Evidence map›Paper›PMID 40619428›Full record

ArticleJournal of neuroinflammation2025

MAVS signaling of long-lived brain-resident myeloid cells is needed during viral encephalitis to adjust the transcriptome of CNS infiltrating CD8

Andreas Pavlou, Luca Ghita, Felix Mulenge, Inken Waltl, Olivia Luise Gern, Pia-Katharina Larsen, Bibiana Costa, Veronica Duran, Lena Mareike Busker, Shelly J Robertson and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Andreas Pavlou *Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, 30625, Germany.
Luca Ghita *Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, 30625, Germany.
Felix MulengeInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, 30625, Germany.
Inken WaltlInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, 30625, Germany.
Olivia Luise GernInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, 30625, Germany.
Pia-Katharina LarsenInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, 30625, Germany.
Bibiana CostaInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, 30625, Germany.
Veronica DuranInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, 30625, Germany.
Lena Mareike BuskerInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, 30625, Germany.
Shelly J RobertsonInnate Immunity & Pathogenesis Section, Laboratory of Neurological Infections and Immunity, Rocky Mountain Laboratories, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.
Yvonne LuederInstitute of Immunology, Hannover Medical School, Hannover, 30625, Germany.
Stephan HalleInstitute of Immunology, Hannover Medical School, Hannover, 30625, Germany.
Reinhold FörsterInstitute of Immunology, Hannover Medical School, Hannover, 30625, Germany.
Sonja M BestInnate Immunity & Pathogenesis Section, Laboratory of Neurological Infections and Immunity, Rocky Mountain Laboratories, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.
Martin StangelDepartment of Neurology, Clinical Neuroimmunology and Neurochemistry, Hannover Medical School, Hannover, 30625, Germany.
Ulrich KalinkeInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, 30625, Germany. ulrich.kalinke@twincore.de.

Funding

Deutsche Forschungsgemeinschaft 39087428 EXC 2155Helmholtz-Gemeinschaft ZT-0027
6 · The paper itself

Abstract

Neurotropic viruses like vesicular stomatitis virus (VSV) can infect the central nervous system (CNS) through the olfactory route. Following intranasal instillation, VSV moves along the axons of olfactory sensory neurons to the olfactory bulb. While within the olfactory bulb the spread of the virus is controlled by microglia activation and the recruitment of peripheral leukocytes, some of the underlying mechanisms remain unknown. To investigate these mechanisms, we used mice with conditional deletions of the mitochondrial antiviral-signaling protein (MAVS), an adaptor for RIG-I-like receptor (RLR) signaling. By selectively deleting MAVS in neurons, astrocytes, or long-lived myeloid cells, we discovered that RLR signaling specifically within brain-resident myeloid cells is crucial for protection against the virus. Infected mice with a MAVS deletion in these myeloid cells showed normal myeloid cell and leukocyte infiltration into the brain. However, the P2RY12

Indexed as

Adaptor Proteins, Signal TransducingBrainCD8-Positive T-LymphocytesEncephalitis, ViralMyeloid CellsSignal TransductionTranscriptomeAnimalsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicAdaptor Proteins, Signal TransducingMAVS protein, mouseBrain infectionCD8+ T cellsCNSCross-presentationMAVS signalingMicrogliaRLR signaling

Identifiers

PMID40619428
PMCPMC12232705

What OpenQuestion holds

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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.