Читать книгу Basic Virology - Martinez J. Hewlett - Страница 31

Pathogenesis can be divided into stages – from initial infection of the host to its eventual full or partial recovery, or its virus‐induced death. A more‐or‐less typical course of infection in a vertebrate host is schematically diagrammed in Figure 2.3. Although individual cases differ, depending on the nature of the viral pathogen and the immune capacity of the host, a general pattern of infection would be as follows:

 Initial infection leads to virus replication at the site of entry, and multiplication and spread into favored tissues. The time between the initial infection and the observation of clinical symptoms of disease defines the incubation period, which can be of variable length, depending on many factors.Figure 2.3 The pathogenesis of virus infection. Typically, infection is followed by an incubation period of variable length in which virus multiplies at the site of initial infection. Local and innate immunity, including the interferon response, counter infection from the earliest stages; and if these lead to clearing, disease never develops. During the incubation period, virus spreads to the target of infection (which may be the same site). The adaptive immune response becomes significant only after virus reaches high enough levels to efficiently interact with cells of the immune system; this usually requires virus attaining high levels or titers in the circulatory system. Virus replication in the target leads to symptoms of the disease in question and is often important in spread of the virus to others. Immunity reaches a maximum level only late in the infection process and remains high for a long period after resolution of the disease.

 The host responds to the viral invasion by marshaling its defense forces, both local and systemic. The earliest defenses include expression of interferon and tissue inflammation. Ultimately the major component of this defense – adaptive immunity – comes into play. For disease to occur, the defenses must lag as the virus multiplies to high levels. At the same time, the virus invades favored sites of replication. Infection of these favored sites is often a major factor in the occurrence of disease symptoms and is often critical for the transmission to other organisms. As the host defenses mount, virus replication declines and there is recovery – perhaps with lasting damage and usually with immunity to a repeat infection. If an insufficient defense is mounted, the host will die.