ArticlePLoS pathogens2011
A novel human cytomegalovirus locus modulates cell type-specific outcomes of infection.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
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Who cites it
116 citing papers in PubMed, 161 citations in OpenAlex.
- Human Cytomegalovirus UL4 is Required for Viral Reactivation via Cellular Reprogramming in Latently Infected CD34+ Progenitor Cells and Humanized Mice.bioRxiv : the preprint server for biology · 2026Article
- Isolation and characterization of broadly-neutralizing anti-HCMV-gB antibodies from human donors using a prefusion-stabilized HCMV gB variant.PLoS pathogens · 2026Article
- Human cytomegalovirus regulates host DNA repair machinery for viral genome integrity.Nucleic acids research · 2026Article
- Joining the dots: maternal cytomegalovirus, HIV and the placenta.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- HCMV infection of terminally differentiated neurons disrupts microtubule organization, resulting in neurite retraction.Microbiology spectrum · 2025Article
- Cytomegalovirus latency-the sum of subtleties.Journal of virology · 2025Review
- Viral and host network analysis of the human cytomegalovirus transcriptome in latency.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- RNA-targeted proteomics identifies YBX1 as critical for efficient HCMV mRNA translation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Viral microRNA regulation of Akt is necessary for reactivation of Human Cytomegalovirus from latency in CD34+ hematopoietic progenitor cells and humanized mice.PLoS pathogens · 2024Article
- Anti-cytomegalovirus antibody levels stratify human immune profiles across the lifespan.GeroScience · 2024Article
- Stabilizing microtubules aids neurite structure and disrupts syncytia formation in human cytomegalovirus-infected human forebrain neurons.bioRxiv : the preprint server for biology · 2024Article
- Distinct early role of PTEN regulation during HCMV infection of monocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- CCR4-NOT differentially controls host versus virus poly(a)-tail length and regulates HCMV infection.EMBO reports · 2023Article
- Stabilization of the human cytomegalovirus UL136p33 reactivation determinant overcomes the requirement for UL135 for replication in hematopoietic cells.Journal of virology · 2023Article
- Review
- Liver X Receptor-Inducible Host E3 Ligase IDOL Targets a Human Cytomegalovirus Reactivation Determinant.Journal of virology · 2023Article
- Mouse Models for Human Herpesviruses.Pathogens (Basel, Switzerland) · 2023Review
- Human cytomegalovirus UL138 interaction with USP1 activates STAT1 in infection.PLoS pathogens · 2023Article
- Critical Role for the Human Cytomegalovirus Major Immediate Early Proteins in Recruitment of RNA Polymerase II and H3K27Ac To an Enhancer-Like Element in OriMicrobiology spectrum · 2023Article
- Human Cytomegalovirus UL138 Interaction with USP1 Activates STAT1 in infection.bioRxiv : the preprint server for biology · 2023Article
56 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Clinical strains of HCMV encode 20 putative ORFs within a region of the genome termed ULb' that are postulated to encode functions related to persistence or immune evasion. We have previously identified ULb'-encoded pUL138 as necessary, but not sufficient, for HCMV latency in CD34+ hematopoietic progenitor cells (HPCs) infected in vitro. pUL138 is encoded on polycistronic transcripts that also encode 3 additional proteins, pUL133, pUL135, and pUL136, collectively comprising the UL133-UL138 locus. This work represents the first characterization of these proteins and identifies a role for this locus in infection. Similar to pUL138, pUL133, pUL135, and pUL136 are integral membrane proteins that partially co-localized with pUL138 in the Golgi during productive infection in fibroblasts. As expected of ULb' sequences, the UL133-UL138 locus was dispensable for replication in cultured fibroblasts. In CD34+ HPCs, this locus suppressed viral replication in HPCs, an activity attributable to both pUL133 and pUL138. Strikingly, the UL133-UL138 locus was required for efficient replication in endothelial cells. The association of this locus with three context-dependent phenotypes suggests an exciting role for the UL133-UL138 locus in modulating the outcome of viral infection in different contexts of infection. Differential profiles of protein expression from the UL133-UL138 locus correlated with the cell-type dependent phenotypes associated with this locus. We extended our in vitro findings to analyze viral replication and dissemination in a NOD-scid IL2Rγ(c) (null)-humanized mouse model. The UL133-UL138(NULL) virus exhibited an increased capacity for replication and/or dissemination following stem cell mobilization relative to the wild-type virus, suggesting an important role in viral persistence and spread in the host. As pUL133, pUL135, pUL136, and pUL138 are conserved in virus strains infecting higher order primates, but not lower order mammals, the functions encoded likely represent host-specific viral adaptations.
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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.