Home › Research › TREM2 and immune genetics
Microglia influence host defense, disease, and repair following murine coronavirus infection of the central nervous system
Mangale V, Syage AR, Ekiz HA, Skinner DD, Cheng Y, Stone CL, Brown RM, O'Connell RM et al.. Glia, 2020-05-25
Topic: Brain proteins, microglia and lab models
Plain-language summary
The present study examines functional contributions of microglia in host defense, demyelination, and remyelination following infection of susceptible mice with a neurotropic coronavirus. Treatment with PLX5622, an inhibitor of colony stimulating factor 1 receptor (CSF1R) that efficiently depletes microglia, prior to infection of the central nervous system (CNS) with the neurotropic JHM strain of mouse hepatitis virus (JHMV) resulted in increased mortality compared with control mice that correlated with impaired control of viral replication. Single cell RNA sequencing (scRNASeq) of CD45+ cells isolated from the CNS revealed that PLX5622 treatment resulted in muted CD4+ T cell activation profile that was associated with decreased expression of transcripts encoding MHC class II and CD86 in macrophages but not dendritic cells.
What this study adds
Evidence grade: Low
In mice, depleting microglia before a brain infection increased death and weakened control of the virus. This is an animal study of viral brain infection, not Alzheimer's disease, so it does not show how to treat, cure or prevent Alzheimer's.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Mangale, V., Syage, A. R., Ekiz, H. A., Skinner, D. D., Cheng, Y., Stone, C. L., et al. (2020). Microglia influence host defense, disease, and repair following murine coronavirus infection of the central nervous system. Glia. https://doi.org/10.1002/glia.23844
Vancouver
Mangale V, Syage AR, Ekiz HA, Skinner DD, Cheng Y, Stone CL, et al. Microglia influence host defense, disease, and repair following murine coronavirus infection of the central nervous system. Glia. 2020. doi:10.1002/glia.23844. PMID: 32449994.
BibTeX
@article{mangale2020-32449994,
author = {Mangale, V. and Syage, A. R. and Ekiz, H. A. and Skinner, D. D. and Cheng, Y. and Stone, C. L. and Brown, R. M. and O'Connell, R. M. and others},
title = {{Microglia influence host defense, disease, and repair following murine coronavirus infection of the central nervous system}},
journal = {Glia},
year = {2020},
doi = {10.1002/glia.23844},
pmid = {32449994},
url = {https://doi.org/10.1002/glia.23844}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- Treatment with PLX5622, an inhibitor of colony stimulating factor 1 receptor (CSF1R) that efficiently depletes microglia, prior to infection of the central nervous system (CNS) with the neurotropic JHM strain of mouse hepatitis virus (JHMV) resulted in increased mortality compared with control mice that correlated with impaired control of viral replication.
- Single cell RNA sequencing (scRNASeq) of CD45+ cells isolated from the CNS revealed that PLX5622 treatment resulted in muted CD4+ T cell activation profile that was associated with decreased expression of transcripts encoding MHC class II and CD86 in macrophages but not dendritic cells.
- Evaluation of spinal cord demyelination revealed a marked increase in white matter damage in PLX5622-treated mice that corresponded with elevated expression of transcripts encoding disease-associated proteins Osteopontin (Spp1), Apolipoprotein E (Apoe), and Triggering receptor expressed on myeloid cells 2 (Trem2) that were enriched within macrophages.
- In addition, PLX5622 treatment dampened expression of Cystatin F (Cst7), Insulin growth factor 1 (Igf1), and lipoprotein lipase (Lpl) within macrophage populations which have been implicated in promoting repair of damaged nerve tissue and this was associated with impaired remyelination.
Why it matters
In mice, depleting microglia before a brain infection increased death and weakened control of the virus. This is an animal study of viral brain infection, not Alzheimer's disease, so it does not show how to treat, cure or prevent Alzheimer's.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 44/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Glia) |
| Journal's citation record | 2 / 4 | Glia: journal h-index 233 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2020 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “murine”) — scores zero |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 71 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 8.9 citations a year over 8 year(s) since 2020 |
| Impact for its field and year | 3 / 6 | Cited 3.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 2 / 4 | Cited 24 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Thomas E. Lane: h-index 62 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Utah: institution h-index 1,238 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 32449994) |
| Free to read | 2 / 2 | Free to read |
| Total | 44 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Related
Studies in the library that share something with this one. The line above each title says what.
Studies this one cites
Referenced by this study and also in the alzhub library, so you can read them here.
Later studies that cite this one
1 study in the alzhub library lists this one in its references.
Related studies in TREM2 and immune genetics from nearby years
Also tagged “small”
900 studies in the library carry the topic tag “small”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 900 tagged studies.