ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
Latent infection by γherpesvirus stimulates profibrotic mediator release from multiple cell types.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- The Role of Herpes Viruses in Pulmonary Fibrosis.Frontiers in medicine · 2021Pooled it
- A Phase I Randomized, Controlled, Clinical Trial of Valganciclovir in Idiopathic Pulmonary Fibrosis.Annals of the American Thoracic Society · 2021Trial
- Comparative study on mouse models of acute exacerbation of pulmonary fibrosis.Experimental and therapeutic medicine · 2026Article
- Concerted action of gammaherpesvirus infection and moderate hyperoxia on lung structural development including effects on critical lung fibroblast functions in neonatal mice.Molecular and cellular pediatrics · 2026Article
- Alveolar Macrophages in Viral Respiratory Infections: Sentinels and Saboteurs of Lung Defense.International journal of molecular sciences · 2025Review
- Current advancements in the mechanisms and animal models of acute exacerbation of pulmonary fibrosis: a systematic review.Frontiers in pharmacology · 2025Review
- Persistent microbial infections and idiopathic pulmonary fibrosis - an insight intoFrontiers in cellular and infection microbiology · 2024Review
- Animal models of acute exacerbation of pulmonary fibrosis.Respiratory research · 2023Review
- Comparison of cytokine profiles induced by nonlethal and lethal doses of influenza A virus in mice.Experimental and therapeutic medicine · 2019Article
- The contribution of infection and the respiratory microbiome in acute exacerbations of idiopathic pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2019Review
- Influenza-induced immune suppression to methicillin-resistant Staphylococcus aureus is mediated by TLR9.PLoS pathogens · 2019Article
- Natural Secretory Immunoglobulins Promote Enteric Viral Infections.Journal of virology · 2018Article
- Proteomics of Bronchoalveolar Lavage Fluid Reveals a Lung Oxidative Stress Response in Murine Herpesvirus-68 Infection.Viruses · 2018Article
- Efferocytosis of apoptotic alveolar epithelial cells is sufficient to initiate lung fibrosis.Cell death & disease · 2018Article
- Plasma membrane wounding and repair in pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- Nanoparticle exposure reactivates latent herpesvirus and restores a signature of acute infection.Particle and fibre toxicology · 2017Article
- Loss of CCR2 signaling alters leukocyte recruitment and exacerbates γ-herpesvirus-induced pneumonitis and fibrosis following bone marrow transplantation.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Viruses in Idiopathic Pulmonary Fibrosis. Etiology and Exacerbation.Annals of the American Thoracic Society · 2015Review
- The anti-fibrotic effect of inhibition of TGFβ-ALK5 signalling in experimental pulmonary fibrosis in mice is attenuated in the presence of concurrent γ-herpesvirus infection.Disease models & mechanisms · 2015Article
- CD8+ T Cell Response to Gammaherpesvirus Infection Mediates Inflammation and Fibrosis in Interferon Gamma Receptor-Deficient Mice.PloS one · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Although γherpesvirus infections are associated with enhanced lung fibrosis in both clinical and animal studies, there is limited understanding about fibrotic effects of γherpesviruses on cell types present in the lung, particularly during latent infection. Wild-type mice were intranasally infected with a murine γherpesvirus (γHV-68) or mock-infected with saline. Twenty-eight days postinfection (dpi), ∼14 days following clearance of the lytic infection, alveolar macrophages (AMs), mesenchymal cells, and CD19-enriched cell populations from the lung and spleen express M(3) and/or glycoprotein B (gB) viral mRNA and harbor viral genome. AMs from infected mice express more transforming growth factor (TGF)-β(1), CCL2, CCL12, TNF-α, and IFN-γ than AMs from mock-infected mice. Mesenchymal cells express more total TGF-β(1), CCL12, and TNF-α than mesenchymal cells from mock-infected mice. Lung and spleen CD19-enriched cells express more total TGF-β(1) 28 dpi compared with controls. The CD19-negative fraction of the spleen overexpresses TGF-β(1) and harbors viral genome, but this likely represents infection of monocytes. Purified T cells from the lung harbor almost no viral genome. Purified T cells overexpress IL-10 but not TGF-β(1). Intracellular cytokine staining demonstrated that lung T cells at 28 dpi produce IFN-γ but not IL-4. Thus infection with a murine γherpesvirus is sufficient to upregulate profibrotic and proinflammatory factors in a variety of lung resident and circulating cell types 28 dpi. Our results provide new information about possible contributions of these cells to fibrogenesis in the lungs of individuals harboring a γherpesvirus infection and may help explain why γHV-68 infection can augment or exacerbate fibrotic responses in mice.
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