Page 890 - Veterinary Immunology, 10th Edition

infected cells to this cytotoxic effect. Under some circumstances,
VetBooks.ir cytotoxic T cells may kill intracellular viruses without killing the

infected cells. This effect is mediated by T cell–derived IFN-γ and
tumor necrosis factor-α (TNF-α). These cytokines activate two
virucidal pathways. One pathway eliminates viral nucleocapsid

particles, including their contained genomes. The second pathway
destabilizes viral RNA.
Some viral antigens may act as superantigens by binding directly

to TCR Vβ chains. For example, rabies virus nucleocapsid binds to
mouse Vβ8 T cells. By stimulating helper T cell activity, rabies
viruses can switch on Th2 cells. This in turn can result in an
enhanced immune response to rabies viruses, as well as a

polyclonal B cell response.
Macrophages develop antiviral activity following activation.
Viruses are readily endocytosed by macrophages and are usually
destroyed. If the viruses are noncytopathic and can grow inside

macrophages, a persistent infection may result. Under these
circumstances, the macrophages must be activated to eliminate the
virus. Thus macrophage activation mediated by IFN-γ is a feature
of some virus diseases (Chapter 18). For example, macrophages

from birds immunized against fowlpox show an enhanced antiviral
effect against Newcastle disease virus and will prevent the
intracellular growth of Salmonella gallinarum, a feature that is not a
property of normal macrophages.

The duration of immunological memory to viruses is highly
variable. Antiviral antibodies may persist for many years in the
absence of the virus. On the other hand, cytotoxic T cells die soon
after virus elimination while memory T cells can persist for many

years (Chapter 18).

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