ArticlePLoS pathogens2015
Rhadinovirus host entry by co-operative infection.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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.
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Who cites it
22 citing papers in PubMed.
- CYTOKINE SIGNALING REGULATES MULTIPLE STAGES OF GAMMA-HERPESVIRUS INFECTION IN MYELOID CELLS.bioRxiv : the preprint server for biology · 2026Article
- Alveolar Macrophages in Viral Respiratory Infections: Sentinels and Saboteurs of Lung Defense.International journal of molecular sciences · 2025Review
- Indirect CD4Journal of virology · 2024Article
- Olfactory Entry Promotes Herpesvirus Recombination.Journal of virology · 2021Article
- Conquering the Host: Determinants of Pathogenesis Learned from Murine Gammaherpesvirus 68.Annual review of virology · 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
- Immune Control ofViral immunology · 2020Article
- A CD4Journal of virology · 2020Article
- Article
- Murine Cytomegalovirus Spread Depends on the Infected Myeloid Cell Type.Journal of virology · 2019Article
- Inhibition of murine herpesvirus-68 replication by IFN-gamma in macrophages is counteracted by the induction of SOCS1 expression.PLoS pathogens · 2018Article
- A gammaherpesvirus provides protection against allergic asthma by inducing the replacement of resident alveolar macrophages with regulatory monocytes.Nature immunology · 2017Article
- Type I Interferon Signaling to Dendritic Cells Limits Murid Herpesvirus 4 Spread from the Olfactory Epithelium.Journal of virology · 2017Article
- The Major Envelope Glycoprotein of Murid Herpesvirus 4 Promotes Sexual Transmission.Journal of virology · 2017Article
- CD8+ T cell evasion mandates CD4+ T cell control of chronic gamma-herpesvirus infection.PLoS pathogens · 2017Article
- Type I Interferons and NK Cells Restrict Gammaherpesvirus Lymph Node Infection.Journal of virology · 2016Article
- Herpes Simplex Virus 1 Interaction with Myeloid Cells In Vivo.Journal of virology · 2016Article
- Type I Interferons Direct Gammaherpesvirus Host Colonization.PLoS pathogens · 2016Article
- Interplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the Host.Frontiers in microbiology · 2016Review
- Alveolar Macrophages Are a Prominent but Nonessential Target for Murine Cytomegalovirus Infecting the Lungs.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Rhadinoviruses establish chronic infections of clinical and economic importance. Several show respiratory transmission and cause lung pathologies. We used Murid Herpesvirus-4 (MuHV-4) to understand how rhadinovirus lung infection might work. A primary epithelial or B cell infection often is assumed. MuHV-4 targeted instead alveolar macrophages, and their depletion reduced markedly host entry. While host entry was efficient, alveolar macrophages lacked heparan - an important rhadinovirus binding target - and were infected poorly ex vivo. In situ analysis revealed that virions bound initially not to macrophages but to heparan⁺ type 1 alveolar epithelial cells (AECs). Although epithelial cell lines endocytose MuHV-4 readily in vitro, AECs did not. Rather bound virions were acquired by macrophages; epithelial infection occurred only later. Thus, host entry was co-operative - virion binding to epithelial cells licensed macrophage infection, and this in turn licensed AEC infection. An antibody block of epithelial cell binding failed to block host entry: opsonization provided merely another route to macrophages. By contrast an antibody block of membrane fusion was effective. Therefore co-operative infection extended viral tropism beyond the normal paradigm of a target cell infected readily in vitro; and macrophage involvement in host entry required neutralization to act down-stream of cell binding.
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Registered trials
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.