Once introduced into a host, the virus infects susceptible cells, frequently in the upper respiratory tract. Viral infections may produce one of three characteristic clinical presentations: (1) acute viral infection, displaying evident signs and symptoms; (2) latent infection, which has no visible signs and symptoms, but the virus is still present in the host cell in a lysogenic state (inserted into the host genome in a resting state); and (3) chronic or persistent infection, in which low levels of virus are detectable and the degree of visible signs or symptoms varies. osby.)
After a local viral infection, a viremia occurs (viruses present in the patient’s blood ), which inoculates secondary target tissue distant from the primary site and releases mediators of human immune cell functions. Secondary viremia may occur in a variety of tissues, such as the skin, salivary glands, kidneys, and brain tissues. Symptomatic disease ensues. Disease resolves when specific antibody and cell-mediated immune mechanisms prevent continued replication of the virus. Tissue is damaged as a result of lysis of virus-infected cells or by immunopathologic mechanisms directed against the virus that are also destructive to neighboring tissue. Most DNA-containing viruses, such as those in the herpes group, remain latent in host tissue with no observable clinical impact. Retro viruses and most DNA viruses establish a latent state after primary infection. During the latent state, viral genome is integrated into the host cell’s chromosome and no viral replication occurs. Latent viruses can reactivate silently, resulting in viral replication and shedding but no clinical symptoms, or they can reactivate and cause symptomatic, even fatal, disease. Reactivation may accompany immune suppression, resulting in the recurrence of clinically apparent disease.
Occasionally, pathogenic viruses stimulate an immune reaction that cross-reacts with related human tissue, resulting in damage to host function; this is called auto immune pathogenesis. When present, it occurs well after the acute viral infection has resolved. Rare viral infection promotes transformation or immortalization of host cells, resulting in uncontrolled cell growth. Viruses with the ability to stimulate uncontrolled growth of host cells are referred to as oncogenic viruses. Some papillomaviruses (wart viruses) are oncogenic, giving rise to human cervical cancer.
Examples of the variety of pathogenic mechanisms of viral infection are illustrated in disease caused by infection with the measles virus. After replication in the upper respiratory tract and subsequent viremia, the virus infects many susceptible cells throughout the body, including endothelial cells in capillaries of the skin. This is accompanied by local inflammation and results in the characteristic rash of measles. Immunocompetent individuals eradicate the virus, resolving the infection, and have life long immunity. In some, antibody produced in response to the measles infection cross reacts with tissue in the central nervous system (CNS), causing a postinfectious encephalitis. In others, slow but continuing replication of damaged virus in the brain gives rise to subacute sclerosing panencephalitis. In severely immunocompromised individuals, ongoing primary infection is not aborted by the usual immune mechanisms, and the result is death (Figure 1). Because the measles virus is not an oncogenic virus, no cancers result from prolonged infection.
Fig1. Viral pathogenesis is illustrated by the mechanisms through which the measles virus spreads in the body. (From Murray PR, Drew WL, Kobayashi GS, et al, editors: Medical microbiology, St Louis, 1990, Mosby.)
