ArticleMucosal immunology2018
B cells are the predominant mediators of early systemic viral dissemination during rectal LCMV infection.
Article in Mucosal immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Nociceptor neurons shape antiviral immunity.Journal of neuroinflammation · 2026Review
- RIG-I Stimulation Enhances the Effector Function and Proliferation of Primary Human CD8+ T Cells.International journal of molecular sciences · 2026Article
- Polyclonal B cells acquire LCMV antigens in a GP1-dependent manner.PLoS pathogens · 2025Article
- Segmented, Negative-Sense RNA Viruses of Humans: Genetic Systems and Experimental Uses of Reporter Strains.Annual review of virology · 2023Review
- Gammaherpesviruses and B Cells: A Relationship That Lasts a Lifetime.Viral immunology · 2020Review
- Low expression of RNA sensors impacts Zika virus infection in the lower female reproductive tract.Nature communications · 2019Article
- Lack of Sprouty 1 and 2 enhances survival of effector CD8Proceedings of the National Academy of Sciences of the United States of America · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Determining the magnitude of local immune response during mucosal exposure to viral pathogens is critical to understanding the mechanism of viral pathogenesis. We previously showed that vaginal inoculation of lymphocytic choriomeningitis virus (LCMV) fails to induce a robust innate immune response in the lower female reproductive tract (FRT), allowing high titer viral replication and a delay in T-cell-mediated viral control. Despite this immunological delay, LCMV replication remained confined mainly to the FRT and the draining iliac lymph node. Here, we show that rectal infection with LCMV triggers type I/III interferon responses, followed by innate immune activation and lymphocyte recruitment to the colon. In contrast to vaginal exposure, innate immunity controls LCMV replication in the colon, but virus rapidly disseminates systemically. Virus-induced inflammation promotes the recruitment of LCMV target cells to the colon followed by splenic viral dissemination by infected B cells, and to a lesser extent by CD8 T cells. These findings demonstrate major immunological differences between vaginal and rectal exposure to the same viral pathogen, highlighting unique risks associated with each of these common routes of sexual viral transmission.
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Registered trials
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