ArticlePLoS pathogens2012
Macrophage activation associated with chronic murine cytomegalovirus infection results in more severe experimental choroidal neovascularization.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Persistent microglial activation following neonatal CMV infection mediates neurodegeneration.Science advances · 2026Article
- Treatment Strategies for Anti-VEGF Resistance in Neovascular Age-Related Macular Degeneration by Targeting Arteriolar Choroidal Neovascularization.Biomolecules · 2024Review
- Article
- Blocking Autophagy in M1 Macrophages Enhances Virus Replication and Eye Disease in Ocularly Infected Transgenic Mice.Journal of virology · 2022Article
- Suppression of myeloid PFKFB3-driven glycolysis protects mice from choroidal neovascularization.British journal of pharmacology · 2022Article
- Retinal and Choroidal Pathologies in Aged BALB/c Mice Following Systemic Neonatal Murine Cytomegalovirus Infection.The American journal of pathology · 2021Article
- Incomplete response to Anti-VEGF therapy in neovascular AMD: Exploring disease mechanisms and therapeutic opportunities.Progress in retinal and eye research · 2021Review
- Immunological Aspects of Age-Related Macular Degeneration.Advances in experimental medicine and biology · 2021Article
- Ocular cytomegalovirus latency exacerbates the development of choroidal neovascularization.The Journal of pathology · 2020Article
- Human Vascular Pericytes and Cytomegalovirus Pathobiology.International journal of molecular sciences · 2019Review
- Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases.Infection and drug resistance · 2019Article
- Suppressor of Cytokine Signaling 1 (SOCS1) and SOCS3 Are Stimulated within the Eye during Experimental Murine Cytomegalovirus Retinitis in Mice with Retrovirus-Induced Immunosuppression.Journal of virology · 2018Article
- Nosocomial Cytomegalovirus Infection Resulting in Worsening of Retinopathy of Prematurity.Indian journal of pediatrics · 2018Article
- Inflammation and outer blood-retina barrier (BRB) compromise following choroidal murine cytomegalovirus (MCMV) infections.Molecular vision · 2018Article
- A Proinflammatory Function of Toll-Like Receptor 2 in the Retinal Pigment Epithelium as a Novel Target for Reducing Choroidal Neovascularization in Age-Related Macular Degeneration.The American journal of pathology · 2017Article
- Intratumoral infection by CMV may change the tumor environment by directly interacting with tumor-associated macrophages to promote cancer immunity.Human vaccines & immunotherapeutics · 2017Review
- Article
- Gene expression regulation in retinal pigment epithelial cells induced by viral RNA and viral/bacterial DNA.Molecular vision · 2015Article
- Ocular neovascularization.Journal of molecular medicine (Berlin, Germany) · 2013Review
- Immuno-modulatory Effect of IFN-gamma in AMD and its Role as a Possible Target for Therapy.Journal of clinical & experimental ophthalmology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
The neovascular (wet) form of age-related macular degeneration (AMD) leads to vision loss due to choroidal neovascularization (CNV). Since macrophages are important in CNV development, and cytomegalovirus (CMV)-specific IgG serum titers in patients with wet AMD are elevated, we hypothesized that chronic CMV infection contributes to wet AMD, possibly by pro-angiogenic macrophage activation. This hypothesis was tested using an established mouse model of experimental CNV. At 6 days, 6 weeks, or 12 weeks after infection with murine CMV (MCMV), laser-induced CNV was performed, and CNV severity was determined 4 weeks later by analysis of choroidal flatmounts. Although all MCMV-infected mice exhibited more severe CNV when compared with control mice, the most severe CNV developed in mice with chronic infection, a time when MCMV-specific gene sequences could not be detected within choroidal tissues. Splenic macrophages collected from mice with chronic MCMV infection, however, expressed significantly greater levels of TNF-α, COX-2, MMP-9, and, most significantly, VEGF transcripts by quantitative RT-PCR assay when compared to splenic macrophages from control mice. Direct MCMV infection of monolayers of IC-21 mouse macrophages confirmed significant stimulation of VEGF mRNA and VEGF protein as determined by quantitative RT-PCR assay, ELISA, and immunostaining. Stimulation of VEGF production in vivo and in vitro was sensitive to the antiviral ganciclovir. These studies suggest that chronic CMV infection may serve as a heretofore unrecognized risk factor in the pathogenesis of wet AMD. One mechanism by which chronic CMV infection might promote increased CNV severity is via stimulation of macrophages to make pro-angiogenic factors (VEGF), an outcome that requires active virus replication.
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