Evidence map›Paper›PMID 31917822›Full record

ArticlePloS one2020

The effect of mutations derived from mouse-adapted H3N2 seasonal influenza A virus to pathogenicity and host adaptation.

Eun-Ji Choi, Young Jae Lee, Jin-Moo Lee, Yeon-Jung Kim, Jang-Hoon Choi, Byeongwoo Ahn, Kisoon Kim, Myung Guk Han

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 17 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Eun-Ji ChoiDivision of Viral Disease Research, Center for Infectious Diseases Research, National Institute of Health, Korea Centers for Disease Control and Prevention, Osong, Republic of Korea.
Young Jae LeeDivision of Viral Disease Research, Center for Infectious Diseases Research, National Institute of Health, Korea Centers for Disease Control and Prevention, Osong, Republic of Korea.
Jin-Moo LeeDivision of Viral Disease Research, Center for Infectious Diseases Research, National Institute of Health, Korea Centers for Disease Control and Prevention, Osong, Republic of Korea.
Yeon-Jung KimDivision of Viral Disease Research, Center for Infectious Diseases Research, National Institute of Health, Korea Centers for Disease Control and Prevention, Osong, Republic of Korea.
Jang-Hoon ChoiDivision of Viral Disease Research, Center for Infectious Diseases Research, National Institute of Health, Korea Centers for Disease Control and Prevention, Osong, Republic of Korea.
Byeongwoo AhnCollege of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea.
Kisoon KimDivision of Viral Disease Research, Center for Infectious Diseases Research, National Institute of Health, Korea Centers for Disease Control and Prevention, Osong, Republic of Korea.
Myung Guk HanDivision of Viral Disease Research, Center for Infectious Diseases Research, National Institute of Health, Korea Centers for Disease Control and Prevention, Osong, Republic of Korea.
Korea Center for Disease Control and Prevention · KRKorea Disease Control and Prevention Agency · KRChungbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elucidating the genetic basis of influenza A viruses (IAVs) is important to understand which mutations will determine the virulence and the host range of mammals. Here, seasonal H3N2 influenza was adapted in mice by serial passage and four mutants, each carrying amino acid substitutions related to mouse adaptation in either the PB2, HA, NP, or NA protein, were generated. To confirm the contribution of each gene to enhanced pathogenicity and mouse adaptation, mice were inoculated with the respective variants, and virulence, replication, histopathology, and infectivity were examined. The virus harboring HA mutations displayed increased infection efficiency and replication competence, resulting in higher mortality in mice relative to those infected with wild-type virus. By contrast, the NP D34N mutation caused rapid and widespread infection in multiple organs without presenting virulent symptoms. Additionally, the PB2 F323L mutation presented delayed but elevated replication competence in the respiratory tract, whereas the S331R mutation in NA showed no considerable effects on mouse adaptation. These results suggested that mouse-adapted changes in HA are major factors in increased pathogenicity and that mutations in NP and PB2 also contribute to cross-species adaptability. Our findings offer a better understanding of the molecular basis for IAV pathogenicity and adaptation in a new host.

Indexed as

MutationAdaptation, PhysiologicalAnimalsFemaleGenome, ViralHost Microbial InteractionsInfluenza A Virus, H3N2 SubtypeLungMiceReassortant VirusesVirulenceVirus Replication

Identifiers

PMID31917822
PMCPMC6952113
OpenAlexW2999219718

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.