Neutralising antibody to an old isolate may not prevent infection by new isolates of virus if antigenic variation occurs in the major epitopes for neutralisation eg with FMDV and influenza. Such changes do not occur with the paramyxoviruses- hence the great success of vaccination against canine distemper and rinderpest.

Certain large viruses e.g. the pox, irido (ASFV) and herpes virus families, are poorly neutralised. T cell immunity controls them best. This explains why vaccination can fail unless T cells are constantly being induced e.g. by the live Marek's disease vaccines which continue to replicate during the life time of the bird.

IgM is pentameric and remains in the plasma as if to counteract viraemia.

IgG enters the tissue spaces and is actively transported across the placenta, into the colostrum and lower respiratory tract. It appears at 7 days when the B cell clones, which have switched to IgG have increased their affinity .

IgA is actively secreted across mucosal surfaces and has a role in gut and upper respiratory tract immunity. It is best produced by B cells which are beneath the mucosal surface in response to virus replicating at that surface. IgA is therefore more prominent after live virus vaccines than inactivated virus vaccines.