Evidence map›Paper›PMID 33927339›Full record

ArticleCommunications biology2021

Slow viral propagation during initial phase of infection leads to viral persistence in mice.

Haifeng C Xu, Ruifeng Wang, Prashant V Shinde, Lara Walotka, Anfei Huang, Gereon Poschmann, Jun Huang, Wei Liu, Kai Stühler, Heiner Schaal and 5 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

15 citing papers in PubMed, 16 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

15 authors at 3 institutions in 2 countries.

Haifeng C Xu *Department of Molecular Medicine II, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.ORCID 0000-0002-4674-4983
Ruifeng Wang *Department of Molecular Medicine II, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.
Prashant V ShindeDepartment of Molecular Medicine II, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.
Lara WalotkaInstitute of Virology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Anfei HuangDepartment of Molecular Medicine II, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.
Gereon PoschmannInstitute of Molecular Medicine I, Proteome research, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.ORCID 0000-0003-2448-0611
Jun HuangDepartment of Molecular Medicine II, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.
Wei LiuDepartment of Molecular Medicine II, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.
Kai StühlerInstitute of Molecular Medicine I, Proteome research, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Heiner SchaalInstitute of Virology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.ORCID 0000-0002-1636-4365
Andreas BergthalerCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID 0000-0003-0597-1976
Aleksandra A PandyraDepartment of Molecular Medicine II, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.
Cornelia HardtInstitute of Immunology, Medical Faculty, University of Duisburg-Essen, Essen, Germany.
Karl S LangInstitute of Immunology, Medical Faculty, University of Duisburg-Essen, Essen, Germany.
Philipp A LangDepartment of Molecular Medicine II, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany. langp@uni-duesseldorf.de.ORCID 0000-0001-5341-0407
Heinrich Heine University Düsseldorf · DEUniversity of Duisburg-Essen · DEAustrian Academy of Sciences · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune evasion of pathogens can modify the course of infection and impact viral persistence and pathology. Here, using different strains of the lymphocytic choriomeningitis virus (LCMV) model system, we show that slower propagation results in limited type I interferon (IFN-I) production and viral persistence. Specifically, cells infected with LCMV-Docile exhibited reduced viral replication when compared to LCMV-WE and as a consequence, infection with LCMV-Docile resulted in reduced activation of bone marrow derived dendritic cells (BMDCs) and IFN-I production in vitro in comparison with LCMV-WE. In vivo, we observed a reduction of IFN-I, T cell exhaustion and viral persistence following infection of LCMV-Docile but not LCMV-WE. Mechanistically, block of intracellular protein transport uncovered reduced propagation of LCMV-Docile when compared to LCMV-WE. This reduced propagation was critical in blunting the activation of the innate and adaptive immune system. When mice were simultaneously infected with LCMV-Docile and LCMV-WE, immune function was restored and IFN-I production, T cell effector functions as well as viral loads were similar to that of mice infected with LCMV-WE alone. Taken together, this study suggests that reduced viral propagation can result in immune evasion and viral persistence.

Indexed as

Virus ReplicationAnimalsArenaviridae InfectionsDendritic CellsLymphocytic choriomeningitis virusMiceMice, Inbred C57BLMice, KnockoutReceptor, Interferon alpha-betaT-LymphocytesIfnar1 protein, mouseReceptor, Interferon alpha-beta

Identifiers

PMID33927339
PMCPMC8084999
OpenAlexW3158578082

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.