Evidence map›Paper›PMID 38953377›Full record

ArticleJournal of virology2024

Six adenoviral vectored African swine fever virus genes protect against fatal disease caused by genotype I challenge.

Raquel Portugal, Hannah Goldswain, Rebecca Moore, Matthew Tully, Katie Harris, Amanda Corla, John Flannery, Linda K Dixon, Christopher L Netherton

Abstract read
In one paragraph

Article in Journal of virology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

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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

9 authors.

Raquel PortugalThe Pirbright Institute, Woking, Surrey, United Kingdom.ORCID 0000-0002-7144-9409
Hannah GoldswainThe Pirbright Institute, Woking, Surrey, United Kingdom.
Rebecca MooreThe Pirbright Institute, Woking, Surrey, United Kingdom.
Matthew TullyThe Pirbright Institute, Woking, Surrey, United Kingdom.
Katie HarrisThe Pirbright Institute, Woking, Surrey, United Kingdom.
Amanda CorlaThe Pirbright Institute, Woking, Surrey, United Kingdom.
John FlanneryThe Pirbright Institute, Woking, Surrey, United Kingdom.
Linda K DixonThe Pirbright Institute, Woking, Surrey, United Kingdom.ORCID 0000-0003-3845-3016
Christopher L NethertonThe Pirbright Institute, Woking, Surrey, United Kingdom.ORCID 0000-0002-1286-8590

Funding

Department for Environment, Food and Rural Affairs, UK Government (Defra) SE1516Department for Environment, Food and Rural Affairs, UK Government (Defra) SE1517, SE1520UK Research and Innovation (UKRI) BBS/E/I/00007031, BBS/E/I/00007037, BBS/E/I/00007039
6 · The paper itself

Abstract

African swine fever virus causes a lethal hemorrhagic disease in domestic swine and wild boar for which currently licensed commercial vaccines are only available in Vietnam. Development of subunit vaccines is complicated by the lack of information on protective antigens as well as suitable delivery systems. Our previous work showed that a pool of eight African swine fever virus genes vectored using an adenovirus prime and modified vaccinia virus boost could prevent fatal disease after challenge with a virulent genotype I isolate of the virus. Here, we identify antigens within this pool of eight that are essential for the observed protection and demonstrate that adenovirus-prime followed by adenovirus-boost can also induce protective immune responses against genotype I African swine fever virus. Immunization with a pool of adenoviruses expressing individual African swine fever virus genes partially tailored to genotype II virus did not protect against challenge with genotype II Georgia 2007/1 strain, suggesting that different antigens may be required to induce cross-protection for genetically distinct viruses. IMPORTANCE: African swine fever virus causes a lethal hemorrhagic disease in domestic pigs and has killed millions of animals across Europe and Asia since 2007. Development of safe and effective subunit vaccines against African swine fever has been problematic due to the complexity of the virus and a poor understanding of protective immunity. In a previous study, we demonstrated that a complex combination of eight different virus genes delivered using two different viral vector vaccine platforms protected domestic pigs from fatal disease. In this study, we show that three of the eight genes are required for protection and that one viral vector is sufficient, significantly reducing the complexity of the vaccine. Unfortunately, this combination did not protect against the current outbreak strain of African swine fever virus, suggesting that more work to identify immunogenic and protective viral proteins is required to develop a truly effective African swine fever vaccine.

Indexed as

AdenoviridaeAfrican Swine FeverAfrican Swine Fever VirusGenetic VectorsGenotypeViral VaccinesAnimalsAntibodies, ViralAntigens, ViralSwineVaccines, SubunitAntibodies, ViralAntigens, ViralVaccines, SubunitViral Vaccinesadenovirus vectorsAfrican swine feverpigvaccinesviral hemorrhagic fever

Identifiers

PMID38953377
PMCPMC11264932

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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.