Page 906 - Veterinary Immunology, 10th Edition

unusually low levels of IgG3.
VetBooks.ir Porcine Respiratory and Reproductive

Syndrome

Porcine respiratory and reproductive syndrome virus (PRRSV) is a

single-stranded, positive-sense RNA virus belonging to the family
Arteriviridae. It causes a syndrome characterized by reproductive
failure, infertility, abortions, anorexia, and secondary pneumonia.
When PRRSV invades the respiratory tract, it damages the
mucociliary transport system, kills alveolar macrophages, and

induces apoptosis of immune cells. Some PRRSV isolates
downregulate TNF-α and IFN-γ while others induce Treg cells and
IL-10, both of which can suppress the immune response within the

lungs. Enhanced IL-10 secretion and suppressed TNF-α and IFN-γ
production result in a Th1/Th2 imbalance. As a result of all this,
PRRSV causes an increase in secondary pneumonia. When PRRSV
infects neonatal piglets, it stimulates B cell activity. The piglets
therefore present with polyclonal B cell activation, autoimmunity

(antibodies specific for Golgi antigens and dsDNA), grossly
enlarged lymph nodes, and hypergammaglobulinemia (a 100- to
1000-fold increase in IgG; a 10- to 100-fold increase in IgM and IgA).

The immunoglobulins produced are not directed against PRRSV,
and the B cell proliferative response is not purely polyclonal. The
antibodies produced are derived from a limited number of
dominant B cell clones and are not neutralizing. It is speculated that
the virus produces some form of B cell superantigen. Affected pigs

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also show a decrease in CD4 T cells and an increase in CD8 cells
after several weeks. Cell-mediated responses and virus-neutralizing
antibodies to PRRSV do not develop for about 4 weeks as a result of
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the loss of CD4 cells. Because of this immunosuppression, PRRSV
may cause persistent infections lasting for up to 6 months. The
levels of IL-1, IL-6, TNF-α, and IFN-α are upregulated earlier and to
a greater extent in pigs infected with a highly pathogenic strain of
PRRSV than in pigs infected with less virulent strains. These

cytokines are produced by alveolar macrophages and they may
reduce adaptive immunity to this virus. When PRRSV infects
mature dendritic cells it reduces the expression of CD80/86 and

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