Year: 2018
Type: article
Abstract: , orchestrated by a surface protein annotated as BBA57, through its modulation of multiple spirochete virulent determinants. BBA57 function is critical for early infection but largely redundant for later stages of spirochetal persistence, either in mammals or in ticks. The protein influences host IFN responses as well as suppresses multiple host microbicidal activities involving serum complement, neutrophils, and antimicrobial peptides. We also discovered a remarkable plasticity in BBA57-mediated spirochete immune evasion strategy because its loss, although resulting in near clearance of pathogens at the inoculum site, triggers nonheritable adaptive changes that exclude detectable nucleotide alterations in the genome but incorporate transcriptional reprograming events. Understanding the malleability in spirochetal immune evasion mechanisms that ensures their host persistence is critical for the development of novel therapeutic and preventive approaches to combat long-term infections like Lyme borreliosis.
Institutions: University of Maryland, College Park, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Tufts University, University of Maryland, Baltimore, National Institute of Allergy and Infectious Diseases, Ikerbasque, CIC bioGUNE, Virginia–Maryland College of Veterinary Medicine
Language: English
Subfield: Parasitology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: bronze
Awards: BBA57-Mediated Borrelial Persistence, Genesis of Inflammation and Immunity, Borella Gene Products Critical For Natural Infection Cycle, G3735318962, A Novel Tick Protein Influences Persistence of Lyme Disease Pathogens, Borrelia gene products critical for natural infection cycle, G7803227287, Bacterium-ECM interactions during infection by the Lyme disease spirochete
OpenAlex ID: W2795423223