ReviewCellular & molecular immunology2015
Cytomegalovirus immune evasion by perturbation of endosomal trafficking.
Review in Cellular & molecular immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Human herpesvirus evasion of humoral immunity and implications for vaccine development.Nature reviews. Microbiology · 2026Review
- Advances in immunotherapy for cytomegalovirus infection following allogeneic hematopoietic stem cell transplantation.Immunotherapy · 2026Review
- Clinical and biological features of CMV reactivation in ARDS: a prospective cohort study.Critical care (London, England) · 2026Article
- The Cell Biologist Potential of Cytomegalovirus to Solve Biogenesis and Maintenance of the Membrane Recycling System.Biomedicines · 2025Article
- Article
- Rab10-associated tubulation as an early marker for biogenesis of the assembly compartment in cytomegalovirus-infected cells.Frontiers in cell and developmental biology · 2024Article
- SNX27:Retromer:ESCPE-1-mediated early endosomal tubulation impacts cytomegalovirus replication.Frontiers in cellular and infection microbiology · 2024Article
- Acute post-renal kidney graft dysfunction due to cytomegalovirus-positive nephrogenic adenoma-case report and review of the literature.Frontiers in medicine · 2024Article
- Article
- Review
- Cytomegalovirus Infections in Children with Primary and Secondary Immune Deficiencies.Viruses · 2021Review
- The m15 Locus of Murine Cytomegalovirus Modulates Natural Killer Cell Responses to Promote Dissemination to the Salivary Glands and Viral Shedding.Pathogens (Basel, Switzerland) · 2021Article
- Article
- Cytomegalovirus Generates Assembly Compartment in the Early Phase of Infection by Perturbation of Host-Cell Factors Recruitment at the Early Endosome/Endosomal Recycling Compartment/Trans-Golgi Interface.Frontiers in cell and developmental biology · 2020Article
- T-cell phenotypes are associated with serum IgE levels in Amish and Hutterite children.The Journal of allergy and clinical immunology · 2019Article
- Function of the cargo sorting dileucine motif in a cytomegalovirus immune evasion protein.Medical microbiology and immunology · 2019Article
- Between Innate and Adaptive Immune Responses: NKG2A, NKG2C, and CD8⁺ T Cell Recognition of HLA-E Restricted Self-Peptides Acquired in the Absence of HLA-Ia.International journal of molecular sciences · 2019Article
- A Prominent Role of the Human Cytomegalovirus UL8 Glycoprotein in Restraining Proinflammatory Cytokine Production by Myeloid Cells at Late Times during Infection.Journal of virology · 2018Article
- Cytomegaloviruses Exploit Recycling Rab Proteins in the Sequential Establishment of the Assembly Compartment.Frontiers in cell and developmental biology · 2018Review
- Infection-Induced Changes Within the Endocytic Recycling Compartment Suggest a Roadmap of Human Cytomegalovirus Egress.Frontiers in microbiology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytomegaloviruses (CMVs), members of the herpesvirus family, have evolved a variety of mechanisms to evade the immune response to survive in infected hosts and to establish latent infection. They effectively hide infected cells from the effector mechanisms of adaptive immunity by eliminating cellular proteins (major histocompatibility Class I and Class II molecules) from the cell surface that display viral antigens to CD8 and CD4 T lymphocytes. CMVs also successfully escape recognition and elimination of infected cells by natural killer (NK) cells, effector cells of innate immunity, either by mimicking NK cell inhibitory ligands or by downregulating NK cell-activating ligands. To accomplish these immunoevasion functions, CMVs encode several proteins that function in the biosynthetic pathway by inhibiting the assembly and trafficking of cellular proteins that participate in immune recognition and thereby, block their appearance at the cell surface. However, elimination of these proteins from the cell surface can also be achieved by perturbation of their endosomal route and subsequent relocation from the cell surface into intracellular compartments. Namely, the physiological route of every cellular protein, including immune recognition molecules, is characterized by specific features that determine its residence time at the cell surface. In this review, we summarize the current understanding of endocytic trafficking of immune recognition molecules and perturbations of the endosomal system during infection with CMVs and other members of the herpesvirus family that contribute to their immune evasion mechanisms.
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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.