The pathogenesis of respiratory viral infection.
Sendai virus is used as a model to study the histological response and the mechanism of recovery of mice from infection. Although mice infected intranasally do not appear ill, the ciliated columnar cells of the bronchial epithelium undergoes rapid necrosis followed later by repair. Interferon is produced at an early stage of infection and antibody formation follows later. Cyclophosphamide given to mice infected with Sendai virus abolishes the humoral antibody response but not interferon production; the mice develop pneumonic lesions. They cannot eliminate virus and they die. On the other hand, deprivation of 'T' lymphocytes by thymectomy, irradiation and bone marrow reconstitution renders mice more susceptible to Sendai virus but they do not die. The humoral response is thus apparently helped by 'T' lymphocytes and interferon production is not vital for recovery.
D000818:Animals; D000914:Antibodies, Viral / Q000096:biosynthesis; D007111:Immunity, Cellular; D007372:Interferons / Q000096:biosynthesis; D008264:Macrophages / Q000276:immunology; D051379:Mice; D009092:Mucous Membrane / Q000473:pathology; D010222:Parainfluenza Virus 1, Human; D018184:Paramyxoviridae Infections / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D012137:Respiratory System / Q000473:pathology; D012141:Respiratory Tract Infections / Q000209:etiology* / Q000276:immunology / Q000473:pathology
D000914:Antibodies, Viral; D007372:Interferons