Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 201, Issue 7, Pages 1084-1095Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/651172
Keywords
-
Categories
Funding
- National Institute of Allergy and Infectious Diseases [R21AI076684, R01AI080615]
Ask authors/readers for more resources
Borrelia burgdorferi, the pathogen of Lyme borreliosis, persists in nature through a tick-rodent transmission cycle. A selective assessment of the microbial transcriptome, limited to gene-encoding putative membrane proteins, reveals that bba52 transcription in vivo is strictly confined to the vector-specific portion of the microbial life cycle, with the highest levels of expression noted in feeding ticks and with swift down-regulation noted in mice. bba52 deletion did not affect murine disease as assessed by the genesis of arthritis and carditis or long-term persistence of pathogens in mice or ticks. However, bba52 deficiency did impair microbial transitions between hosts and vector, defects that could be fully rescued when bba52 expression was genetically restored to the original genomic locus. These studies establish that BBA52 facilitates vector-host transitions by the pathogen and therefore is a potential antigenic target for interference with transmission of B. burgdorferi from ticks to mammalian hosts.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available