Page 895 - Veterinary Immunology, 10th Edition

clades are sufficiently antigenically different as to require both in
VetBooks.ir vaccines.

A second form of immune evasion by viruses is seen in caprine
arthritis-encephalitis (CAE), Aleutian disease of mink, and African

swine fever. Although infected animals respond to these viruses,
their antibodies are incapable of virus neutralization. Thus
parvovirus-antibody complexes from Aleutian disease-infected
mink are fully infectious. Goats with CAE make large amounts of

anti-envelope antibodies, but they develop negligible levels of
neutralizing antibodies. In this case, goats fail to recognize and
respond to the virus-neutralizing epitopes. If rabbits are immunized
with CAE virus, they can readily produce virus-neutralizing

antibodies; even goats will produce these antibodies if immunized
with large amounts of an adjuvanted viral antigen. The antibodies
produced in these hyperimmunized goats are very specific and will
react only with the immunizing strain of the virus.

Notwithstanding the absence of neutralizing antibodies, other
antibodies can bind to CAE virions, and the opsonized virions are
endocytosed by macrophages. Unfortunately, this virus grows
within macrophages so that opsonizing antibodies merely speed up

virus replication, an example of antibody-mediated enhancement.
Attempts to vaccinate goats against CAE lead only to more severe
disease.
A third mechanism by which viruses can evade destruction by

antibodies is seen in yet another lentiviral infection, maedi-visna, in
sheep. (Maedi is a chronic pneumonia; visna is a chronic
neurological disease caused by the same virus.) In maedi-visna
infections, neutralizing antibodies are produced slowly. These

neutralizing antibodies are unable to reduce the viral burden in
infected sheep, and cyclical relapses do not occur. The antibodies
have a low affinity for viral epitopes and take at least 20 minutes to
bind to the virus and 30 minutes to neutralize it. In contrast, it takes

only 2 minutes for this virus to infect a cell. Thus the virus can
spread between cells much faster than it can be neutralized. The
maedi-visna virus also invades monocytes and macrophages. In
most of these cells, the replication of the virus stops after its RNA
has been reversely transcribed into proviral DNA. As a result, the

cells are persistently infected by the virus without expressing viral

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