Most viral infections are limited by nonspecific defenses, which (1) restrict initial virus multiplication to manageable levels, (2) initiate recovery from established infections that is then completed by a combination of these early nonspecific and subsequent antigen-specific immune defenses, and (3) enable the host to cope with the peak numbers of virus that, if presented as the infecting dose, could be lethal. Although immune and nonimmune (nonspecific) defenses operate together to control viral infections, this chapter considers only nonspecific defenses. Some nonspecific defenses exist independently of infection (e.g., genetic factors, anatomic barriers, nonspecific inhibitors in body fluids, and phagocytosis). Others (e.g., fever, inflammation, and interferon) are produced by the host in response to infection. All nonspecific defenses begin to act before the specific defense responses develop and can potentiate some of the established immune effector mechanisms.
The fact that viruses replicate intracellularly and the ability of some viruses to spread by inducing cell fusion partly protect viruses against such extracellular defenses as neutralizing antibody, phagocytosis, and nonspecific inhibitors. However, because they replicate within the cell, viruses are vulnerable to intracellular alterations caused by host responses to infection. Nonspecific responses that alter the intracellular environment include fever, inflammation, and interferon.
These multiple defenses function with great complexity because of their interactions with one another. This complexity is compounded by the varying effectiveness of the defenses that results from the diversity of viruses, hosts, and sites and stages of infection.
Copyright © 1996, The University of Texas Medical Branch at Galveston.