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However, the role of these cells during herpes simplex encephalitis (HSE) has not been fully characterized. We sought to identify different microglia\/microglia-like cells and describe the potential mechanisms and signaling pathways involved during HSE.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The transcriptional response of CD11b\n                      <jats:sup>+<\/jats:sup>\n                      immune cells, including microglia\/microglia-like cells, was investigated using single-cell RNA sequencing (scRNA-seq) on cells isolated from the ventral posterolateral nucleus (VPL)-enriched thalamic regions of C57BL\/6\u00a0N mice intranasally infected with herpes simplex virus-1 (HSV-1) (6\u2009\u00d7\u200910\n                      <jats:sup>5<\/jats:sup>\n                      PFUs\/20 \u00b5l). We further performed scanning electronic microscopy (SEM) analysis in VPL regions on day 6 post-infection (p.i.) to provide insight into microglial functions.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We describe a novel microglia-like transcriptional response associated with a rare cell population (7% of all analyzed cells), named \u201cin transition\u201d microglia\/microglia-like cells in HSE. This new microglia-like transcriptional signature, found in the highly infected thalamic regions, was enriched in specific genes (\n                      <jats:italic>Retnlg<\/jats:italic>\n                      ,\n                      <jats:italic>Cxcr2<\/jats:italic>\n                      ,\n                      <jats:italic>Il1f9<\/jats:italic>\n                      ) usually associated with neutrophils. Pathway analysis of this cell-type transcriptome showed increased NLRP3-inflammasome-mediated interleukin IL-1\u03b2 production, promoting a pro-inflammatory response. These cells' increased expression of viral transcripts suggests that the distinct \u201cin transition\u201d transcriptome corresponds to the intrinsic antiviral immune signaling of HSV-1-infected microglia\/microglia-like cells in the thalamus. In accordance with this phenotype, we observed several TMEM119\n                      <jats:sup>+<\/jats:sup>\n                      \/IBA-I\n                      <jats:sup>+<\/jats:sup>\n                      microglia\/microglia-like cells immunostained for HSV-1 in highly infected regions.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>A new microglia\/microglia-like state may potentially shed light on how microglia could react to HSV-1 infection. Our observations suggest that infected microglia\/microglia-like cells contribute to an exacerbated CNS inflammation. Further characterization of this transitory state of the microglia\/microglia-like cell transcriptome may allow the development of novel immunomodulatory approaches to improve HSE outcomes by regulating the microglial immune response.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12974-022-02437-7","type":"journal-article","created":{"date-parts":[[2022,4,6]],"date-time":"2022-04-06T10:02:55Z","timestamp":1649239375000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Single-cell transcriptomics of the ventral posterolateral nucleus-enriched thalamic regions from HSV-1-infected mice reveal a novel microglia\/microglia-like transcriptional response"],"prefix":"10.1186","volume":"19","author":[{"given":"Olus","family":"Uyar","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan Manuel","family":"Dominguez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maude","family":"Bordeleau","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lina","family":"Lapeyre","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fernando Gonz\u00e1lez","family":"Ib\u00e1\u00f1ez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luc","family":"Valli\u00e8res","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie-Eve","family":"Tremblay","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacques","family":"Corbeil","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guy","family":"Boivin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,4,6]]},"reference":[{"issue":"3","key":"2437_CR1","doi-asserted-by":"publisher","first-page":"541","DOI":"10.1086\/514600","volume":"26","author":"RJ Whitley","year":"1998","unstructured":"Whitley RJ, Kimberlin DW, Roizman B. 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