A virus enters the host through any opportunistic opening of the body. Minute breaks in the skin barrier or mucosal linings of the eye, nose, gastrointestinal, and urogenital tracts create portals for the virus to enter host cells and underlying tissues. Replicating virus may establish a localized infection, or the virus, traveling as free virions or associated with immune cells, may spread to other areas of the body. Replication can continue at the initial site of infection or move to secondary organs and tissues. During an active infection, virus particles may be shed through nasal and respiratory secretions, urine, and stool.
An incubation period is the time between exposure to virus and the manifestation of symptoms of infection. Initial symptoms may be slight, such as a rash or fever, and may not initially prompt patients to seek medical care. Diagnostic samples are taken when people seek medical treatment; therefore, the presence of virus and virus-specific antibodies depends on the incubation period. This observation has important implications for the identification of new viral infections or epidemics. Virus may be detected and isolated for infections with short incubations; however, antibodies may not yet have developed, see Figure 4.2. For example, infections with influenza and adenovirus have very short incubation periods, 1-2 days, before myalgias and fever manifest. Many viruses have invaded the body for over a week before symptoms become apparent. Dengue, measles, and rotavirus are relatively asymptomatic during the first 5-8 days, but may rapidly progress to severe illness soon after. Longer incubation
A. Acute infection
B. Chronic Infection
Time figure 4.2 (A) Adaptive immune response in an acute resolving infection. Low-affinity antibodies of the IgM isotype develop initially, and partially control circulating virus. T cells undergo clonal expansion upon virus antigen stimulation. In response to effector T cells and often higher-affinity IgG antibodies, virus levels decline and the immune system differentiates into memory T cells. Such memory T cells and neutralizing antibody may persist for the life of the patient. (B) Adaptive immune response in a chronic virus infection. Antibodies and T cells develop but are unable to eliminate virus. Virus levels, although typically lower than in the acute stage, are continuously present despite a measurable immune response. Mechanisms leading to chronic infection include generation of viral mutants that escape the adaptive immune response, induction of immune exhaustion or tolerance, and a quiescent state called latency for some DNA and RNA viruses.
periods may be caused by chronic infections. For example, rabies virus may remain silent for 30-100 days after an animal bite before causing sudden disease demanding medical treatment. Other stealth viruses, such as HIV, hepatitis B and C, and papilloma viruses, may bring about a mild ailment initially that may gradually progress to a fatal disease. Patients with chronic infections may seroconvert and have detectable virus even in the presence of antibodies. Others may be persistently infected by a virus, yet never develop symptoms. These carriers may have low levels of virus, which could potentially be transmitted to other individuals despite being below the level of assay detection. An understanding of how the host responds to viral infection aids investigators and health care workers in identifying and treating infection.
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