ArticleJournal of virology2009
Liver sinusoidal endothelial cells are a site of murine cytomegalovirus latency and reactivation.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 99 citations in OpenAlex.
- Liver sinusoidal endothelial cells in liver diseases and hepatocellular carcinoma: molecular mechanisms, physiology, and therapies.Molecular biomedicine · 2026Review
- Cytomegalovirus latency-the sum of subtleties.Journal of virology · 2025Review
- Why Are Cytomegalovirus-Encoded G-Protein-Coupled Receptors Essential for Infection but Only Variably Conserved?Pathogens (Basel, Switzerland) · 2025Review
- Immune surveillance of cytomegalovirus in tissues.Cellular & molecular immunology · 2024Review
- Immunosenescence and Cytomegalovirus: Exploring Their Connection in the Context of Aging, Health, and Disease.International journal of molecular sciences · 2024Review
- Modulation of cytomegalovirus immune evasion identifies direct antigen presentation as the predominant mode of CD8 T-cell priming during immune reconstitution after hematopoietic cell transplantation.Frontiers in immunology · 2024Article
- Article
- Mouse Models for Human Herpesviruses.Pathogens (Basel, Switzerland) · 2023Review
- Fibroblasts are a site of murine cytomegalovirus lytic replication and Stat1-dependent latent persistence in vivo.Nature communications · 2023Article
- Latent CMV infection of Lymphatic endothelial cells is sufficient to drive CD8 T cell memory inflation.PLoS pathogens · 2023Article
- Infection of liver sinusoidal endothelial cells with Muromegalovirus muridbeta1 involves binding to neuropilin-1 and is dynamin-dependent.Frontiers in cellular and infection microbiology · 2023Article
- Impact of cytomegalovirus infection on biliary disease after liver transplantation - maybe an essential factor.World journal of clinical cases · 2021Article
- Direct Evidence for Viral Antigen Presentation during Latent Cytomegalovirus Infection.Pathogens (Basel, Switzerland) · 2021Article
- Human Herpesviruses Increase the Severity of Hepatitis.Biology · 2021Article
- Review
- Cytomegalovirus Hepatitis in Immunocompetent and Immunocompromised Hosts.Journal of clinical and translational hepatology · 2021Review
- Therapeutic Vaccination of Hematopoietic Cell Transplantation Recipients Improves Protective CD8 T-Cell Immunotherapy of Cytomegalovirus Infection.Frontiers in immunology · 2021Article
- Stochastic Episodes of Latent Cytomegalovirus Transcription Drive CD8 T-Cell "Memory Inflation" and Avoid Immune Evasion.Frontiers in immunology · 2021Article
- Insufficient Antigen Presentation Due to Viral Immune Evasion Explains Lethal Cytomegalovirus Organ Disease After Allogeneic Hematopoietic Cell Transplantation.Frontiers in cellular and infection microbiology · 2020Article
- Cytomegaloviruses and Macrophages-Friends and Foes From Early on?Frontiers in immunology · 2020Review
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Latent cytomegalovirus (CMV) is frequently transmitted by organ transplantation, and its reactivation under conditions of immunosuppressive prophylaxis against graft rejection by host-versus-graft disease bears a risk of graft failure due to viral pathogenesis. CMV is the most common cause of infection following liver transplantation. Although hematopoietic cells of the myeloid lineage are a recognized source of latent CMV, the cellular sites of latency in the liver are not comprehensively typed. Here we have used the BALB/c mouse model of murine CMV infection to identify latently infected hepatic cell types. We performed sex-mismatched bone marrow transplantation with male donors and female recipients to generate latently infected sex chromosome chimeras, allowing us to distinguish between Y-chromosome (gene sry or tdy)-positive donor-derived hematopoietic descendants and Y-chromosome-negative cells of recipients' tissues. The viral genome was found to localize primarily to sry-negative CD11b(-) CD11c(-) CD31(+) CD146(+) cells lacking major histocompatibility complex class II antigen (MHC-II) but expressing murine L-SIGN. This cell surface phenotype is typical of liver sinusoidal endothelial cells (LSECs). Notably, sry-positive CD146(+) cells were distinguished by the expression of MHC-II and did not harbor latent viral DNA. In this model, the frequency of latently infected cells was found to be 1 to 2 per 10(4) LSECs, with an average copy number of 9 (range, 4 to 17) viral genomes. Ex vivo-isolated, latently infected LSECs expressed the viral genes m123/ie1 and M122/ie3 but not M112-M113/e1, M55/gB, or M86/MCP. Importantly, in an LSEC transfer model, infectious virus reactivated from recipients' tissue explants with an incidence of one reactivation per 1,000 viral-genome-carrying LSECs. These findings identified LSECs as the main cellular site of murine CMV latency and reactivation in the liver.
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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.