Table 3.
Infectivity of B. burgdorferi expressing vlsE and ospA from the ospC promoter
| B. burgdorferi strain | No. of infected mice/no. of mice injecteda | |
|---|---|---|
| WT | SCID | |
| WT | 6/8 | 9/10 |
| WT/pCpvlsE1 | 2/10 | 0/5 |
| WT/pCpvlsE2 | 1/5 | NDc |
| WT/pCpospA | 4/5 | 5/5 |
| WT/pKFSS1b | 5/5 | ND |
| ΔospC | 0/10 | 0/10 |
| ΔospC/pCpvlsE1 | 0/5 | 0/5 |
| ΔospC/pCpvlsE2 | 0/5 | ND |
| ΔospC/pCpospA | 0/5 | 0/5 |
Both immunocompetent WT mice and immunodeficient C3H-SCID mice were injected intradermally with 104 of the designated B. burgdorferi strain. At three weeks post-injection, WT mice were retro-orbitally bled to test for infection by immunoblot for seroconversion to B. burgdorferi proteins, and all mice were euthanized for attempted isolation of spirochaetes from the ear, bladder, and tibiotarsal joint. All WT mice positive by serology were also positive by isolation from all three tissues.
The pBSV2G-ospCp-vlsE shuttle vector (pCpvlsE1) was displaced from the WT/pCpvlsE1 strain by introduction of the incompatible pKFSS1 shuttle vector. This strain was then injected into wild-type mice at a dose of 104 to confirm that the loss of the pBSV2G-ospCp-vlsE shuttle vector restored infectivity to wild-type levels.
No data. These strains were only tested in WT mice.