Lack of Activation Marker Induction and Chemokine Receptor Switch in Human Neonatal Myeloid Dendritic Cells in Response to Human Respiratory Syncytial Virus

Author:

Le Nouën Cyril1,Hillyer Philippa2ORCID,Levenson Eric3,Martens Craig4,Rabin Ronald L.2ORCID,Collins Peter L.1,Buchholz Ursula J.1

Affiliation:

1. RNA Viruses Section, Laboratory of Infectious Diseases (LID), NIAID, NIH, Bethesda, Maryland, USA

2. Center for Biologics Evaluation and Research, U.S. Food and Drug Administration, Silver Spring, Maryland, USA

3. Norovirus Section, Laboratory of Infectious Diseases (LID), NIAID, NIH, Bethesda, Maryland, USA

4. Research Technologies Section, Rocky Mountain Laboratories, NIAID, NIH, Hamilton, Montana, USA

Abstract

Respiratory syncytial virus (RSV) causes disease early in life and can reinfect symptomatically throughout life without undergoing significant antigenic change. In contrast, reinfection by influenza A virus (IAV) requires antigenic change. The adaptive immune response depends on antigen presentation by dendritic cells (DC). We used myeloid DC (mDC) from cord blood and adult blood donors to evaluate whether immunological immaturity contributes to the inability to mount a fully protective immune response to RSV. While IAV induced some activation and chemokine receptor switching in cord blood mDC, RSV did not. This appeared to be due to a lack of activation and a weak and mostly reversible inhibition of DC functions. Both viruses induced a stronger activation of mDC from adults than mDC from cord blood. Thus, inefficient stimulation of mDC by RSV and immunological immaturity may contribute to reduced immune responses and increased susceptibility to RSV disease and reinfection in young infants.

Funder

The Intramural Research Program of the NIAID, NIH

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

Reference29 articles.

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