Abstract
The landscape of infant bronchiolitis and viral pneumonia may be altered by preventive interventions against respiratory syncytial virus under evaluation today. Pediatric wards in 2018 in developing countries may differ from those attended by future generation pediatricians who may not witness the packed emergency rooms, lack of available beds, or emergency situations that all physicians caring for children with RSV experience every year. In this review, we describe and discuss different prevention strategies under evaluation to protect pediatric patients. Then, we outline a number of potential challenges, benefits, and concerns that may result from successful interventions after licensure.
Highlights
Reviewed by: Juan Pablo Jaworski, National Council for Scientific and Technical Research (CONICET), Argentina Bernhard Resch, Medical University of Graz, Austria
Pediatric wards in 2018 in developing countries may differ from those attended by future generation pediatricians who may not witness the packed emergency rooms, lack of available beds, or emergency situations that all physicians caring for children with respiratory syncytial virus (RSV) experience every year
The only available intervention licensed to prevent severe disease today is the administration of a neutralizing anti-RSV humanized monoclonal antibody, palivizumab R
Summary
Humans are the only natural host for RSV. The virus is spread from person to person via respiratory droplets, and spreads into the respiratory tract, where it preferentially targets apical ciliated epithelial cells [4]. Natural immunity includes innate responses by polymorphonuclear (PMN) and mononuclear cells, activation of numerous pattern recognition receptors (e.g., TLR3, TLR2/6, TLR7/8, NOD-like, and RIG-I-like receptors), and type I and III interferon responses [6,7,8,9] These responses are important, as PMNs and macrophages have been postulated to enhance and prevent severe disease, and PRRs have been reported to modulate numerous responses during RSV infection [5, 10]. Upon infection with wild type RSV during the winter of 19661967, non-protective, low avidity IgG coupled with the virus to activate the complement cascade and in synergy with a strong Th2 polarization of the immune response led to increased hospitalization rates and two deaths in toddlers due to this enhanced form of RSV disease presenting with wheezing and bronchopneumonia [20, 24,25,26]. Generation of an IgG response dominated by low avidity, non-neutralizing antibodies against RSV F (Figure 1), and priming for a Th2 bias upon RSV infection are considered undesirable features for RSV vaccine candidates
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