Syncitial virus respiratory infections in children – immunological aspects

Abstract

Out of all respiratory viral infections, those with human respiratory syncytial virus (HRSV) are the most frequent registered worldwide being responsible for bronchiolitis, pneumonia, and asthma in all age groups, especially in children. As children have an immature immune system, severe HRSV infection can lead to death. In this paper we will revise the most recent findings regarding the immune response in the HRSV infection focusing on children. Extensive studies indicate that viral and host factors modulate the severity of infection. The viral infection first triggers a strong innate immune response followed by a further adaptive immune antiviral response. Although HRSV infection is common, there is still no efficient therapy available. The hurdles in obtaining an efficient therapy reside in several issues: the immaturity of the immune system of infants and young children, the differences in the virulence potential of the viral strains that induce a different cytokine/chemokine host response, with the involvement of multiple molecular, still unknown pathways. Identification of antiviral immune mechanisms and the comprehensive characterization of virus-specific immune responses using new cellular and animal models would help to define the crosstalk between viral and host factors that would modulate the severity of infection. Moreover identifying the molecular mechanisms of acute airway disease would shed light also on associated long-term consequences like developing asthma in the adulthood. As HRSV is globally circulating for more than 60 years, an effective therapy remains a public health priority.

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“…In children, the figures are even higher. Worldwide, every year, over 1 million children and infants under 5 years die from acute respiratory infections (2), this disease represents in developing countries the cause of death of 30% of children under five years (3,4). When RTI have an increased frequency, over 60% of the cases have a primary immunodeficiency in humoral immunity.…”