The gut microbiota controls gammaherpesvirus infection and viral gene expression 4581

Abstract Description Gammaherpesviruses, such as Epstein-Barr Virus, are ubiquitous pathogens that cause acute lytic infections and establish latency, leading to chronic infections with potential severe health consequences, including malignancies. Recent studies highlight the role of the microbiota in viral infections and immune responses. However, its impact on gammaherpesvirus infections remains unexplored. This research investigates the microbiota’s influence on both acute and chronic gammaherpesvirus infection using a murine model, γHV68, coupled with antibiotic-induced microbial dysbiosis. Mice were treated with broad-spectrum antibiotics or a vehicle control before or during the intraperitoneal infection with γHV68. We found that the antibiotic-treated mice had consistently higher viral loads in the spleen, liver, and lungs compared to controls. Furthermore, the establishment of latency in splenocytes and peritoneal cavity was equal between the two groups; however, the ex vivo reactivation of latent infection was significantly higher in splenocytes but not in the peritoneal cells from antibiotic-treated mice. These findings suggest that the microbiota plays a crucial role in modulating acute viral infection and the reactivation of latency, with tissue- and cell-specific effects. Understanding the microbiota’s impact on viral infections and host immunity is vital for improving clinical strategies, especially in the context of chronic infections and widespread antibiotic use. Topic Categories Viral Immunology (VIR)

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Publication Details

Journal
The Journal of Immunology
Published
2025-11-01
DOI
https://doi.org/10.1093/jimmun/vkaf283.2248
Primary Topic
Viral-associated cancers and disorders
Type
article
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article

The gut microbiota controls gammaherpesvirus infection and viral gene expression 4581

Aakanksha Agarwal, Ashley Steed, Gautam Anand, Ivana Ling et al.
The Journal of Immunology
Viral-associated cancers and disorders
article

The gut microbiota controls gammaherpesvirus infection and viral gene expression 4581

Aakanksha Agarwal, Ashley Steed, Gautam Anand, Ivana Ling, Colin Clark Dinovo
article en

Abstract

Abstract Description Gammaherpesviruses, such as Epstein-Barr Virus, are ubiquitous pathogens that cause acute lytic infections and establish latency, leading to chronic infections with potential severe health consequences, including malignancies. Recent studies highlight the role of the microbiota in viral infections and immune responses. However, its impact on gammaherpesvirus infections remains unexplored. This research investigates the microbiota’s influence on both acute and chronic gammaherpesvirus infection using a murine model, γHV68, coupled with antibiotic-induced microbial dysbiosis. Mice were treated with broad-spectrum antibiotics or a vehicle control before or during the intraperitoneal infection with γHV68. We found that the antibiotic-treated mice had consistently higher viral loads in the spleen, liver, and lungs compared to controls. Furthermore, the establishment of latency in splenocytes and peritoneal cavity was equal between the two groups; however, the ex vivo reactivation of latent infection was significantly higher in splenocytes but not in the peritoneal cells from antibiotic-treated mice. These findings suggest that the microbiota plays a crucial role in modulating acute viral infection and the reactivation of latency, with tissue- and cell-specific effects. Understanding the microbiota’s impact on viral infections and host immunity is vital for improving clinical strategies, especially in the context of chronic infections and widespread antibiotic use. Topic Categories Viral Immunology (VIR)

The Journal of ImmunologyVol. 214(Supplement_1)
Washington University in St. Louis (US)
Openalex Percentile: Top 52%
Viral-associated cancers and disorders
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The gut microbiota controls gammaherpesvirus infection and viral gene expression 4581 — Aakanksha Agarwal, Ashley Steed, et al. · The Journal of Immunology (2025) | TGRS Research Map | TGRS