Back to Search Start Over

VirB10 vaccination for protection against Anaplasma phagocytophilum.

Authors :
Crosby FL
Lundgren AM
Hoffman C
Pascual DW
Barbet AF
Source :
BMC microbiology [BMC Microbiol] 2018 Dec 18; Vol. 18 (1), pp. 217. Date of Electronic Publication: 2018 Dec 18.
Publication Year :
2018

Abstract

Background: Human granulocytic anaplasmosis (HGA) is a tick-borne disease caused by the etiologic agent Anaplasma phagocytophilum. HGA was designated a nationally notifiable disease in the United States in 1998. Currently there are no vaccines available against HGA. Conserved membrane proteins that are subdominant in Anaplasma species, such as VirB9 and VirB10, may represent better vaccine targets than the variable immunodominant surface proteins. VirB9 and VirB10 are constituents of the Type 4 secretion system (T4SS) that is conserved amongst many intracellular bacteria and performs essential functions for invasion and survival in host cells.<br />Results: Immunogenicity and contribution to protection, provided after intramuscular vaccination of plasmid DNA encoding VirB9-1, VirB9-2, and VirB10 followed by inoculation of homologous recombinant proteins, in a prime-boost immunization strategy was evaluated in a murine model of HGA. Recombinant VirB9-1-, VirB9-2-, and VirB10-vaccinated mice developed antibody responses that specifically reacted with A. phagocytophilum organisms. However, only the mice vaccinated with VirB10 developed a significant increase in IFN-γ CD4 <superscript>+</superscript> T cells and partial protection against challenge with A. phagocytophilum.<br />Conclusions: This work provides evidence that A. phagocytophilum T4SS VirB10 is partially protective in a murine model against infection in an IFN-γ-dependent fashion and suggests that this protein may be a potential vaccine candidate against this and possibly other pathogenic bacteria with a T4SS.

Details

Language :
English
ISSN :
1471-2180
Volume :
18
Issue :
1
Database :
MEDLINE
Journal :
BMC microbiology
Publication Type :
Academic Journal
Accession number :
30563470
Full Text :
https://doi.org/10.1186/s12866-018-1346-x