ArticleThe Journal of experimental medicine2001
A secreted chemokine binding protein encoded by murine gammaherpesvirus-68 is necessary for the establishment of a normal latent load.
Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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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.
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Who cites it
41 citing papers in PubMed, 100 citations in OpenAlex.
- The human cytomegalovirus chemokine binding protein UL22A is necessary for efficient reactivation from latency in CD34Journal of virology · 2026Article
- Serine Proteases and Chemokines in Neurotrauma: New Targets for Immune Modulating Therapeutics in Spinal Cord Injury.Current neuropharmacology · 2021Review
- Immune Control ofViral immunology · 2020Article
- Addition of a Viral Immunomodulatory Domain to Etanercept Generates a Bifunctional Chemokine and TNF Inhibitor.Journal of clinical medicine · 2019Article
- BAFF receptor deficiency limits gammaherpesvirus infection.Journal of virology · 2014Article
- Article
- Murine gammaherpesvirus 68 glycoprotein 150 does not contribute to latency amplification in vivo.Virology journal · 2012Article
- Gammaherpesvirus 68 infection of endothelial cells requires both host autophagy genes and viral oncogenes for optimal survival and persistence.Journal of virology · 2011Article
- Chemokine binding protein M3 of murine gammaherpesvirus 68 modulates the host response to infection in a natural host.PLoS pathogens · 2011Article
- T-bet-mediated differentiation of the activated CD8+ T cell.European journal of immunology · 2011Article
- Prospects of a novel vaccination strategy for human gamma-herpesviruses.Immunologic research · 2010Review
- Article
- Characterization of a novel wood mouse virus related to murid herpesvirus 4.The Journal of general virology · 2010Article
- Pathogenesis of a model gammaherpesvirus in a natural host.Journal of virology · 2010Article
- Induction of protective immunity against murine gammaherpesvirus 68 infection in the absence of viral latency.Journal of virology · 2010Article
- In vivo imaging of murid herpesvirus-4 infection.The Journal of general virology · 2009Article
- A single CD8+ T cell epitope sets the long-term latent load of a murid herpesvirus.PLoS pathogens · 2008Article
- Role for MyD88 signaling in murine gammaherpesvirus 68 latency.Journal of virology · 2008Article
- Toll-like receptors, Notch ligands, and cytokines drive the chronicity of lung inflammation.Proceedings of the American Thoracic Society · 2007Review
- Control of virus reactivation arrests pulmonary herpesvirus-induced fibrosis in IFN-gamma receptor-deficient mice.American journal of respiratory and critical care medicine · 2007Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Herpesviruses encode a variety of proteins with the potential to disrupt chemokine signaling, and hence immune organization. However, little is known of how these might function in vivo. The B cell-tropic murine gammaherpesvirus-68 (MHV-68) is related to the Kaposi's sarcoma-associated herpesvirus (KSHV), but whereas KSHV expresses small chemokine homologues, MHV-68 encodes a broad spectrum chemokine binding protein (M3). Here we have analyzed the effect on viral pathogenesis of a targeted disruption of the M3 gene. After intranasal infection, an M3 deficiency had surprisingly little effect on lytic cycle replication in the respiratory tract or the initial spread of virus to lymphoid tissues. However, the amplification of latently infected B cells in the spleen that normally drives MHV-68-induced infectious mononucleosis failed to occur. Thus, there was a marked reduction in latent virus recoverable by in vitro reactivation, latency-associated viral tRNA transcripts detectable by in situ hybridization, total viral DNA load, and virus-driven B cell activation. In vivo CD8(+) T cell depletion largely reversed this deficiency, suggesting that the chemokine neutralization afforded by M3 may function to block effective CD8(+) T cell recruitment into lymphoid tissue during the expansion of latently infected B cell numbers. In the absence of M3, MHV-68 was unable to establish a normal latent load.
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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.