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dc.contributor.authorHart, Thomas M.
dc.contributor.authorDupuis, Alan P. 2nd
dc.contributor.authorTufts, Danielle M.
dc.contributor.authorBlom, Anna M.
dc.contributor.authorStarkey, Simon R.
dc.contributor.authorRego, Ryan O.M.
dc.contributor.authorRam, Sanjay
dc.contributor.authorKraiczy, Peter
dc.contributor.authorKramer, Laura D.
dc.contributor.authorDiuk-Wasser, Maria A.
dc.contributor.authorKolokotronis, Sergios-Orestis
dc.contributor.authorLin, Yi-Pin
dc.date2022-08-11T08:10:01.000
dc.date.accessioned2022-08-23T16:52:28Z
dc.date.available2022-08-23T16:52:28Z
dc.date.issued2021-07-29
dc.date.submitted2022-02-03
dc.identifier.citation<p>Hart TM, Dupuis AP 2nd, Tufts DM, Blom AM, Starkey SR, Rego ROM, Ram S, Kraiczy P, Kramer LD, Diuk-Wasser MA, Kolokotronis SO, Lin YP. Host tropism determination by convergent evolution of immunological evasion in the Lyme disease system. PLoS Pathog. 2021 Jul 29;17(7):e1009801. doi: 10.1371/journal.ppat.1009801. PMID: 34324600; PMCID: PMC8354441. <a href="https://doi.org/10.1371/journal.ppat.1009801">Link to article on publisher's site</a></p>
dc.identifier.issn1553-7366 (Linking)
dc.identifier.doi10.1371/journal.ppat.1009801
dc.identifier.pmid34324600
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42058
dc.description.abstractPathogens possess the ability to adapt and survive in some host species but not in others-an ecological trait known as host tropism. Transmitted through ticks and carried mainly by mammals and birds, the Lyme disease (LD) bacterium is a well-suited model to study such tropism. Three main causative agents of LD, Borrelia burgdorferi, B. afzelii, and B. garinii, vary in host ranges through mechanisms eluding characterization. By feeding ticks infected with different Borrelia species, utilizing feeding chambers and live mice and quail, we found species-level differences in bacterial transmission. These differences localize on the tick blood meal, and specifically complement, a defense in vertebrate blood, and a polymorphic bacterial protein, CspA, which inactivates complement by binding to a host complement inhibitor, Factor H (FH). CspA selectively confers bacterial transmission to vertebrates that produce FH capable of allele-specific recognition. CspA is the only member of the Pfam54 gene family to exhibit host-specific FH-binding. Phylogenetic analyses revealed convergent evolution as the driver of such uniqueness, and that FH-binding likely emerged during the last glacial maximum. Our results identify a determinant of host tropism in Lyme disease infection, thus defining an evolutionary mechanism that shapes host-pathogen associations.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=34324600&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © 2021 Hart et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectNymphs
dc.subjectBlood
dc.subjectQuails
dc.subjectSpirochetes
dc.subjectLyme disease
dc.subjectBorrelia infection
dc.subjectBorrelia burgdorferi
dc.subjectTropism
dc.subjectBacterial Infections and Mycoses
dc.subjectImmunopathology
dc.titleHost tropism determination by convergent evolution of immunological evasion in the Lyme disease system
dc.typeJournal Article
dc.source.journaltitlePLoS pathogens
dc.source.volume17
dc.source.issue7
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=5893&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/4860
dc.identifier.contextkey27978610
refterms.dateFOA2022-08-23T16:52:28Z
html.description.abstract<p>Pathogens possess the ability to adapt and survive in some host species but not in others-an ecological trait known as host tropism. Transmitted through ticks and carried mainly by mammals and birds, the Lyme disease (LD) bacterium is a well-suited model to study such tropism. Three main causative agents of LD, Borrelia burgdorferi, B. afzelii, and B. garinii, vary in host ranges through mechanisms eluding characterization. By feeding ticks infected with different Borrelia species, utilizing feeding chambers and live mice and quail, we found species-level differences in bacterial transmission. These differences localize on the tick blood meal, and specifically complement, a defense in vertebrate blood, and a polymorphic bacterial protein, CspA, which inactivates complement by binding to a host complement inhibitor, Factor H (FH). CspA selectively confers bacterial transmission to vertebrates that produce FH capable of allele-specific recognition. CspA is the only member of the Pfam54 gene family to exhibit host-specific FH-binding. Phylogenetic analyses revealed convergent evolution as the driver of such uniqueness, and that FH-binding likely emerged during the last glacial maximum. Our results identify a determinant of host tropism in Lyme disease infection, thus defining an evolutionary mechanism that shapes host-pathogen associations.</p>
dc.identifier.submissionpathoapubs/4860
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pagese1009801


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Copyright © 2021 Hart et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Except where otherwise noted, this item's license is described as Copyright © 2021 Hart et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.