AMR Lab · DeCure for X

DeCure for Human papilloma virus infection

DeCure's autonomous AMR AI scientist is researching a drug-repurposing hypothesis for human papilloma virus infection — screening already-approved drugs against its 4-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.

Disease module4 genesLead labAMR
All cures
AMRDOID:11166$DeCureAMR

The disease map

Disease moduleHuman papilloma virus infection maps to a 4-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.

Research record

01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash

Current lead

No approved-drug candidate for human papilloma virus infection is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.

Molecular view

programmed cell death 1 (PDCD1)PDCD1 is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.

Loading structure…
helix sheet apo structuredrag to rotate · scroll to zoom

RCSB Protein Data Bank · entry 9Q8L · 1.85 Å · ligand none (apo structure). Experimental structure, not a prediction.

What the evidence adds up to

Human papillomavirus infection is common in the genital tract and causes cancer of stratified epithelium. The viral proteins E6 and E7 inhibit epithelial cell differentiation and stimulate proliferation to create an environment that supports viral genome replication. In high-risk HPV type 16, expression of E6-E7 oncogenes leads to chromosomal aneuploidy, which favours integration of the viral genome into cellular chromosomes. Integration sites are randomly distributed across the genome. For HPV type 18, integration appears required for progression to invasive phenotype, but for HPV 16 it may not always be necessary.

The mere presence of HPV is not sufficient for neoplasia to develop. Genetic and other co-factors are needed for expression of the invasive phenotype. One identified genetic susceptibility involves codon 98 of the fragile histidine triad gene. Interactions between HIV and HPV are complex and favour persistence and progression of cervical disease. More organs are now recognised as susceptible to HPV-driven malignant transformation, including oropharynx, rectum, anal area, and reproductive tracts of both women and men.

As of 2024, there is no drug that specifically stops HPV replication. The 2005 review noted that future research should pave the way for therapeutic vaccine development, but the 2024 clinical case report confirms that no such specific antiviral exists. Early detection, patient information, observation, and timely treatment remain the mainstays of management, alongside prevention of infection.

What is still missing is a drug that directly targets the virus to halt its replication. No clinical trial data for any repurposed or novel antiviral against HPV were presented in these abstracts. Patient stratification by HPV type, integration status, and co-factors such as HIV status or genetic susceptibility has not been incorporated into a treatment trial. Funding for therapeutic vaccine development or antiviral screening against HPV remains absent from these reports.

Evidence

Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.

Science s STKE · 2005 · 17 citations

Human Papillomaviruses and Cell Signaling

AbstractHuman papillomaviruses cause cancer of the stratified epithelium, and the incidence of infection with these viruses in the genital tract is high. The alterations in the biology of normal epithelial cells that lead to malignancy are a consequence of the activity of certain viral proteins, whose function is to create an environment conducive to the replication of the viral genome through inhibition of epithelial cell differentiation and stimulation of proliferation.

https://doi.org/10.1126/stke.2882005pe29
Current Opinion in Obstetrics & Gynecology · 2005 · 14 citations

Update on pathophysiologic mechanisms of human papillomavirus

AbstractPURPOSE OF REVIEW: The role of the human papillomavirus in the pathogenesis has been the subject of many publications in the recent literature. The physical state of the human papillomavirus and the role of chromosomal aneuploidy has been reported. This review discusses the recent pathological mechanisms described in the genesis of human papillomavirus-related disease. RECENT FINDINGS: The mere presence of the human papillomavirus is not sufficient for the development of neoplasia. Genetic and other co-factors seem to be necessary for the expression of the invasive phenotype. The expression of human papillomavirus 16 E6-E7 oncogenes results in chromosomal aneuploidy, favouring the integration of high-risk human papillomavirus genomes into cellular chromosomes. The integration of human papillomavirus 16 may not always be required for the progression to the invasive phenotype unlike human papillomavirus 18 DNA. Such integration sites are randomly distributed over the whole genome. The genetic susceptibility of codon 98 of the fragile histadine triad has been elucidated. SUMMARY: Various molecular mechanisms of human papillomavirus-associated neoplasia are discussed. The interaction between HIV and human papillomavirus are complex and favour the persistence and progression of cervical disease. Future research should pave the way for therapeutic vaccine development.

https://doi.org/10.1097/00001703-200502000-00011
Frontiers in Medicine · 2023 · 1 citations · open access

Treatment of condylomata acuminata caused by low-risk human papillomavirus with chloroquine phosphate gel

AbstractObjective To observe the stability and therapeutic effect of chloroquine phosphate gel on human condylomata acuminata (CA) caused by low-risk human papillomavirus (HPV). Methods The appearance, viscosity, pH, chloroquine concentration, deethylchloroquine concentration and content uniformity of chloroquine phosphate gel were examined for 24 months, the gel met the quality standards throughout the 24-month observation. A nude mouse model harboring CA xenografts was used to observe the therapeutic effect of this gel on CA in vivo . Results After 14 days of gel administration, compared with the control group, the treatment group had significantly smaller warts and significantly reduced DNA copy numbers of HPV6 and HPV11 in the wart tissues. Immunohistochemistry analysis of p53 protein expression in the wart tissues of the treatment group was significantly increased. Conclusion Chloroquine phosphate gel was stable and effective against CA, possibly through the promotion of p53 protein expression to induce apoptosis, leading to the involution of warts.

https://doi.org/10.3389/fmed.2023.1171550
Lekarstvennye sredstva i racionalʹnaâ farmakoterapiâ. · 2024 · 0 citations

RECURRENT PAPILLOMATOSIS: DIAGNOSTICS AND TREATMENT. CLINICAL CASE

AbstractAbstract. The human papillomavirus is a serious problem of the 21st century, due to its widespread prevalence, contagiousness and the possible consequences of malignancy of the epithelium affected by it. More and more organs are susceptible to transformation of epithelial cells by the virus into a malignant process (oropharynx, rectum and anal area, as well as the reproductive sections of women and men). There is also the lack of a drug that specifically affects the virus to stop its replication. Therefore, early detection, informing the patient about the possible consequences, observation and timely treatment if necessary, as well as prevention of infection with the human papilloma virus are very important.

https://doi.org/10.56356/27827259_2024_10_63

Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.

DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.