Abstract

The V-1 antigen of Mycoplasma pulmonis is exposed on the surface of the mycoplasma and has an immunoblot banding pattern that varies in vitro between and within strains. To determine if V-1 variation occurs in vivo, we infected C3H/HeNCr mice intranasally with 5 × 10 8 colony-forming units of M. pulmonis strain 5782C. We isolated M. pulmonis clones from the respiratory tracts of mice up to 28 days post-infection, then used anti-V-1 monoclonal antibody P39 to visualize their V-1 immunoblot banding patterns. By the 28th day following infection, 92% of the recovered clones had variant V-1 banding patterns. Additionally, there was a significant correlation between the severity of lung lesions and the percentage of V-1 variant clones recovered from the respiratory tracts of individual mice. These studies prove that V-1 variation does occur in vivo, and suggest that mice with more severe pulmonary lesions tend to have more V-1 variant clones as a percentage of the M. pulmonis population. Thus, variation in the V-1 protein may be a mechanism by which M. pulmonis persists in the in vivo environment, possibly by evasion of host immune surveillance or by alteration of its surface membrane to take better advantage of its environmental niche in the host.

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