Evidence map›Paper›PMID 28721397›Full record

ArticleHeliyon2017

HIVIS-DNA or HIVISopt-DNA priming followed by CMDR vaccinia-based boosts induce both humoral and cellular murine immune responses to HIV.

J Hinkula, S Petkov, K Ljungberg, D Hallengärd, A Bråve, M Isaguliants, T Falkeborn, S Sharma, V Liakina, M Robb and 8 more

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.3field-weighted citation impact, top 23% of its field
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

2 citing papers in PubMed, 13 citations in OpenAlex.

  1. Trial
  2. 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

18 authors at 7 institutions in 3 countries.

J HinkulaDepartment of Clinical and Experimental Medicine, Linköping University, 58183 Linköping, Sweden.
S PetkovDepartment of Microbiology Tumor and Cell Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
K LjungbergDepartment of Microbiology Tumor and Cell Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
D HallengärdDepartment of Microbiology Tumor and Cell Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
A BråveDepartment of Microbiology Tumor and Cell Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
M IsaguliantsDepartment of Microbiology Tumor and Cell Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
T FalkebornDepartment of Clinical and Experimental Medicine, Linköping University, 58183 Linköping, Sweden.
S SharmaDepartment of Clinical and Experimental Medicine, Linköping University, 58183 Linköping, Sweden.
V LiakinaFaculty of Medicine, Vilnius University 2, 08661 Vilnius, Lithuania.
M RobbU.S. Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, 20892 MD, USA.
M EllerU.S. Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, 20892 MD, USA.
B MossLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, 20892 MD, USA.
G BiberfeldDepartment of Microbiology Tumor and Cell Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
E SandströmDepartment of South Hospital, Karolinska Institutet, 11883 Stockholm, Sweden.
C NilssonDepartment of Microbiology Tumor and Cell Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
K MarklandClinical Research Center and Vecura, Karolinska University Hospital, 17176 Stockholm, Sweden.
P BlombergClinical Research Center and Vecura, Karolinska University Hospital, 17176 Stockholm, Sweden.
B WahrenDepartment of Microbiology Tumor and Cell Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
Karolinska Institutet · SELinköping University · SEKarolinska University Hospital · SEHenry M. Jackson Foundation · USNational Institute of Allergy and Infectious Diseases · USVilnius University · LTWalter Reed Army Institute of Research · US

Funding

Recombinant Virus VaccinesZIAAI000416 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MOSS, BERNARD · 2009 to 2025
$17.3M
6 · The paper itself

Abstract

backgroundIn order to develop a more effective prophylactic HIV-1 vaccine it is important optimize the components, improve Envelope glycoprotein immunogenicity as well as to explore prime-boost immunization schedules. It is also valuable to include several HIV-1 subtype antigens representing the world-wide epidemic.

methodsHIVIS-DNA plasmids which include Env genes of subtypes A, B and C together with Gag subtypes A and B and RTmut/Rev of subtype B were modified as follows: the Envelope sequences were shortened, codon optimized, provided with an FT4 sequence and an immunodominant region mutated. The reverse transcriptase (RT) gene was shortened to contain the most immunogenic N-terminal fragment and fused with an inactivated viral protease vPR gene. HIVISopt-DNA thus contains fewer plasmids but additional PR epitopes compared to the native HIVIS-DNA. DNA components were delivered intradermally to young Balb/c mice once, using a needle-free Biojector® immediately followed by dermal electroporation. Vaccinia-based MVA-CMDR boosts including Env gene E and Gag-RT genes A were delivered intramuscularly by needle, once or twice.

resultsBoth HIVIS-DNA and HIVISopt-DNA primed humoral and cell mediated responses well. When boosted with heterologous MVA-CMDR (subtypes A and E) virus inhibitory neutralizing antibodies were obtained to HIV-1 subtypes A, B, C and AE. Both plasmid compositions boosted with MVA-CMDR generated HIV-1 specific cellular responses directed against HIV-1 Env, Gag and Pol, as measured by IFNγ ELISpot. It was shown that DNA priming augmented the vector MVA immunological boosting effects, the HIVISopt-DNA with a trend to improved (Env) neutralization, the HIVIS-DNA with a trend to better (Gag) cell mediated immune reponses.

conclusionsHIVIS-DNA was modified to obtain HIVISopt-DNA that had fewer plasmids, and additional epitopes. Even with one DNA prime followed by two MVA-CMDR boosts, humoral and cell-mediated immune responses were readily induced by priming with either DNA construct composition. Priming by HIV-DNA augmented neutralizing antibody responses revealed by boosting with the vaccinia-based heterologous sequences. Cellular and antibody responses covered selected strains representing HIV-1 subtypes A, B, C and CRF01_AE. We assume this is related to the inclusion of heterologous full genes in the vaccine schedule.

Indexed as

ImmunologyInfectious diseaseVaccinesVirology

Identifiers

PMID28721397
PMCPMC5496381
OpenAlexW2725479583

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.