Haemagglutinins of pathogenic avian mycoplasmas.

The pathogenic avian mycoplasmas, Mycoplasma gallisepticum, Mycoplasma synoviae, Mycoplasma meleagridis, Mycoplasma iowae and Mycoplasma imitans, synthesize haemagglutinins that are immunogenic, variably expressed, surface proteins. The haemagglutinins of M. gallisepticum (pMGA), M. synoviae (VlhA) and M. imitans are lipoproteins, encoded by related multigene families that appear to have arisen by horizontal gene transfer. M. gallisepticum also has genes encoding cytadhesins in its genome but these are present as a single copies, while the pMGA gene family contains 30 to 70 genes. The switch in expression of distinct pMGA genes (e.g. pMGA1.1 to pMGA1.9) generates antigenic variation, which is thought to be important in immune evasion but also has significance in the preparation of M. gallisepticum antigens for serological diagnosis. In the majority of M. synoviae strains, post-translational cleavage of the VlhA protein generates an amino-terminal part (the lipoprotein MSPB) and a carboxyl-terminal part (MSPA), which mediates binding to erythrocytes. The 5'vlhA gene region, which encodes proline-rich repeats in the amino-terminal part of MSPB, is highly polymorphic among M. synoviae strains. Insertions or deletions in the part of vlhA encoding the proline-rich repeats cause MSPB length variation in different M. synoviae strains. Recombination between the 5'vlhA gene and pseudogenes in the genome generates changes in antigenic determinants in the carboxyl two-thirds of the MSPB molecule, and in MSPA, resulting in changes in the domains involved in the binding of M. synoviae to erythrocytes. Variant haemagglutinins of M. gallisepticum (pMGA1.7) and M. synoviae (diverse VlhA forms) share sequences that may be responsible for antigenic cross-reactions between M. gallisepticum and M. synoviae. Shared epitopes have been demonstrated using specific antibodies against MSPB that also recognize proteins of M. gallisepticum and of M. iowae (serotype N). Size and antigenic variants have also been reported for M. meleagridis and M. iowae proteins, but it is not known if these are their haemagglutinins. Advances in the molecular characterization of M. gallisepticum (pMGA, pvpA) and M. synoviae (vlhA) genes and their sequencing in numerous strains is likely to enable significantly improved epidemiological studies and improved tracing of M. gallisepticum and M. synoviae strains in different flocks.