ArticleJournal of virology2004
Underwhelming the immune response: effect of slow virus growth on CD8+-T-lymphocyte responses.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
31 citing papers in PubMed.
- Article
- An Innate Checkpoint Determines Immune Dysregulation and Immunopathology during Pulmonary Murine Coronavirus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- An integrative systems biology view of host-pathogen interactions: The regulation of immunity and homeostasis is concomitant, flexible, and smart.Frontiers in immunology · 2022Article
- Viral vector-mediated reprogramming of the fibroblastic tumor stroma sustains curative melanoma treatment.Nature communications · 2021Article
- An epidemic Zika virus isolate suppresses antiviral immunity by disrupting antigen presentation pathways.Nature communications · 2021Article
- Sustained Coevolution in a Stochastic Model of Cancer-Immune Interaction.Cancer research · 2020Article
- Article
- Defining Kinetic Properties of HIV-Specific CD8⁺ T-Cell Responses in Acute Infection.Microorganisms · 2019Article
- Immunological Paradigms, Mechanisms, and Models: Conceptual Understanding Is a Prerequisite to Effective Modeling.Frontiers in immunology · 2019Review
- Stochastic modeling of tumor progression and immune evasion.Journal of theoretical biology · 2018Article
- Virological and Clinical Characteristics of Hepatitis B Virus Genotype A.Journal of gastroenterology · 2018Review
- The impact of KIR-HLA genotype on hepatitis B virus clearance in Iranian infected individuals.Medical microbiology and immunology · 2017Article
- Semi-Functional Quantitative Flow Cytometry Assay for Lymphocytic Choriomeningitis Virus Titration.Immune network · 2017Article
- A Dynamic Model of Immune Responses to Antigen Presentation Predicts Different Regions of Tumor or Pathogen Elimination.Cell systems · 2017Article
- N6-Methyladenosine in Flaviviridae Viral RNA Genomes Regulates Infection.Cell host & microbe · 2016Article
- Article
- Understanding Experimental LCMV Infection of Mice: The Role of Mathematical Models.Journal of immunology research · 2015Review
- Efficient norovirus and reovirus replication in the mouse intestine requires microfold (M) cells.Journal of virology · 2014Article
- Stability Analysis of an Improved HBV Model with CTL Immune Response.International scholarly research notices · 2014Article
- Effects of route of inoculation and viral genetic variation on antibody responses to polyomavirus SV40 in Syrian golden hamsters.Comparative medicine · 2012Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
Abstract
The speed of virus replication has typically been seen as an advantage for a virus in overcoming the ability of the immune system to control its population growth. Under some circumstances, the converse may also be true: more slowly replicating viruses may evoke weaker cellular immune responses and therefore enhance their likelihood of persistence. Using the model of lymphocytic choriomeningitis virus (LCMV) infection in mice, we provide evidence that slowly replicating strains induce weaker cytotoxic-T-lymphocyte (CTL) responses than a more rapidly replicating strain. Conceptually, we show a "bell-shaped" relationship between the LCMV growth rate and the peak CTL response. Quantitative analysis of human hepatitis C virus infections suggests that a reduction in virus growth rate between patients during the incubation period is associated with a spectrum of disease outcomes, from fulminant hepatitis at the highest rate of viral replication through acute resolving to chronic persistence at the lowest rate. A mathematical model for virus-CTL population dynamics (analogous to predator [CTL]-prey [virus] interactions) is applied in the clinical data-driven analysis of acute hepatitis B virus infection. The speed of viral replication, through its stimulus of host CTL responses, represents an important factor influencing the pathogenesis and duration of virus persistence within the human host. Viruses with lower growth rates may persist in the host because they "sneak through" immune surveillance.
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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.