RSV associated with poor proinflammatory cytokine production

A comparison of previously healthy infants between 28 days and 6 months who were hospitalized with their first respiratory syncytial virus–acute lower respiratory infection and a group of age-matched healthy infants provided new insights into the immunologic pathogenesis of the disease, as well as variations between children with moderate and severe courses of infection.

Researchers enrolled 75 children with lab-confirmed RSV infection and 24 healthy controls at the Roberto del Rio Children’s Hospital in Santiago, Chile. They compared the in vivo immune response via plasma cytokine concentrations and the phenotyping of peripheral blood lymphocytes and natural killer cells among the two groups, as well as among those with different RSV clinical severity levels. The researchers concluded:

Children with RSV had lower absolute blood cell CD4+, CD8+ and CD19+ lymphocytes and natural killer cells compared with controls.
Those with more severe RSV had the lowest cell counts, particularly among CD8+ lymphocytes (P=.03) and nonactive natural killer cells that express CD94 antigen (P=.046), a molecule associated with the major histocompatibility complex class Ib system.
Concentrations of activated natural killer cells that do not express CD94 were higher in children with RSV compared with patients in the control group (percentage of cells: P=.004).
Children with RSV had poor expression of circulating proinflammatory mediators such as interferon-gamma, tumor necrosis factor-alpha and interleukin-17 cytokine values compared with controls.
IL-17 cytokine was detected in larger concentrations among moderately ill patients compared with those who were severely ill (P=.033).
Severely ill patients had significantly higher IL-8 chemokine compared with controls (P=.024).

“The lack of regulation of the natural killer system, mediated by a poor expression of CD94-NKG2 receptors could lead to increased lung damage, either through increased direct RSV damage on epithelial cells in the absence of an effective immune response or through apoptotic signals in the lung or in blood,” the researchers wrote.

Larrañaga CL. Pediatr Infect Dis J. 2009;28:867-871.