Abstract
Groups of male BALB/c mice were primed intraperitoneally with uninfected HEp-2 cell cultures (HEp-2), live RSV infected cell cultures (L-RSV), or sucrose density gradient purified RSV antigen (P-RSV), in combination with alum and killed Bordetella pertussis as adjuvants. The animals were subsequently challenged intranasally (I/N) with HEp-2 or L-RSV. All animals developed severe pulmonary histopathology after I/N challenge with HEp-2 or RSV, regardless of whether priming immunization was carried out with infected HEp-2 cells alone or with RSV. cellular proteins of P-RSV, HEp-2, BALB/c lung, cotton rat lung (CRL), Buffalo green monkey kidney (BGM), and human buccal epithelial cells (HBE) were separated on SDS-PAGE and tested for reactivity against the sera of these animals for immunologic cross reactivity by Western (immuno)blot procedures. Pre-immunization sera exhibited no binding to the proteins of different cells. Sera from L-RSV and HEp-2 immunized animals reacted with one or more components of all cell types tested. Significantly, however, sera from P-RSV immunized animals reacted with cellular components of HEp-2 and HBE, but not with CRL or BALB/c lung. These observations provide evidence that development of pulmonary immunopathology in RSV infection is mediated in part by the induction of autoreactive or cross-reactive antibody response to the host proteins in which virus replication occurred in this experimentally induced infection and possibly during naturally acquired or induced RSV infection in previously sensitized human infants.
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Piedra, P., Ogra, P. DEVELOPMENT OF ANTIBODY RESPONSE TO HOST PROTEINS AS A POSSIBLE MECHANISM OF IMMUNOPATHOLOGY DURING RESPIRATORY SYNCYTIAL VIRUS (RSV) INFECTION. Pediatr Res 21 (Suppl 4), 332 (1987). https://doi.org/10.1203/00006450-198704010-00988
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DOI: https://doi.org/10.1203/00006450-198704010-00988