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J Gen Virol 70 (1989), 325-333; DOI 10.1099/0022-1317-70-2-325
© 1989 Society for General Microbiology

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Immune Response to Experimentally Induced Infection with Respiratory Syncytial Virus: Possible Role in the Development of Pulmonary Disease

Pedro A. Piedra1,5,{dagger}, Giovanni Camussi3,4,6, and Pearay L. Ogra1,2,5,

1 Department of Pediatrics
2 Department of Microbiology
3 Department of Pathology
and4 Department of Medicine, State University of New York
5 Division of Infectious Diseases and Microbiology Laboratories, Children's Hospital, Buffalo, New York 14222
and6 Kidney Research Laboratory, Buffalo General Hospital, Buffalo, New York 14209, U.S.A.

Groups of mice were immunized intraperitoneally with HEp-2 lysate or respiratory syncytial virus (RSV)-infected HEp-2 cells with or without adjuvant(s). The animals were subsequently challenged intranasally (i.n.) with RSV and/or HEp-2 lysate and studied for RSV shedding in the lung, antigen-specific antibody response and pulmonary histopathology. A significant decrease in virus shedding was detected in each of four groups of animals immunized with a virus preparation and in two of four groups that received a HEp-2 lysate. Mice immunized with adjuvant(s) developed higher antibody-specific responses. All vaccinated animals developed pulmonary histopathology only on subsequent i.n. inoculation with RSV and/or HEp-2 lysate. Denatured extracts of purified RSV, HEp-2, BALB/c lung, cotton rat lung, Buffalo green monkey kidney and human buccal epithelium were tested for reactivity against the sera of immunized mice by an immunoblot method. Sera from all groups of immunized mice reacted with the extracts tested. The data suggest a possible role of reactivity to viral as well as non-viral components in the pathogenesis of RSV vaccine-induced pulmonary inflammation in the mouse model system.

Keywords: RSV, immune response, inflammatory cells

{dagger} Present address: Department of Microbiology and Immunology, Baylor College of Medicine, One Baylor Plaza, Houston, Tex. 77030, U.S.A.

Received 5 July 1988; accepted 17 October 1988.


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