Evidence map›Paper›PMID 39350162›Full record

ArticleBMC biotechnology2024

HPV16 mutant E6/E7 construct is protective in mouse model.

Maryam Moazami Goodarzi, Ghasem Mosayebi, Ali Ganji, Ehsan Raoufi, Samira Sadelaji, Saeid Babaei, Hamid Abtahi

Abstract read
In one paragraph

Article in BMC biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Maryam Moazami GoodarziDepartment of Medical Biotechnology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran.
Ghasem MosayebiDepartment of Microbiology and Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran.
Ali GanjiDepartment of Microbiology and Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran.
Ehsan RaoufiVaccine research center, Iran University of Medical Sciences, Tehran, Iran.
Samira SadelajiDepartment of Microbiology and Immunology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran.
Saeid BabaeiDepartment of Anatomy, School of Medicine, Arak University of Medical Sciences, Arak, Iran.
Hamid AbtahiMolecular and Medicine Research Center, Arak University of Medical Sciences, Arak, Iran. abtahi@arakmu.ac.ir.

Funding

Arak University of Medical Sciences 1296
6 · The paper itself

Abstract

backgroundHuman papillomavirus type 16 (HPV-16) infection is strongly associated with considerable parts of cervical, neck, and head cancers. Performed investigations have had moderate clinical success, so research to reach an efficient vaccine has been of great interest. In the present study, the immunization potential of a newly designed HPV-16 construct was evaluated in a mouse model.

resultsInitially, a construct containing HPV-16 mutant (m) E6/E7 fusion gene was designed and antigen produced in two platforms (i.e., DNA vaccine and recombinant protein). Subsequently, the immunogenicity of these platforms was investigated in five mice) C57BL/6 (groups based on several administration strategies. Three mice groups were immunized recombinant protein, DNA vaccine, and a combination of them, and two other groups were negative controls. The peripheral blood mononuclear cells (PBMCs) proliferation, Interleukin-5 (IL-5) and interferon-γ (IFN-γ) cytokines, IgG1 and IgG2a antibody levels were measured. After two weeks, TC-1 tumor cells were injected into all mice groups, and subsequently further analysis of tumor growth and metastasis and mice survival were performed according to the schedule. Overall, the results obtained from in vitro immunology and tumor cells challenging assays indicated the potential of the mE6/E7 construct as an HPV16 therapeutic vaccine candidate. The results demonstrated a significant increase in IFN-γ cytokine (P value < 0.05) in the Protein/Protein (D) and DNA/Protein (E) groups. This finding was in agreement with in vivo assays. Control groups show a 10.5-fold increase (P value < 0.001) and (C) DNA/DNA group shows a 2.5-fold increase (P value < 0.01) in tumor growth compared to D and E groups. Also, a significant increase in survival of D and E (P value < 0.001) and C (P value < 0.01) groups were observed.

conclusionsSo, according to the findings, the recombinant protein could induce stronger protection compared to the DNA vaccine form. Protein/Protein and DNA/Protein are promising administration strategies for presenting this construct to develop an HPV-16 therapeutic vaccine candidate.

Indexed as

Human papillomavirus 16Mice, Inbred C57BLOncogene Proteins, ViralPapillomavirus E7 ProteinsPapillomavirus VaccinesRepressor ProteinsVaccines, DNAAnimalsDisease Models, AnimalFemaleHumansMicePapillomavirus InfectionsRecombinant Fusion ProteinsE6 protein, Human papillomavirus type 16oncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsPapillomavirus VaccinesRecombinant Fusion ProteinsRepressor ProteinsVaccines, DNADNA vaccineFusion geneHPV-16Prime-boost strategyRecombinant proteinTherapeutic vaccineTumor-specific antigens (TSAs)

Identifiers

PMID39350162
PMCPMC11443707

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.