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Abstract
Respiratory syncytial virus (RSV) causes recurrent infections throughout life. Vaccine development may depend upon understanding the molecular basis for induction of ineffective immunity. Because dendritic cells (DCs) are critically involved in early responses to infection, their interaction with RSV may determine the immunological outcome of RSV infection. Therefore, we investigated the ability of RSV to infect and activate primary mDCs and pDCs using recombinant RSV expressing green fluorescent protein (GFP). At a multiplicity of infection of 5, initial studies demonstrated ∼6.8% of mDC1 and ∼0.9% pDCs were infected. We extended these studies to include CD1c−CD141+ mDC2, finding mDC2 infected at similar frequencies as mDC1. Both infected and uninfected cells upregulated phenotypic markers of maturation. Divalent cations were required for infection and maturation, but maturation did not require viral replication. There is evidence that attachment and entry/replication processes exert distinct effects on DC activation. Cell-specific patterns of RSV-induced maturation and cytokine production were detected in mDC1, mDC2, and pDC. We also demonstrate for the first time that RSV induces significant TIMP-2 production in all DC subsets. Defining the influence of RSV on the function of selected DC subsets may improve the likelihood of achieving protective vaccine-induced immunity.
Highlights
Respiratory syncytial virus (RSV) is a pneumovirus in the family Paramyxoviridae and has a non-segmented negative-sense singlestranded RNA genome [1]
Both myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) are recruited to the respiratory tract in virally-infected infants, and differences in dendritic cells (DCs) recruitment and function have been observed in children who experienced bronchiolitis compared to mild upper respiratory infection or in infants infected with RSV compared to those infected with influenza [41,42,43]
Because the initial exposure to RSV antigens during primary infection of infants may play a role in establishing susceptibility to subsequent reinfection, it is important to understand the effects of RSV exposure on the maturation and function of primary human mDCs and pDCs
Summary
Respiratory syncytial virus (RSV) is a pneumovirus in the family Paramyxoviridae and has a non-segmented negative-sense singlestranded RNA genome [1]. More than 95% of children are infected with RSV by 2 years of age, and ,50% of children infected in the first year of life are reinfected during the second year [5]. Natural RSV infection fails to induce immunity that prevents reinfection despite relatively minor genetic variation between strains [6,7]. Reinfection during childhood causes significant morbidity [12], and in adults with normal immune function, symptoms are typically restricted to the upper airway. There is evidence that RSV interferes with development of both humoral and cell-mediated immune mechanisms which results in an overall immunological state that cannot protect the upper airway from reinfection
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