hrHPV positivity between baseline and follow-up, stratified by HIV status. This figure presents only the subset of participants (n = 176) who had persistent hrHPV infection at follow-up.

Figure 2.

HPV genotype group transitions from baseline to 12-month follow-up among participants with persistent infection (n = 176), stratified by HIV status.

P3–P5 genotype group positivity increased modestly over time in both WLWH (29.3%–32.4%) and participants without HIV (31.5%–34.4%). Patterns in P1 and P2 positivity between baseline and follow-up varied by HIV status: P1 increased slightly in WLWH (6.4%–7.4%) but declined in the group without HIV (9.7%–8.3%). P2 positivity was higher at baseline among WLWH (14.4%) than among participants without HIV (8.9%). Among women initially positive for P2, WLWH were more likely to shift to P3–P5 at follow-up, while women without HIV most often remained positive for P2 only.

Discussion

In this cohort of Malawian HPV-positive women undergoing hrHPV-based screen-and-treat with TA, 35.6% had persistent high-risk HPV 12 months after treatment. WLWH were significantly more likely to have persistence than HIV-negative or unknown-status participants (46.0% versus 32.0%), underscoring the persistent immunologic and clinical vulnerabilities despite widespread ART access. These results align with findings from South Africa and other high-burden settings, emphasizing that immunosuppression has been consistently associated with higher HPV persistence following TA in integrated care models.^11,12

The predominance of P3–P5 genotype group persistence (37.7%) post-treatment – including HPV types 31, 33, 35, 39, 51, 52, 56, 58, 59, 66, and 68 – may reflect regional genotype patterns as well as increased reactivation of certain latent virus types in WLWH.^4,21 Although P1 (HPV16) and P2 (HPV18/45) remain the most oncogenic globally,¹ repeat positivity of HPV 16 and 18 was less frequent in this cohort. Notably, repeat positivity of P3–P5 (persistence) was significantly higher in WLWH (51.8% versus 33.7%), supporting hypotheses that immunocompromised individuals may be more susceptible to sequential or multi-genotype infections, particularly in pooled channel groupings.¹⁶ While Xpert-based grouping limits inferences about HPV type-specific persistence, the higher persistence of non-16/18/45 genotypes in WLWH is consistent with studies from Kenya, Mali, and South Africa, where HPV35 and HPV52 were especially prevalent in population-based samples.^22–24

These results reinforce a report from South Africa¹⁶ that described higher 12-month hrHPV persistence in WLWH (61.5%) versus women without HIV (34.8%) post-TA, with WLWH also more likely to exhibit new channel detection at follow-up, potentially reflecting broader susceptibility. However, that study¹⁶ further identified P1 and P2 persistence – not P3 – as most predictive of CIN2⁺, indicating that while P3–P5 genotypes commonly persist, their association with high-grade disease is expected to be weaker. Our data similarly support genotype-informed stratification post-treatment, especially where resources limit histologic surveillance.

Given the substantial proportion of women with persistent hrHPV infection after TA, particularly among those living with HIV, adjunct approaches to enhance viral clearance warrant further investigation. Therapeutic HPV vaccines and topical antiviral agents, such as intravaginal artesunate and 5-fluorouracil, have shown early promise in reducing post-treatment HPV persistence and may represent feasible strategies in resource-limited settings.^25,26

Limitations

The study’s strengths include its pragmatic integration within an implementation trial, a large and demographically representative sample, and the use of standardized testing at both study time points. However, several limitations merit consideration. First, we did not collect histologic outcomes, which precludes assessment of clinical progression. Second, the GeneXpert assay’s pooled channel format prevents assessment of type-specific HPV persistence or reinfection. Third, we lacked access to HIV clinical markers, such as CD4 count or viral load, limiting our ability to evaluate immunologic correlates of persistence. Fourth, the study’s modest power may have limited sensitivity to detect smaller or more nuanced associations. Lastly, the 12-month follow-up cohort may be biased toward women more engaged in care or symptomatic.

Despite these limitations, our definition of HPV persistence – repeat detection of the same GeneXpert channel – aligns with other Xpert-based screening studies and underscores important risks in this population.^11,16

Conclusions

In this cohort, hrHPV persistence 12 months after TA was more frequent among WLWH, with a higher prevalence of P3–P5 genotype group persistence. The relatively high rate of repeat hrHPV positivity following TA treatment raises concerns about treatment durability in this population and points to the need for additional treatment strategies alongside or after ablation to reduce cancer risk. Tailored follow-up protocols – such as targeted re-screening, genotyping, or adjuvant vaccination – may help close gaps in protection for WLWH and should be prioritized within national cervical cancer prevention frameworks in LMICs.

Supplemental Material

sj-pdf-1-whe-10.1177_17455057261428547 – Supplemental material for Persistent human papillomavirus after thermal ablation in Malawian women with and without HIV: Implications for risk-based cervical cancer prevention in low- and middle-income countries

Supplemental material, sj-pdf-1-whe-10.1177_17455057261428547 for Persistent human papillomavirus after thermal ablation in Malawian women with and without HIV: Implications for risk-based cervical cancer prevention in low- and middle-income countries by Jessica Gingles, Yating Zou, Lameck Chinula, Jennifer H. Tang, Ivy Kaliati, Tawonga Mkochi, Lizzie Msowoya, Charity Nakanga, Friday Saidi, Jennifer S. Smith and Chemtai Mungo in Women's Health

Footnotes

Acknowledgements

The authors are grateful to the study participants and the clinical and laboratory teams at UNC Project – Malawi and collaborating health facilities in Lilongwe for their invaluable contributions to this research.

ORCID iDs

Jessica Gingles

Yating Zou

Jennifer H. Tang

Ivy Kaliati

Tawonga Mkochi

Friday Saidi

Jennifer S. Smith

Chemtai Mungo

Ethical considerations

Approved by the University of North Carolina at Chapel Hill Institutional Review Board (IRB #21-3266) and the Malawi National Health Sciences Research Committee (NHSRC Protocol #21/11/2831).

Consent to participate

Informed consent was waived as only de-identified data were abstracted from clinical and laboratory registers

Consent for publication

Not applicable.

Author contributions

Jessica Gingles: Methodology; Data curation; Investigation; Formal analysis; Visualization; Writing – review & editing; Writing – original draft.

Yating Zou: Data curation; Formal analysis; Writing – review & editing.

Lameck Chinula: Conceptualization; Methodology; Funding acquisition; Supervision; Writing – review & editing.

Jennifer H. Tang: Methodology; Conceptualization; Writing – review & editing; Supervision; Funding acquisition.

Ivy Kaliati: Methodology; Project administration; Resources.

Tawonga Mkochi: Data curation; Software; Formal analysis; Validation.

Lizzie Msowoya: Resources; Project administration.

Charity Nakanga: Resources; Project administration.

Friday Saidi: Resources; Project administration.

Jennifer S. Smith: Conceptualization; Supervision; Formal analysis; Visualization; Writing – review & editing.

Chemtai Mungo: Conceptualization; Supervision; Writing – review & editing.

Funding

The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by internal funding from the University of North Carolina Lineberger Comprehensive Cancer Center.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data availability statement

Data supporting the findings are available upon reasonable request to the corresponding author.

Supplemental material

Supplemental material for this article is available online.

Use of generative artificial intelligence (AI)

Portions of this manuscript were prepared with the assistance of OpenAI’s ChatGPT (GPT-5) to support grammar editing. The authors reviewed, edited, and approved all content generated and take full responsibility for the accuracy, integrity, and originality of the final manuscript.

References

Cohen

Jhingran

Oaknin

, et al. Cervical cancer. Lancet 2019; 393(10167): 169–182.

Okunade

KS.

Human papillomavirus and cervical cancer. J Obstet Gynaecol 2020; 40(5): 602–608.

Denny

Franceschi

De Sanjosé

, et al. Human papillomavirus, human immunodeficiency virus and immunosuppression. Vaccine 2012; 30(Suppl 5): F168–F174.

Murenzi

Tuyisenge

Kanyabwisha

, et al. Type-specific persistence, clearance, and incidence of high-risk HPV among screen-positive Rwandan women living with HIV. Infect Agent Cancer 2021; 16(1):16.

Stelzle

Tanaka

Lee

, et al. Estimates of the global burden of cervical cancer associated with HIV. Lancet Glob Health 2021; 9(2): e161–e169.

Hull

Mbele

Makhafola

, et al. Cervical cancer in low- and middle-income countries. Oncol Lett 2020; 20(3): 2058–2074.

World Health Organization. Global strategy to accelerate the elimination of cervical cancer as a public health problem. World Health Organization, 2020.

Ferlay

Ervik

Lam

, et al. Global cancer observatory: cancer today. International Agency for Research on Cancer, 2024.

Wolock

Flaxman

Chimpandule

, et al. Subnational HIV incidence trends in Malawi: large, heterogeneous declines across space. medRxiv 2023; 2023: 2023.02.02.23285334.

10.

Pinder

Parham

Basu

, et al. Thermal ablation versus cryotherapy or loop excision to treat women positive for cervical precancer. Lancet Oncol 2020; 21(1): 175–184.

11.

Denny

Saidu

Boa

, et al. Point-of-care testing with Xpert HPV for single-visit, screen-and-treat for cervical cancer prevention: a demonstration study in South Africa. Sci Rep 2023; 13: 16182.

12.

Mungo

Osongo

Ambaka

, et al. Efficacy of thermal ablation for treatment of biopsy-confirmed high-grade cervical precancer among women living with HIV in Kenya. Int J Cancer 2023; 153(12): 1971–1977.

13.

Armstrong

Ragupathy

Test of cure and beyond: superiority of thermal ablation over LLETZ in the treatment of high-grade CIN. Arch Gynecol Obstet 2022; 306: 1815–1820.

14.

Joshi

Muwonge

Kulkarni

, et al. Can we increase the cervical cancer screening interval with an HPV test for women living with HIV? Int J Cancer 2023; 152(2): 249–258.

15.

Castle

Einstein

Sahasrabuddhe

VV.

Cervical cancer prevention and control in women living with human immunodeficiency virus. CA Cancer J Clin 2021; 71(6): 505–526.

16.

Jenkins

Saidu

Boa

, et al. Performance of thermoablation among women treated for high-risk human papillomavirus in a screen-and-treat program in South Africa. Int J Cancer 2025; 157(8): 1709–1722.

17.

Chung

De Vuyst

Greene

, et al. Human papillomavirus persistence and association with recurrent cervical intraepithelial neoplasia after cryotherapy vs loop electrosurgical excision procedure among HIV-positive women: a secondary analysis of a randomized clinical trial. JAMA Oncol 2021; 7(10): 1514–1520.

18.

Tang

Smith

McGue

, et al. Prevention of cervical cancer through two HPV-based screen-and-treat implementation models in Malawi: protocol for a cluster randomized feasibility trial. Pilot Feasibility Stud 2021; 7(1): 98.

19.

World Health Organization. WHO guidelines for the use of thermal ablation for cervical pre-cancer lesions. World Health Organization, 2019.

20.

Von Elm

Altman

Egger

, et al. The strengthening the reporting of observational studies in epidemiology (STROBE) statement: guidelines for reporting observational studies. PLoS Med 2007;4(10): e296.

21.

Rositch

Koshiol

Hudgens

, et al. Patterns of persistent genital human papillomavirus infection among women worldwide: a literature review and meta-analysis. Int J Cancer 2013; 133: 1271–1285.

22.

Mbulawa

ZZA

Phohlo

Garcia-Jardon

, et al. High human papillomavirus (HPV)-35 prevalence among South African women with cervical intraepithelial neoplasia warrants attention. PLoS One 2022; 17(3): e0264498.

23.

Tounkara

Téguété

Guédou

, et al. Type-specific incidence, persistence, and factors associated with human papillomavirus infection among female sex workers in West Africa. Int J Infect Dis 2021(106): 348–357.

24.

Njue

Muturi

Kamau

, et al. Human papillomavirus types associated with cervical dysplasia among HIV- and non-HIV-infected women attending reproductive health clinics in Eastern Kenya. Biomed Res Int 2021; 2021: 2250690.

25.

Mungo

Sorgi

Misiko

, et al. Phase I study on the pharmacokinetics of intravaginal, self-administered artesunate vaginal pessaries among women in Kenya. PLoS One 2025; 20(4): e0316334.

26.

Mungo

Omoto

Ogollah

, et al. Safety and adherence to self-administered intravaginal 5-fluorouracil cream following cervical intraepithelial neoplasia (CIN) 2/3 treatment among HIV-positive women in Kenya: a phase 1 clinical trial. Int J Gynaecol Obstet 2025; 169(2): 781–787.

Supplementary Material

Please find the following supplemental material available below.

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