ArticlePLoS pathogens2012
Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 53 citations in OpenAlex.
- Conserved gammaherpesvirus protein kinase counters myeloid cell-specific type I IFN receptor but not IRF-3 expression to promote the establishment of chronic latent infection in the spleen.Journal of virology · 2026Article
- HIGH DOSE GAMMAHERPESVIRUS INFECTION IN MACROPHAGES RESULTS IN INFLAMMATORY MULTIMODAL CELL DEATH.bioRxiv : the preprint server for biology · 2026Article
- CYTOKINE SIGNALING REGULATES MULTIPLE STAGES OF GAMMA-HERPESVIRUS INFECTION IN MYELOID CELLS.bioRxiv : the preprint server for biology · 2026Article
- STAT1 and herpesviruses: Making lemonade from lemons.Virology · 2025Review
- Tissue and cellular tropism ofVeterinary pathology · 2024Article
- Indirect CD4Journal of virology · 2024Article
- Macrophages drive KSHV B cell latency.Cell reports · 2023Article
- Lytic Replication and Reactivation from B Cells Is Not Required for Establishing or Maintaining Gammaherpesvirus LatencyJournal of virology · 2022Article
- Olfactory Entry Promotes Herpesvirus Recombination.Journal of virology · 2021Article
- Conserved Gammaherpesvirus Protein Kinase Counters the Antiviral Effects of Myeloid Cell-Specific STAT1 Expression To Promote the Establishment of Splenic B Cell Latency.Journal of virology · 2021Article
- Interferon Regulatory Factor 3 Supports the Establishment of Chronic Gammaherpesvirus Infection in a Route- and Dose-Dependent Manner.Journal of virology · 2021Article
- Gammaherpesvirus Usurps Host IL-17 Signaling To Support the Establishment of Chronic Infection.mBio · 2021Article
- Optimized Detection of Acute MHV68 Infection With a Reporter System Identifies Large Peritoneal Macrophages as a Dominant Target of Primary Infection.Frontiers in microbiology · 2021Article
- Deletion of Murine Gammaherpesvirus GeneJournal of virology · 2020Article
- Deletion of immune evasion genes provides an effective vaccine design for tumor-associated herpesviruses.NPJ vaccines · 2020Article
- Review
- Immune Control ofViral immunology · 2020Article
- Article
- Glycoprotein K8.1A of Kaposi's Sarcoma-Associated Herpesvirus Is a Critical B Cell Tropism Determinant Independent of Its Heparan Sulfate Binding Activity.Journal of virology · 2019Article
- Gammaherpesvirus BoHV-4 infects bovine respiratory epithelial cells mainly at the basolateral side.Veterinary research · 2019Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
Gamma-herpesviruses persist in lymphocytes and cause disease by driving their proliferation. Lymphocyte infection is therefore a key pathogenetic event. Murid Herpesvirus-4 (MuHV-4) is a rhadinovirus that like the related Kaposi's Sarcoma-associated Herpesvirus persists in B cells in vivo yet infects them poorly in vitro. Here we used MuHV-4 to understand how virion tropism sets the path to lymphocyte colonization. Virions that were highly infectious in vivo showed a severe post-binding block to B cell infection. Host entry was accordingly an epithelial infection and B cell infection a secondary event. Macrophage infection by cell-free virions was also poor, but improved markedly when virion binding improved or when macrophages were co-cultured with infected fibroblasts. Under the same conditions B cell infection remained poor; it improved only when virions came from macrophages. This reflected better cell penetration and correlated with antigenic changes in the virion fusion complex. Macrophages were seen to contact acutely infected epithelial cells, and cre/lox-based virus tagging showed that almost all the virus recovered from lymphoid tissue had passed through lysM(+) and CD11c(+) myeloid cells. Thus MuHV-4 reached B cells in 3 distinct stages: incoming virions infected epithelial cells; infection then passed to myeloid cells; glycoprotein changes then allowed B cell infection. These data identify new complexity in rhadinovirus infection and potentially also new vulnerability to intervention.
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