ArticleJournal of virology2007
Early antibodies specific for the neutralizing epitope on the receptor binding subunit of the lymphocytic choriomeningitis virus glycoprotein fail to neutralize the virus.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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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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
38 citing papers in PubMed, 48 citations in OpenAlex.
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- Chronic infection perturbs the affinity hierarchy of antiviral B cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- B cell immunity to the Lassa virus glycoprotein is a correlate of vaccination-induced virus control in mice.Nature communications · 2026Article
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- Orf virus-based vectors induce potent germinal center B cell, Tfh cell, and CD8Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Polyclonal B cells acquire LCMV antigens in a GP1-dependent manner.PLoS pathogens · 2025Article
- Patrolling monocytes mediate virus neutralizing IgG effector functions: beyond neutralization capacity.Frontiers in immunology · 2025Article
- The Adaptive Immune Response againstViruses · 2024Review
- Central tolerance shapes the neutralizing B cell repertoire against a persisting virus in its natural host.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Structural basis for antibody-mediated neutralization of lymphocytic choriomeningitis virus.Cell chemical biology · 2023Article
- Arenaviruses: Old viruses present new solutions for cancer therapy.Frontiers in immunology · 2023Review
- Single-cell immune repertoire sequencing of B and T cells in murine models of infection and autoimmunity.Genes and immunity · 2022Article
- Antibody bivalency improves antiviral efficacy by inhibiting virion release independently of Fc gamma receptors.Cell reports · 2022Article
- Persistent RNA virus infection is short-lived at the single-cell level but leaves transcriptomic footprints.The Journal of experimental medicine · 2021Article
- Viral nucleoprotein antibodies activate TRIM21 and induce T cell immunity.The EMBO journal · 2021Article
- Spatiotemporal regulation of type I interferon expression determines the antiviral polarization of CD4Nature immunology · 2020Article
- Chronic Viral Infection Promotes Efficient Germinal Center B Cell Responses.Cell reports · 2020Article
- Xenoantigen-Dependent Complement-Mediated Neutralization of Lymphocytic Choriomeningitis Virus Glycoprotein-Pseudotyped Vesicular Stomatitis Virus in Human Serum.Journal of virology · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lymphocytic choriomeningitis virus (LCMV) is a murine arenavirus whose glycoprotein consists of a transmembrane subunit (GP-2) and a receptor-binding subunit (GP-1). LCMV-neutralizing antibodies (nAbs) are directed against a single site on GP-1 and occur 1 month after the infection of cytotoxic-T-lymphocyte (CTL) deficient mice. In wild-type mice, however, CTLs control early infection, and weak nAb titers emerge very late (after 70 to 150 days) if at all. Production of recombinant GP-1 in native conformation enabled us to study the emergence of GP-1-binding antibodies directed against the neutralizing epitope. By combining binding and neutralization assays, we correlated the development of binding antibodies versus nAbs in wild-type and CTL-deficient mice after infection with different LCMV doses. We found that wild-type mice developed GP-1-specific antibodies already by day 8 after exposure to high but not low doses, demonstrating that naive GP-1-specific B cells were infrequent. Furthermore, the induced antibodies bound to the neutralizing GP-1 epitope but failed to neutralize the virus and therefore were of low affinity. In CTL-deficient mice, where massive viremia quickly levels initial differences in viral load, low and high doses induced low-affinity non-neutralizing GP-1-binding antibodies with kinetics similar to high-dose-infected wild-type mice. Only in CTL-deficient mice, however, the GP-1-specific antibodies developed into nAbs within 1 month. We conclude that LCMV uses a dual strategy to evade nAb responses in wild-type mice. First, LCMV exploits a "hole" in the murine B-cell repertoire, which provides only a small and narrow initial pool of low-affinity GP-1-specific B cells. Second, affinity maturation of the available low-affinity non-neutralizing antibodies is impaired.
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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.