ArticlePLoS pathogens2016
Natural Killer Cell Evasion Is Essential for Infection by Rhesus Cytomegalovirus.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- HCMV Variants Expressing ULBP2 Enhance the Function of Human NK Cells via its Receptor NKG2D.European journal of immunology · 2025Article
- Rhesus Cytomegalovirus-encoded Fcγ-binding glycoproteins facilitate viral evasion from IgG-mediated humoral immunity.Nature communications · 2025Article
- Proceedings of the Conference "CMV Vaccine Development-How Close Are We?" (27-28 September 2023).Vaccines · 2024Article
- Human cytomegalovirus UL18 prevents priming of MHC-E- and MHC-II-restricted CD8Science immunology · 2024Article
- Cytomegalovirus vaccine vector-induced effector memory CD4 + T cells protect cynomolgus macaques from lethal aerosolized heterologous avian influenza challenge.Nature communications · 2024Article
- Uncloaking the viral glycocalyx: How do viruses exploit glycoimmune checkpoints?Advances in virus research · 2024Review
- Programming cytomegalovirus as an HIV vaccine.Trends in immunology · 2023Review
- Characterization of natural killer cells in the blood and airways of cynomolgus macaques during Mycobacterium tuberculosis infection.Journal of medical primatology · 2023Article
- Cytomegalovirus-vaccine-induced unconventional T cell priming and control of SIV replication is conserved between primate species.Cell host & microbe · 2022Article
- The human cytomegalovirus protein UL147A downregulates the most prevalent MICA allele: MICA*008, to evade NK cell-mediated killing.PLoS pathogens · 2021Article
- Modulation of MHC-E transport by viral decoy ligands is required for RhCMV/SIV vaccine efficacy.Science (New York, N.Y.) · 2021Article
- Pseudorabies Virus Infection Causes Downregulation of Ligands for the Activating NK Cell Receptor NKG2D.Viruses · 2021Article
- Recent Approaches and Strategies in the Generation of Anti-human Cytomegalovirus Vaccines.Methods in molecular biology (Clifton, N.J.) · 2021Article
- In vitro and in vivo characterization of a recombinant rhesus cytomegalovirus containing a complete genome.PLoS pathogens · 2020Article
- RhCMV serostatus and vaccine adjuvant impact immunogenicity of RhCMV/SIV vaccines.Scientific reports · 2020Article
- Animal Models of Congenital Cytomegalovirus Transmission: Implications for Vaccine Development.The Journal of infectious diseases · 2020Review
- Immune Correlates of Protection Against Human Cytomegalovirus Acquisition, Replication, and Disease.The Journal of infectious diseases · 2020Article
- Endoplasmic Reticulum (ER) Reorganization and Intracellular Retention of CD58 Are Functionally Independent Properties of the Human Cytomegalovirus ER-Resident Glycoprotein UL148.Journal of virology · 2020Article
- Intrahost cytomegalovirus population genetics following antibody pretreatment in a monkey model of congenital transmission.PLoS pathogens · 2020Article
- Characterization of a live-attenuated HCMV-based vaccine platform.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
The natural killer cell receptor NKG2D activates NK cells by engaging one of several ligands (NKG2DLs) belonging to either the MIC or ULBP families. Human cytomegalovirus (HCMV) UL16 and UL142 counteract this activation by retaining NKG2DLs and US18 and US20 act via lysomal degradation but the importance of NK cell evasion for infection is unknown. Since NKG2DLs are highly conserved in rhesus macaques, we characterized how NKG2DL interception by rhesus cytomegalovirus (RhCMV) impacts infection in vivo. Interestingly, RhCMV lacks homologs of UL16 and UL142 but instead employs Rh159, the homolog of UL148, to prevent NKG2DL surface expression. Rh159 resides in the endoplasmic reticulum and retains several NKG2DLs whereas UL148 does not interfere with NKG2DL expression. Deletion of Rh159 releases human and rhesus MIC proteins, but not ULBPs, from retention while increasing NK cell stimulation by infected cells. Importantly, RhCMV lacking Rh159 cannot infect CMV-naïve animals unless CD8+ cells, including NK cells, are depleted. However, infection can be rescued by replacing Rh159 with HCMV UL16 suggesting that Rh159 and UL16 perform similar functions in vivo. We therefore conclude that cytomegaloviral interference with NK cell activation is essential to establish but not to maintain chronic infection.
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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.