TY - JOUR
T1 - Residual brain infection in relapsing-fever borreliosis
AU - Cadavid, Diego
AU - Sondey, Marie
AU - Garcia, Edwin
AU - Lawson, Catherine L.
N1 - Funding Information:
Received 24 August 2005; accepted 9 December 2005; electronically published 4 April 2006. Potential conflicts of interest: none reported. Financial support: Foundation of the University of Medicine and Dentistry of New Jersey (grant to D.C.); Heritage Affiliate of the American Heart Association (Scientist Development Grant 0235464T to D.C.). a Present affiliations: Department of Biochemistry, University of Medicine and Dentistry of New Jersey–New Jersey Medical School, Newark (M.S.); New York College of Osteopathic Medicine, Old Westbury (E.G.) Reprints or correspondence: Dr. Diego Cadavid, University of Medicine and Dentistry of New Jersey–New Jersey Medical School, 185 S. Orange Ave., MSB H506, Newark, NJ 07103 (cadavidi@umdnj.edu).
PY - 2006/5/15
Y1 - 2006/5/15
N2 - Background. Neurological involvement is common in the spirochetal infection relapsing fever (RF) in both humans and experimental animals. RF is best known for antigenic variation caused by the sequential expression of variable outer membrane lipoproteins of 2 sizes, variable small (Vsp) and variable large (VIp) proteins. Less understood is the persistence of RF borreliae in the brain after they are cleared from the blood, referred to as residual brain infection (RBI). Our goal was to investigate the phenomenon of RBI in RF. Methods. We studied RBI in immunocompetent mice by culturing blood and perfused brain samples 1 month after intraperitoneal inoculation with Borrelia turicatae serotype 1 (Bt1). Mice deficient in Toll-like receptor 2 (TLR2-/-) or in B and T cells (scid) were included for comparison. Results. All scid mice had persistent infection in blood and brain. RBI was found in 3 (19%) of 16 immunocompetent and TLR2-/- mice. RBI was caused by either persistence of the original serotype (Bt1) or newly emerged Vsp (n = 1, renamed Bt3) or Vlp serotypes. The Vsp of Bt1 (Vspl) and Bt3 (Vsp3) were 75% identical. Conclusions. RBI in RF is relatively frequent and can occur by persistence of the original or newly emerged serotypes.
AB - Background. Neurological involvement is common in the spirochetal infection relapsing fever (RF) in both humans and experimental animals. RF is best known for antigenic variation caused by the sequential expression of variable outer membrane lipoproteins of 2 sizes, variable small (Vsp) and variable large (VIp) proteins. Less understood is the persistence of RF borreliae in the brain after they are cleared from the blood, referred to as residual brain infection (RBI). Our goal was to investigate the phenomenon of RBI in RF. Methods. We studied RBI in immunocompetent mice by culturing blood and perfused brain samples 1 month after intraperitoneal inoculation with Borrelia turicatae serotype 1 (Bt1). Mice deficient in Toll-like receptor 2 (TLR2-/-) or in B and T cells (scid) were included for comparison. Results. All scid mice had persistent infection in blood and brain. RBI was found in 3 (19%) of 16 immunocompetent and TLR2-/- mice. RBI was caused by either persistence of the original serotype (Bt1) or newly emerged Vsp (n = 1, renamed Bt3) or Vlp serotypes. The Vsp of Bt1 (Vspl) and Bt3 (Vsp3) were 75% identical. Conclusions. RBI in RF is relatively frequent and can occur by persistence of the original or newly emerged serotypes.
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U2 - 10.1086/503367
DO - 10.1086/503367
M3 - Article
C2 - 16619194
AN - SCOPUS:33646344227
SN - 0022-1899
VL - 193
SP - 1451
EP - 1458
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 10
ER -