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Review
. 1999 Apr;12(2):298-309.
doi: 10.1128/CMR.12.2.298.

Respiratory syncytial virus infection: immune response, immunopathogenesis, and treatment

J B Domachowske  1 , H F Rosenberg
Affiliations
Review

Respiratory syncytial virus infection: immune response, immunopathogenesis, and treatment

J B Domachowske et al. Clin Microbiol Rev. 1999 Apr.

Abstract

Respiratory syncytial virus (RSV) is the single most important cause of lower respiratory tract infection during infancy and early childhood. Once RSV infection is established, the host immune response includes the production of virus-neutralizing antibodies and T-cell-specific immunity. The humoral immune response normally results in the development of anti-RSV neutralizing-antibody titers, but these are often suboptimal during an infant's initial infection. Even when the production of RSV neutralizing antibody following RSV infection is robust, humoral immunity wanes over time. Reinfection during subsequent seasons is common. The cellular immune response to RSV infection is also important for the clearance of virus. This immune response, vital for host defense against RSV, is also implicated in the immunopathogenesis of severe lower respiratory tract RSV bronchiolitis. Many details of the immunology and immunopathologic mechanisms of RSV disease known at present have been learned from rodent models of RSV disease and are discussed in some detail. In addition, the roles of immunoglobulin E, histamine, and eosinophils in the immunopathogenesis of RSV disease are considered. Although the treatment of RSV bronchiolitis is primarily supportive, the role of ribavirin is briefly discussed. Novel approaches to the development of new antiviral drugs with promising anti-RSV activity in vitro are also described.

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Figures

FIG. 1
FIG. 1
RSV-infected respiratory epithelial cells. Respiratory epithelial cells (HEp-2, laryngeal carcinoma cell line) on day 1 (A), day 3 (B), and day 5 (C) following infection with RSV. Magnification, ×400. After 1 day, the cells continue to appear healthy. After 3 days, many of the cells have fused, forming large syncytia. After 5 days, most of the syncytia have detached from the surface and the majority of the cells are dead.
FIG. 2
FIG. 2
RSV RNA genome. Shown is a schematic of the 15.2-kb RSV genomic RNA. The genome is nonsegmented; the order of the genes from 3′ to 5′ is as depicted. RSV-specific proteins encoded by these genes, and their functions, when known, are listed in Table 1.
FIG. 3
FIG. 3
Structural formula of ribavirin. Ribavirin is a synthetic nucleoside with the empirical formula C8H12N4O5. While the mechanism of action of its antiviral properties remain unknown, the reversal of the in vitro antiviral activity by guanosine or xanthosine that suggests ribavirin may act as an analogue of these cellular metabolites.
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