ArticleJournal of virology2011
Protein pUL128 of human cytomegalovirus is necessary for monocyte infection and blocking of migration.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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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.
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Who cites it
69 citing papers in PubMed.
- Mapping the monoclonal antibody landscape of human cytomegalovirus.Journal of virology · 2026Review
- Rapid phylogenomic analysis for viral surveillance and metagenomic profiling with Omni2Tree.bioRxiv : the preprint server for biology · 2026Article
- Cytomegalovirus disrupts Lamin A/C to control microtubule-mediated nuclear movement and cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Dissecting the cytomegalovirus CC chemokine: Chemokine activity and gHgLchemokine-dependent cell tropism are independent players in CMV infection.PLoS pathogens · 2023Article
- Review
- Distribution of CMV envelope glycoprotein B, H and N genotypes in infants with congenital cytomegalovirus symptomatic infection.Frontiers in pediatrics · 2023Article
- Lessons from Acquired Natural Immunity and Clinical Trials to Inform Next-Generation Human Cytomegalovirus Vaccine Development.Annual review of virology · 2022Review
- The Role of CMV Infection in Primary Lesions, Development and Clinical Expression of Atherosclerosis.Journal of clinical medicine · 2022Review
- Identification of functionally important domains of human cytomegalovirus gO that act after trimer binding to receptors.PLoS pathogens · 2022Article
- Article
- Modulation of host cell signaling during cytomegalovirus latency and reactivation.Virology journal · 2021Review
- Human Cytomegalovirus RNA2.7 Is Required for Upregulating Multiple Cellular Genes To Promote Cell Motility and Viral Spread Late in Lytic Infection.Journal of virology · 2021Article
- Murine Cytomegalovirus MCK-2 FacilitatesJournal of virology · 2021Article
- Common Polymorphisms in the Glycoproteins of Human Cytomegalovirus and Associated Strain-Specific Immunity.Viruses · 2021Review
- Targeted mutagenesis on PDGFRα-Fc identifies amino acid modifications that allow efficient inhibition of HCMV infection while abolishing PDGF sequestration.PLoS pathogens · 2021Article
- Insight for Immunotherapy of HCMV Infection.International journal of biological sciences · 2021Review
- Analysis of Cytomegalovirus Glycoprotein and Cellular Receptor Interactions.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Rat Cytomegalovirus Virion-Associated Proteins R131 and R129 Are Necessary for Infection of Macrophages and Dendritic Cells.Pathogens (Basel, Switzerland) · 2020Article
- Control of Cytokines in Latent Cytomegalovirus Infection.Pathogens (Basel, Switzerland) · 2020Review
- Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously shown that only endotheliotropic strains of human cytomegalovirus (HCMV), such as TB40E, infect monocytes and impair their chemokine-driven migration. The proteins encoded by the UL128-131A region (UL128, UL130, and UL131A) of the HCMV genome, which assemble into a pentameric gH-gL-UL128-UL130-UL131A envelope complex, have been recognized as determinants for HCMV endothelial cell tropism. The genes for these proteins are typically inactivated by mutations in all fibroblast-adapted strains that have lost the diversified tropism of clinical isolates. By using mutant HCMV reconstituted from TB40E-derived bacterial artificial chromosomes (BAC) encoding a wild-type (wt) or mutated form of UL128, we show here that UL128-131A products are essential determinants of infection in monocytes and that pUL128, in particular, can block chemokine-driven motility. The virus BAC4, encoding wt UL128, established infection in monocytes, induced the intracellular retention of several chemokine receptors, and rendered monocytes unresponsive to different chemokines. In contrast, the virus BAC1, encoding a mutated UL128, failed to infect monocytes and to downregulate chemokine receptors. BAC1-exposed monocytes did not express immediate-early (IE) products, retained virions in cytoplasmic vesicles, and exhibited normal chemokine responsiveness. A potential role of second-site mutations in the observed phenotype was excluded by using the revertant viruses BAC1rep and BAC4mut. By incubating noninfected monocytes with soluble recombinant pUL128, we observed both the block of migration and the chemokine receptor internalization. We propose that among the gH-gL-UL128-UL130-UL131A complex subunits, the UL128 protein is the one that triggers monocyte paralysis.
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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 Socratic graph.