Causes and pathogenesis of respiratory syncytial infection
Last reviewed: 23.04.2024
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Respiratory syncytial infection is widespread, recorded year-round, but outbreaks occur more often in winter and spring. The source of infection are sick and rarely - virus carriers. Patients excrete the virus within 10-14 days. Infection is transmitted exclusively by airborne droplets during direct contact. Transmission of infection through third parties and household items is unlikely. Susceptibility of different age groups to respiratory syncytial infection is not the same. Children under the age of 4 months are relatively insensitive, as many of them have specific antibodies received from the mother. The only exception is premature babies, they do not have passive immunity and therefore are susceptible to PC infection from the first days of life. The greatest susceptibility to respiratory syncytial infection is observed at the age of 4-5 months to 3 years. At this age, all children manage to survive respiratory syncytial infection (especially in children's groups). Serious antibodies of IgA appear in the serum and the mucous membrane of the nose. Secretory antibodies are an important factor of immunity in respiratory syncytial infection. Since the acquired immunity is not stable, in repeated meetings with the respiratory syncytial virus, children can again get respiratory syncytial infection. Such diseases are erased, but maintain the intensity of specific immunity. Consequently, with the complete disappearance of specific antibodies against the respiratory syncytial virus, a manifest form of the disease appears, and against the background of residual immunity, an erased, or inapparent, infection.
Causes of respiratory syncytial infection
The respiratory syncytial infection virus contains RNA, from other paramyxoviruses it is distinguished by great polymorphism, the diameter of the particles is on the average 120-200 nm, is not very stable in the external environment. There are 2 serovars of the virus having a common complement-binding antigen. The virus develops well in primary and transplantable cell lines (HeLa cells, Hep-2, etc.), where syncytium and pseudo-giant cells are formed. Unlike other paramyxoviruses, neither hemagglutinin nor neuraminidase has been detected in respiratory syncytial viruses.
Pathogenesis of respiratory syncytial infection
The virus enters the body by airborne droplets. Reproduction occurs in the epithelial cells of the mucous membrane of the respiratory tract. The pathological process quickly spreads to small bronchi and bronchioles, especially in young children. The persistence of the respiratory syncytial virus in epithelial cells causes their hyperplasia with the formation of symplasts, pseudo-gigantic cells and the phenomenon of hypersecretion, which leads to a narrowing of the lumen of small bronchi and bronchioles and complete blockage of their lumen with thick viscous mucus, deflated epithelium, leukocytes and lymphocytes. Drainage function of the bronchi is broken, stasis develops, small atelectasis, interalveolar septa thickens, which leads to disruption of oxygen metabolism and development of oxygen starvation. The lungs are emphysematically dilated, dyspnea and tachycardia occur. The further course of respiratory syncytial infection is determined by the severity of respiratory failure and the layering of bacterial infection.
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