ArticleInfection and immunity2004
Whole-genome DNA array analysis of the response of Borrelia burgdorferi to a bactericidal monoclonal antibody.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
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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
13 citing papers in PubMed, 20 citations in OpenAlex.
- Protective efficacy of mutant strains ofInfection and immunity · 2026Article
- Microarray-Based Comparative Genomic and Transcriptome Analysis of Borrelia burgdorferi.Microarrays (Basel, Switzerland) · 2016Review
- Absence of sodA Increases the Levels of Oxidation of Key Metabolic Determinants of Borrelia burgdorferi.PloS one · 2015Article
- Assessment of transcriptional activity of Borrelia burgdorferi and host cytokine genes during early and late infection in a mouse model.Vector borne and zoonotic diseases (Larchmont, N.Y.) · 2013Article
- B1b lymphocyte-derived antibodies control Borrelia hermsii independent of Fcα/μ receptor and in the absence of host cell contact.Immunologic research · 2011Review
- Oligopeptide permease A5 modulates vertebrate host-specific adaptation of Borrelia burgdorferi.Infection and immunity · 2011Article
- CsrA modulates levels of lipoproteins and key regulators of gene expression critical for pathogenic mechanisms of Borrelia burgdorferi.Infection and immunity · 2011Article
- Overexpression of CsrA (BB0184) alters the morphology and antigen profiles of Borrelia burgdorferi.Infection and immunity · 2009Article
- Deletion of BBA64, BBA65, and BBA66 loci does not alter the infectivity of Borrelia burgdorferi in the murine model of Lyme disease.Infection and immunity · 2008Article
- Demonstration of cotranscription and 1-methyl-3-nitroso-nitroguanidine induction of a 30-gene operon of Borrelia burgdorferi: evidence that the 32-kilobase circular plasmids are prophages.Journal of bacteriology · 2005Article
- Comparative transcriptional profiling of Borrelia burgdorferi clinical isolates differing in capacities for hematogenous dissemination.Infection and immunity · 2005Article
- Interactions of OspA monoclonal antibody C3.78 with Borrelia burgdorferi within ticks.Infection and immunity · 2005Article
- Combined effects of blood and temperature shift on Borrelia burgdorferi gene expression as determined by whole genome DNA array.Infection and immunity · 2004Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Identification and characterization of genes that contribute to infection with Borrelia burgdorferi and, of those, genes that are targets of host responses is important for understanding the pathogenesis of Lyme disease. The complement-independent bactericidal monoclonal antibody (MAb) CB2 recognizes a carboxy-terminal, hydrophilic epitope of the outer surface protein B (OspB). CB2 kills B. burgdorferi by an unknown bactericidal mechanism. Upon binding of CB2 to OspB, differentially expressed gene products may be responsible for, or associated with, the death of the organism. A time course of the response of B. burgdorferi to CB2 was completed to analyze the differential gene expression in the bacteria over a period of visual morphological changes. Bacteria were treated with a sublethal concentration in which spirochetes were visibly distressed by the antibody but not lysed. Preliminary whole-genome DNA arrays at various time points within 1 h of incubation of B. burgdorferi with the antibody showed that most significant changes occurred at 25 min. Circular plasmid 32 (cp32)-encoded genes were active in this period of time, including the blyA homologs, phage holin system genes. DNA array data show that three blyA homologs were upregulated significantly, >/==" BORDER="0">2 standard deviations from the mean of the log ratios, and a P value of </=0.01. Quantitative real-time PCR analysis verified blyA and blyB upregulation over an 18- to 35-min time course. The hypothesis to test is whether the killing mechanism of CB2 is through uncontrolled expression of the blyA and blyB phage holin system.
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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.