Key result
Primary HMPV infection in BALB/c mice elicited weak innate and aberrant adaptive immune responses with a Th2-type cytokine response, increased IL-10 expression, and persistent virus replication.
HMPV infection in BALB/c mice induces a weak innate and aberrant Th2-skewed adaptive immune response leading to persistent viral replication, distinct from the immune response to RSV.
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Distinguishes HMPV from RSV immunity in mice; leaves open human translation and vaccine implications.
Human metapneumovirus (HMPV), recently identified in isolates from children hospitalized with acute respiratory tract illness, is associated with clinical diagnosis of pneumonia, asthma exacerbation, and acute bronchiolitis in young children. HMPV has been shown to cocirculate with respiratory syncytial virus (RSV) and mediate clinical disease features similarly to RSV. Little is known regarding the pathophysiology or immune response associated with HMPV infection; thus, animal models are needed to better understand the mechanisms of immunity and disease pathogenesis associated with infection. In this study, we examine features of the innate and adaptive immune response to HMPV infection in a BALB/c mouse model. Primary HMPV infection elicits weak innate and aberrant adaptive immune responses characterized by induction of a Th2-type cytokine response at later stages of infection that coincides with increased interleukin-10 expression and persistent virus replication in the lung. Examination of the cytotoxic T lymphocyte and antibody response to HMPV infection revealed a delayed response, but passive transfer of HMPV-specific antibodies provided considerable protection. These features are consistent with virus persistence and indicate that the immune response to HMPV is unique compared to the immune response to RSV.
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Alvarez et al. (2005) studied Human metapneumovirus (HMPV) infection. Primary HMPV infection was evaluated on Innate and adaptive immune response. Primary HMPV infection in BALB/c mice elicited weak innate and aberrant adaptive immune responses with a Th2-type cytokine response, increased IL-10 expression, and persistent virus replication.
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