ArticleJournal of immunology (Baltimore, Md. : 1950)2023
Host Genetic Variation Has a Profound Impact on Immune Responses Mediating Control of Viral Load in Chronic Gammaherpesvirus Infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Natural genetic variation in wild-derived mice controls host survival and transcriptional responses during endotoxic shock.ImmunoHorizons · 2025Article
- Indirect CD4Journal of virology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic infection with the gammaherpesvirus EBV is a risk factor for several autoimmune diseases, and poor control of EBV viral load and enhanced anti-EBV responses elevate this risk further. However, the role of host genetic variation in the regulation of immune responses to chronic gammaherpesvirus infection and control of viral replication remains unclear. To address this question, we infected C57BL/6J (B6) and genetically divergent wild-derived inbred PWD/PhJ (PWD) mice with murine gammaherpesvirus-68 (MHV-68), a gammaherpesvirus similar to EBV, and determined the effect of latent gammaherpesvirus infection on the CD4 T cell transcriptome. Chronic MHV-68 infection of B6 mice resulted in a dramatic upregulation of genes characteristic of a cytotoxic Th cell phenotype, including Gzmb, Cx3cr1, Klrg1, and Nkg7, a response that was highly muted in PWD mice. Flow cytometric analyses revealed an expansion of CX3CR1+KLRG1+ cytotoxic Th cell-like cells in B6 but not PWD mice. Analysis of MHV-68 replication demonstrated that in spite of muted adaptive responses, PWD mice had superior control of viral load in lymphoid tissue, despite an absence of a defect in MHV-68 in vitro replication in PWD macrophages. Depletion of NK cells in PWD mice, but not B6 mice, resulted in elevated viral load, suggesting genotype-dependent NK cell involvement in MHV-68 control. Taken together, our findings demonstrate that host genetic variation can regulate control of gammaherpesvirus replication through disparate immunological mechanisms, resulting in divergent long-term immunological sequelae during chronic infection.
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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.