domingo, 1 de septiembre de 2013

Borrelia burgdorferi bba66 gene inactivation re... [Infect Immun. 2013] - PubMed - NCBI

Borrelia burgdorferi bba66 gene inactivation re... [Infect Immun. 2013] - PubMed - NCBI

2013 Jul;81(7):2488-98. doi: 10.1128/IAI.00140-13. Epub 2013 Apr 29.

Borrelia burgdorferi bba66 gene inactivation results in attenuated mouse infection by tick transmission.


National Center for Emerging and Zoonotic Infectious Diseases, Division of Vector-Borne Diseases, Bacterial Diseases Branch, Centers for Disease Control and Prevention, Fort Collins, Colorado, USA.


The impact of the Borrelia burgdorferi surface-localized immunogenic lipoprotein BBA66 on vector and host infection was evaluated by inactivating the encoding gene, bba66, and characterizing the mutant phenotype throughout the natural mouse-tick-mouse cycle. The BBA66-deficient mutant isolate, Bb(ΔA66), remained infectious in mice by needle inoculation of cultured organisms, but differences in spirochete burden and pathology in the tibiotarsal joint were observed relative to the parental wild-type (WT) strain. Ixodes scapularis larvae successfully acquired Bb(ΔA66) following feeding on infected mice, and the organisms persisted in these ticks through the molt to nymphs. A series of tick transmission experiments (n = 7) demonstrated that the ability of Bb(ΔA66)-infected nymphs to infect laboratory mice was significantly impaired compared to that of mice fed upon by WT-infected ticks. trans-complementation of Bb(ΔA66) with an intact copy of bba66 restored the WT infectious phenotype in mice via tick transmission. These results suggest a role for BBA66 in facilitating B. burgdorferi dissemination and transmission from the tick vector to the mammalian host as part of the disease process for Lyme borreliosis.

[PubMed - indexed for MEDLINE]
[Available on 2014/1/1]

No hay comentarios:

Publicar un comentario