SEARCH · PubMed Health

Results for “HPV persistence”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

14 recordsLinked to original sources

PubMed2026

Prevalence and persistence of high-risk HPV genotypes in unvaccinated asymptomatic women: a six-year study in Peru.

OBJECTIVE: This study was to determine the frequency of HPV-hr and describe the distribution by categories (HPV16, HPV18, HPV-hr non16/18) among unvaccinated asymptomatic women in Peru over a 6-year period (2013-2018). In addition, the disease clearance rate is assessed in a percentage of cases. RESULTS: Of the 6,665 samples, 2,240 (33.6%) tested positive for HPV. Among the positive cases, single-genotype infections were caused by HPV-16 (14.8%), followed by HPV-18 (2.2%) and clustered high-risk HPV (HR-HPV) genotypes (66.7%). Multiple HPV-16 infections were more common than HPV-18 infections. In addition, 22 cases (1%) presented with infection with HPV-16, HPV-18, and HR-HPV genotypes. A subset of 116 samples from patients with 1 to 2 years of follow-up was analyzed further. Clearance rates were high, at 68.8% for HPV-16 infections and 67.5% for HR-HPV infections. However, the elimination rate of multiple infections with HPV-16 and HR-HPV genotypes was slightly lower, at 55.6%.

Prevalence↗

PubMed2026

Human papillomavirus viral load as promising surrogate biomarker of cervical cancer risk and clinical outcome.

INTRODUCTION: Persistent high-risk human papillomavirus (HR-HPV) causes cervical precancerous lesions and cancer. While molecular HPV DNA testing offers superior sensitivity over cytology as a primary screening method, its limited specificity leads to unnecessary follow-up procedures. Therefore, identifying surrogate biomarkers to distinguish transient infections from clinically relevant, persistent ones is essential for improving risk stratification. A comprehensive literature search across PubMed/MEDLINE, Embase, Scopus, and Web of Science databases up to December 2025 identified studies evaluating HR-HPV viral load in cervical lesion progression. AREAS COVERED: Oncogenic HPV viral load, the quantity of HPV genomes in a sample, is a promising biomarker. Levels correlated positively with HR-HPV persistence, increasing the risk of high-grade lesions and invasive cervical cancer. Furthermore, quantification provides prognostic information regarding disease severity, therapeutic response, and post-treatment recurrence. EXPERT OPINION: Recent standardization and validation of multiplex real-time PCR techniques supports integrating HPV viral load into clinical pratice. Incorporating viral load assessment into screening and management algorithms could significantly enhance diagnostic precision, enable personalized follow-up, and guide therapeutic decisions for women with HR-HPV-associated cervical disease. Refining these protocols will ultimately minimize over-treatment while ensuring rigorous monitoring for high-risk patients.

Humans↗

PubMed2026

Longitudinal analysis of high-risk HPV infections reveals within-host viral genome changes over time.

Persistent infection with high-risk (HR)-HPV causes cervical cancer, however, it is unclear why most infections resolve while a minority progress. We deep sequenced the HPV genomes of 1,228 HR-HPV-positive serial samples from 351 women with persistent infections (2-10 serial samples per woman over 1-8 years), including 279 controls and 72 precancer/cancer cases, to assess HR-HPV genome changes during infection and relation to infection outcomes. Seventy-seven percent of persistent infections (45-97% by HPV type) were infections with the same exact viral genome isolate; for HPV16, only 52% were persistent with the same isolate. This may suggest some infections include a type-specific isolate switch or new isolate infection during persistence. We additionally observed within-host change to the HPV genome estimated as gradual changes to intrahost single nucleotide variant (iSNV) frequency, and changes varied by HPV type, with HPV33 infections showing the most iSNV changes. Cases exhibited fewer viral genome changes during infection compared to controls (OR = 0.31, 95% CI = 0.1 - 0.86, p = 0.019), suggesting a more stable and clonal viral genome in cases. By viral gene, E7 had fewer nonsynonymous mutations in the cases compared to controls that cleared within 2 years of infection (p = 0.012), which confirms the importance of E7 conservation and suggests mutations to E7 reduce persistence associated with progression. There was a similar pattern in E4 (p = 0.013), while E5 had more changes in the cases (p = 0.008). A subset of 28 infections had an intervening HPV-negative sample between HPV-positive visits; 93% of these infections had the same exact viral genome isolate in the samples before and after the negative, consistent with subclinical persistence and subsequent re-detection. Our data suggests that HR-HPV type-persistence can include a collection of viral isolates, and viral mutations during infection, particularly in E7, reduce HR-HPV persistence and thus carcinogenic potential.

Humans↗

PubMed2026

Lipid reprogramming of stratified squamous epithelium by the high-risk HPV E6 and E6/E7 oncoproteins.

INTRODUCTION: High risk human papillomavirus (HPV) infection and genome integration with pronounced expression of the viral E6/E7 oncogenes is the major cause of cervical cancer. Emerging evidence suggests that HPV reprograms host metabolism to support viral persistence and cellular transformation. However, global HPV oncogene-induced lipidomic reprogramming remains poorly understood, particularly at early stages of HPV-induced transformation. OBJECTIVE: We sought to define the regulation of lipid metabolism in squamous epithelia of transgenic mice expressing the HPV16 oncogene E6 alone or in conjunction with E7. METHODS: Untargeted lipidomics was used to identify novel lipid biomarkers in the skin and female reproductive tract (FRT) of HPV16 E6 and E6/E7 transgenic compared to wild-type (WT) mice. To investigate enzymatic dysregulation of lipids by HPV oncogene expression, we employed Lipid Network Explorer (LINEX2), which analyzes lipidomics data through lipid enrichment analysis. We also used the Global Natural Product Social Molecular Networking (GNPS) platform to enhance lipid identification, exploring molecular networking to improve feature annotation. RESULTS: Our lipidomic analysis produced several new observations. First, E6 expression caused a consistent alteration of glycerophospholipids, with particularly significant substrate-product shifts in the phosphatidylcholine (PC) to lysophosphatidylcholine (LPC) pathway in the skin. Second, E6/E7 expression caused a dysregulation of glucosylceramide (GlcCer) biosynthesis. Third, both E6/E7 expressing skin and FRT tissues exhibited a redox imbalance and increased levels of oxidized lipids, including oxylipins and several oxidized PCs. These findings suggest that HPV oncoproteins drive lipid reprogramming, potentially contributing to early HPV-related tumorigenesis. CONCLUSIONS: These findings provide new insights into HPV‑induced lipid reprogramming and establish a framework for future studies examining the functional and clinical relevance of lipid alterations in HPV‑associated cancers.

Animals↗

PubMed1979

Mechanism of persistence of rubella virus in LLC-MK2 cells.

LLC-MK2 cells chronically infected with two strains of rubella virus, HPV-77 and Thomas, have been examined over several months to find out the mechanism of persistence. Evidence is given for the presence of defective particles in these cultures by finding virion RNA which sedimented at 12S instead of the 40S typical of the fully infectious virus. A 'provirus' DNA copy of the rubella virus genome was not detected by methods which included filter hybridization and in situ hybridization, or by treatment of the chronically infected cells with mitomycin C, antinomycin D or 5-bromodeoxyuridine. In addition, the chronically infected cells contained RNA-dependent RNA polymerase activity, but no RNA-dependent DNA polymerase activity.

Animals↗

PubMed2026

Molecular insights and therapeutic innovations in low-risk human papillomavirus-associated cutaneous wart.

Human papillomavirus (HPV) is a DNA virus that belongs to the Papillomaviridae family. Among the various types, high-risk strains are associated to malignancy, whereas low-risk types cause benign skin warts due to persistent infection. Unlike high-risk HPVs, low-risk HPV genomes remain in an episomal state while expressing E6/E7 proteins. These proteins exhibit a reduced ability to degrade pRb and p53, which finally leads to controlled epithelial hyperplasia instead of developing malignancy. Infection with low-risk HPV activates distinct host signaling pathways, ultimately promoting the proliferation of keratinocytes and formation of warts. Simultaneously, it triggers host innate and adaptive immune responses that often clear the lesion. This review focuses on low-risk types that cause skin warts by analyzing the molecular pathways, particularly the integrin-FAK-PI3K/AKT, Hippo-YAP/TAZ pathway along with MAPK-ERK pathways that promotes cutaneous benign wart formation. This article further studies clinical management strategies for HPV associated warts, including primary destructive treatment (cryotherapy, keratolytics, excision), immunotherapies (imiquimod, interferon injections or intralesional antigen), and novel adjunctive therapies with clinical evidence including photodynamic therapy, intralesional chemotherapeutics, and emerging HPV vaccination strategies. Among these, for benign skin warts, intralesional immunotherapy, particularly Candida antigen, and intralesional HPV vaccination have shown encouraging responses clinically. But extensive controlled clinical studies are necessary to establish their efficacy and clinical value as a standard medicine. This review therefore, generates a comprehensive overview of papilloma virus mediated skin warts and their management for both clinicians and researchers.

Humans↗

PubMed1978

Isolation and characterization of a new rubella variang with DNA polymerase activity.

A rubella variant (HPV-RV) was isolated from high passage rubella virus preparations propagated at 37 degrees C in baby hamster kidney BHK21/WI-2 cells. HPV-RV formed clear plaques in HeLa cells and primary cells of the Rhesus monkey kidney although wild type rubella virus did not produce plaques in these cells. Cells persistently infected with rubella virus were insensitive to infection by HPV-RV at both 34 degrees and 39.5 degrees C. HPV-RV agglutinated one day old chick, human group O and sheep erythrocytes. This hemagglutinating activity was inhibited by anti-BHK latent virus serum but not by anti-rubella virus serum. The plaque forming ability of HPV-RV was neutralized by anti-BHK latent virus serum although the same antiserum did not affect the plaque forming ability of wild type rubella virus. Furthermore, HPV-RV was found to have the complement fixation antigen of rubella virus and DNA polymerase activity. From these findings, it is concluded that HPV-RV is a hybrid between rubella virus and a latent virus of BHK21/WI-2 cells.

Antigens, Viral↗

PubMed1978

Persistence of antibody after administration of monovalent and combined live attenuated measles, mumps, and rubella virus vaccines.

Hemagglutination-inhibiting antibodies were retained in comparable levels eight years after vaccination with Enders' original Edmonston and more attenuated Moraten (Attenuvax) and Schwarz line measles vaccines. Neutralizing antibody persisted without substantial decline in titer for at least 9.5 years after administration of Jeryl Lynn mumps virus vaccine (Mumpsvax). Antibodies were retained without important decline in children and adults for at least 7.5 and 7 years, respectively, after administration of HPV-77 duck-modified rubella vaccine (Meruvax). The patterns of antibody persistence 7.5 years after administration of combined measles-mumps-rubella (M-M-R) and mumps-rubella (Biavax) vaccines, 6 years after administration of measles-rubella vaccine (M-R-VAX), and 4 years after administration of measles-mumps vaccine (M-M-VAX) were the same as for the monovalent vaccines, indicating no alteration in the retention of immunity. Subclinical reinfection evidenced by increase in homologous antibody titer was observed to follow vaccination the same as occurs after natural infection.

Adult↗

PubMed2025

Repression of CADM1 transcription by HPV type 18 is mediated by three-dimensional rearrangement of promoter-enhancer interactions.

Upon infection, human papillomavirus (HPV) manipulates host cell gene expression to create an environment that is supportive of a productive and persistent infection. The virus-induced changes to the host cell's transcriptome are thought to contribute to carcinogenesis. Here, we show by RNA-sequencing that oncogenic HPV18 episome replication in primary human foreskin keratinocytes (HFKs) drives host transcriptional changes that are consistent between multiple HFK donors. We have previously shown that HPV18 recruits the host protein CTCF to viral episomes to control the differentiation-dependent viral transcriptional programme. Since CTCF is an important regulator of host cell transcription via coordination of epigenetic boundaries and long-range chromosomal interactions, we hypothesised that HPV18 may also manipulate CTCF to contribute to host transcription reprogramming. Analysis of CTCF binding in the host cell genome by ChIP-Seq revealed that while the total number of CTCF binding sites is not altered by the virus, there are a sub-set of CTCF binding sites that are either enriched or depleted of CTCF. Many of these altered sites are clustered within regulatory elements of differentially expressed genes, including the tumour suppressor gene cell adhesion molecule 1 (CADM1), which supresses epithelial cell growth and invasion. We show that HPV18 establishment results in reduced CTCF binding at the CADM1 promoter and upstream enhancer. Loss of CTCF binding is coincident with epigenetic repression of CADM1, in the absence of CpG hypermethylation, while adjacent genes including the transcriptional regulator ZBTB16 are activated. These data indicate that the CADM1 locus is subject to topological rearrangement following HPV18 establishment. We tested this hypothesis using 4C-Seq (circular chromosome confirmation capture-sequencing) and show that HPV18 establishment causes a loss of long-range chromosomal interactions between the CADM1 transcriptional start site and the upstream transcriptional enhancer. These data show that HPV18 manipulates host cell promoter-enhancer interactions to drive transcriptional reprogramming that may contribute to HPV-induced disease progression.

Humans↗

PubMed2026

HPV circulating tumor DNA as a potential prognostic and predictive biomarker in head and neck squamous cell carcinoma: a systematic review.

PURPOSE: Human papillomavirus circulating tumor DNA (HPVctDNA) has emerged as a promising prognostic biomarker in HPV-related head and neck squamous cell carcinoma (HNSCC). This systematic review aimed to synthesize current evidence on the diagnostic accuracy and prognostic value of HPVctDNA in HNSCC management. MATERIAL/METHODS: We systematically reviewed a PubMed-indexed database of studies published between January 2012 and September 2025. Eligible studies were assessed for design, primary tumor site and stage, treatment modality, HPVctDNA detection method, diagnostic accuracy (sensitivity and specificity), and reported clinical endpoints. Descriptive syntheses were performed; sensitivity and specificity were standardized to proportions and summarized as median values per group. RESULTS: A total of 60 studies, including 8,234 patients were analyzed, of which 41 (68.3%) focused exclusively on oropharyngeal squamous cell carcinoma (OPSCC) and 17 (28.3%) included mixed HPV-related HNSCC subsites and HPV-positive cancers of unknown primary. The median follow-up across the included studies was 23 months. Among the included studies, 19 were retrospective (31.7%) and 33 were prospective (55.0%), with a small proportion of cross-sectional and randomized clinical trials. Overall, 40 (66.7%) evaluated the role of HPVctDNA in a curative setting. Plasma was the most common sample type, analyzed in 55 studies (91.7%), while 5 studies also included saliva. Detection methods varied: 40 employed droplet digital PCR (ddPCR), 16 used quantitative PCR (qPCR) and 4 applied NGS-based assays. Most of these studies (38, 63.3%) evaluated the prognostic utility of HPVctDNA, while only 4 (6.7%) assessed HPVctDNA in a screening or diagnostic setting. Regarding diagnostic accuracy, the median sensitivity across evaluable studies was 91.1%, while the median specificity was 99.4%. In OPSCC-only cohorts, the median sensitivity and specificity were 89.4% and 99.4%, respectively. Dynamic changes in HPVctDNA levels during or after treatment were consistently associated with outcomes: clearance or sustained negativity correlated with higher response rates, improved progression-free survival and overall survival, while persistent positivity or increasing levels predicted disease progression and recurrence. CONCLUSIONS: HPVctDNA demonstrates high diagnostic and prognostic accuracy in HPV-related HNSCC, especially OPSCC, supporting its use for prognosis, treatment monitoring and early detection of recurrence. However, prospective interventional studies are still required to demonstrate that HPVctDNA-guided treatment decisions improve clinical outcomes before routine implementation.

Humans↗

PubMed2026

Conserved host-exclusive oligonucleotide motifs enriched in pathogenic genes of human oncogenic viruses.

Comparative viral genomics can reveal sequence-level constraints influencing virus-host interactions. Relative minimal absent words (rMAWs) are short oligonucleotide motifs present in viral genomes but completely absent from the host, potentially reflecting selective pressures related to host adaptation and immune evasion. Using the EAGLE algorithm and the GRCh38 human reference genome, we systematically screened for prevalent rMAWs (prMAWs) across six major human oncogenic viruses: Epstein-Barr virus (EBV), hepatitis B virus (HBV), hepatitis C virus (HCV), human papillomavirus (HPV), human T-cell leukemia virus type 1 (HTLV-1), and human herpesvirus 8/Kaposi's sarcoma-associated herpesvirus (HHV-8/KSHV). highly conserved 11- and 12-bp prMAWs were identified in EBV, HBV, HTLV-1, and HHV-8/KSHV, with sequence prevalences ranging from 91.5% to 97.9%. Conversely, no short prMAWs were detected in HCV or HPV, likely reflecting differences in genome architecture, mutation rates, and long-term host adaptation to the human host. Importantly, the identified host-exclusive motifs exhibited non-random genomic distribution and were preferentially embedded within viral genes central to replication, persistence, immune modulation, and oncogenesis, including EBNA-1 (EBV), HBx (HBV), Tax-associated regions (HTLV-1), and lytic replication genes of HHV-8/KSHV. Notably, all detected prMAWs were enriched in GC nucleotides and exhibited marked CpG over-representation, suggesting sequence constraints associated with epigenetic regulation and viral persistence. Collectively, these highly conserved, host-exclusive signatures offer promising, candidates for sequence-directed approaches in the diagnosis, monitoring, and investigation of virus-associated cancers.

Humans↗

PubMed1979

Further evaluation of the optimum age for rubella vaccine administration.

The hemagglutination-inhibition (HI) antibody responses of 452 children to HPV-77, DE5 rubella vaccine were studied. Results indicated that seroconversion rates and geometric mean titers in infants inoculated at 12 through 14 months of age are comparable with those achieved in older children. "Vaccine failures" seem to occur randomly in vaccinees after 1 year of age; the infectivity of individual vaccines is questioned. The persistence of HI antibody was evaluated through serial sampling up to three years postinoculation.

Age Factors↗

PubMed2025

Wastewater Sequencing Reveals Persistent Circulation and Rising Prevalence of Several Oncogenic Viruses Across Texas.

BACKGROUND: Oncogenic viruses cause high-risk cancers in humans and are responsible for nearly 20% of all cancer cases worldwide. Currently, very limited data exists in the realm of wastewater-based viral epidemiology (WBE) of cancer-causing viruses, with existing studies using targeted approaches (i.e PCR-based approaches) which lack scalability. Our study aims to carry out WBE with hybrid-capture probes to detect and track multiple oncogenic viruses simultaneously in wastewater across Texas, USA, overcoming the drawbacks associated with targeted approaches. METHODS: Here, we used a hybrid-capture approach to detect, filter and sequence oncogenic virus signals from wastewater samples collected over a duration of three years, from May 2022 to May 2025. Once viral reads were sequenced, we utilized established computational tools to characterize reads into their respective virus of origin. Next, viral abundances of each characterized oncogenic virus were tracked over time and read coverage across their genomes was measured using read mapping techniques. FINDINGS: We detected six known oncogenic viruses, along with three suspected oncogenic viruses across all sampling locations within Texas. Over three years, viral abundance gradually increased, with distinct peaks and dips over the summer and winter months. The prevalence of high-risk viruses such as HPV and EBV rose sharply, with increases in abundance observed post-2024. We also obtained nearly 100% genome coverage with viral reads captured using a hybrid-capture technique for almost all oncogenic viruses and their types. INTERPRETATIONS: Our study shows that a hybrid-capture method can efficiently overcome the challenges faced with using targeted approaches for WBE. Using this method, we get broader read coverage, coupled with concurrent and consistent real-time tracking dynamics of multiple oncogenic viruses. Our findings also emphasize the persistent circulation and rising prevalence of high-risk cancer-causing viruses, underscoring the need for sustained public health interventions to protect communities and assess viral prevalence in high-risk populations. FUNDING: This work was supported by S.B. 1780, 87th Legislature, 2021 Reg. Sess. (Texas 2021), the Baylor College of Medicine and the Alkek Foundation Seed Funds.

Journal Article↗

PubMed1978

Immunological studies in epidermodysplasia verruciformis.

Immunofluorescence and cell mediated immunity studies have been performed in 14 cases of epidermodysplasia verruciformis (EV), 3 of those abortive or regressing in members of the families of the patients with EV. Two different types of human papillomavirus (HPV)--HPV3 and HPV4--have been found in cases of EV. HPV3 was detected also in flat warts without features of EV. There was no cross-reactivity between these two viruses, neither with HPV1 responsible for plantar warts nor with HPV2 inducing common warts. There was a relationship between the type of HPV and the clinical picture of EV as well as the malignant transformation, namely HPV4 has been found to be more oncogenic. Cell mediated immunity (CMI) seems to be an important factor because it was depressed in a vast majority of active cases and preserved in regressing and abortive cases (in the members of the families of EV patients). However, low CMI has been found in EV cases infected with HPV3 and in persistent flat warts also due to HPV3, which did not undergo malignant transformation. In contrast, in a case of EV due to HPV4 a malignant transformation occured in spite of still preserved, although lowered CMI. Various human papillomaviruses seem to differ in their oncogenic potential. HPV1 responsible for plantar warts, and HPV2 for common warts have no evident oncogenic potential, HPV3 inducing both EV and flat warts has a low oncogenicity, whereas HPV4 inducing some cases of EV seems more oncogenic.

Adult↗