Evidence map›Paper›PMID 17984202›Full record

ArticleInfection and immunity2008

Role of the BBA64 locus of Borrelia burgdorferi in early stages of infectivity in a murine model of Lyme disease.

Mahulena Maruskova, M Dolores Esteve-Gassent, Valerie L Sexton, J Seshu

Abstract read
In one paragraph

Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed.

  1. Protective efficacy of mutant strains ofInfection and immunity · 2026
    Article
  2. Article
  3. Probing the Role ofInfection and immunity · 2021
    Article
  4. Article
  5. TheFrontiers in microbiology · 2021
    Article
  6. Gene Regulation and Transcriptomics.Current issues in molecular biology · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Seroprevalence of Borrelia burgdorferi antibodies in white-tailed deer from Texas.International journal for parasitology. Parasites and wildlife · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Mahulena MaruskovaSouth Texas Center for Emerging Infectious Diseases and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas 7824, USA.
M Dolores Esteve-Gassent
Valerie L Sexton
J Seshu

Funding

UTSA RISE Research Training ProgramR25GM060655 · NIGMS · UNIVERSITY OF TEXAS SAN ANTONIO · PI BAREA-RODRIGUEZ, EDWIN J · 2000 to 2022
$21.6M
Genetic Analysis of Borrelia burgdorferi lp54 LociR21AI065953 · NIAID · UNIVERSITY OF TEXAS SAN ANTONIO · PI SESHU, JANAKIRAM · 2005 to 2006
$400k
NIAID NIH HHS AI-065953NIAID NIH HHS R21 AI065953NIGMS NIH HHS GM-60655NIGMS NIH HHS R25 GM060655
6 · The paper itself

Abstract

Borrelia burgdorferi, the causative agent of Lyme disease, undergoes rapid adaptive gene expression in response to environmental signals encountered during different stages of its life cycle in the arthropod vector or the mammalian host. Among all the plasmid-encoded genes of B. burgdorferi, several linear plasmid 54 (lp54)-encoded open reading frames (ORFs) exhibit the greatest differential expression in response to mammalian host-specific temperature, pH, and other uncharacterized signals. These ORFs include members of the paralogous gene family 54 (pgf 54), such as BBA64, BBA65, and BBA66, present on lp54. In an attempt to correlate transcriptional up-regulation of these pgf 54 members to their role in infectivity, we inactivated BBA64 and characterized the phenotype of this mutant both in vitro and in vivo. There were no major differences in the protein profiles between the BBA64 mutant and the control strains, while immunoblot analysis indicated that inactivation of BBA64 resulted in increased levels of BBA65. Moreover, there was no significant difference in the ability of the BBA64 mutant to infect C3H/HeN mice compared to that of its parental or complemented control strains as determined by culturing of viable spirochetes from infected tissues. However, enumeration of spirochetes using quantitative real-time PCR revealed tissue-specific differences, suggesting a minimal role for BBA64 in the survival of B. burgdorferi in select tissues. Infectivity analysis of the BBA64 mutant suggests that B. burgdorferi may utilize multiple determinants to establish infection in mammalian hosts.

Indexed as

AnimalsArthritis, InfectiousBacterial ProteinsBorrelia burgdorferiDisease Models, AnimalGene Expression Regulation, BacterialJointsLyme DiseaseMiceMice, Inbred C3HMutationBacterial Proteins

Identifiers

PMID17984202
PMCPMC2223643

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.