Because the immune system plays a key role in protection against infections, viral damage to it can exacerbate the severity of disease or predispose to superinfection with other infectious agents The most dramatic effect of viral suppression of the immune system occurs in infections with the human immunodeficiency virus (HIV), the agent that causes the acquired immunodeficiency syndrome (AIDS). The virus damages the immune system in several different ways. It replicates preferentially in CD41 T lymphocytes and in cells of the monocyte/macrophage lineage, in the latter, cytopathic effects are slight, but the cell functions of phagocytosis, antigen processing/ presentation, and cytokine production may be inhibited. In Th cells, viral cDNA is integrated into the chromosomes, and viral replication occurs only following activation of these lymphocytes by certain cytokines. Death of CD4 T cells can occur by apoptosis, or following fusion with other T cells to form syncytia, or by lysis by CD8^ Tc cells. Deletion of CD4 T cells leads to profound immunosuppression, which can be measured by any of a multitude of indicators of loss of Th, (Td) and Th2 (helper T) cell function, that is, impaired delayed-type hypersensitivity and helper functions, as well as diminished cytokine production. Toward the end of the long incubation period (1 to 10 or more years), the CD4 T-cell count drops below 200 per cubic millimeter and the patient falls victim to a succession of opportunistic infections with a range of other viruses, bacteria, fungi, and protozoa, or to cancer. Death follows inexorably, usually within a year of the development of AIDS.
Infections with certain other viruses may temporarily suppress humoral and/or cell-mediated immune responses. Many viruses are capable of productive or abortive replication in macrophages (see Table 7-3) Cytomegalovirus and Epstein-Barr virus replicate nonproductively in B cells, transforming them and altering their function, and several viruses have been shown to grow productively or abortively in activated T lymphocytes, A good example of the latter is measles virus, which replicates nonproductively in T lymphocytes. It has been known since the work of von Pirquet in 1908 that measles infection depressed skin responses to tuberculin and reactivated latent tuberculosis. Other immunologic abnormalities found during the acute phase of measles include spontaneous proliferation of peripheral blood lymphocytes and increased plasma interferon 7. The depressed delayed-fype hypersensitivity response, decreased NK cell activity, increased plasma IgE, and increased soluble IL-2 receptor persist for up to 4 weeks after the onset of the rash. These and other immunologic abnormalities probably account tor the susceptibility to secondary infections that causes most of the mortality during outbreaks of measles.
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