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Central Nervous System inflammation due to respiratory syncytial virus infection.

Karen Bohmwald1, Janyra A. Espinoza1, Susan M. Bueno1, 2, Claudia A. Riedel3 and Alexis M. Kalergis1, 2, 4*
  • 1 Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile
  • 2 INSERM U1064, Nantes, France
  • 3 Millennium Institute on Immunology and Immunotherapy, Departamento de Ciencias Biológicas, Facultad de Ciencias Biológicas y Facultad de Medicina, Universidad Andrés Bello, Santiago, Chile
  • 4 Departamento de Inmunología Clínica y Reumatología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile

Human Respiratory Syncytial Virus (hRSV) is the major cause of lower respiratory tract illness in infants and young children worldwide, including severe bronchiolitis and pneumonia. Recently, neurologic alterations have been associated with hRSV infection in children, which include seizures, central apnea, lethargy, feeding or swallowing difficulty, abnormalities in muscle tone, strabismus, abnormalities in the cerebrospinal fluid and encephalopathy. We have previously shown the presence of hRSV nucleic acid and proteins in brain tissues of mice intranasally challenged with the virus. Further, hRSV impairs behavioral and learning processes in mice and rats, probably due to either an altered production of pro-inflammatory cytokines or to an infection of astrocytes, microglia and neurons at the central nervous system (CNS). To approach these questions, we evaluated the pattern of cytokine expression by RT-qPCR, as well as the presence of hRSV in the CNS of mice intranasally challenged with the virus. The peak of viral load in brain was observed at day 3 and a significant down regulation of CD200 was seen at day 3, 7, 10 and 15 postinfection. Also, we found an elevated expression of pro-inflammatory citokine such as IL-1β, IL-6 and TNF-α at different days after hRSV infection. Further, we evaluated the ability of hRSV to infect CNS cells both in vivo and in vitro. We performed immunofluorescence of brain tissue of hRSV infected mice and found that astrocytes were infected by the virus. Also, we evaluated the infection in human and murine astrocyte primary cultures and observed the peak of viral load at 24 h postinfection. Moreover, we evaluated the ability of hRSV to infect microglia in murine primary cultures and we did not observe infection. Our results suggest that hRSV infection promotes the CNS inflammation through the down regulation of CD200, which works as an immunomodulator of microglia activation. In addition, infected astrocytes can exacerbate the production of pro-inflammatory cytokines, which could promote the behavioral and learning impairment.

Acknowledgements

This work was supported by funding from the Millennium Institute on Immunology and Immunotherapy from Chile (P09/016-F for AMK and SB), KB and JAE are Comisión Nacional de Investigación Científica y Tecnológica—Chile fellows

Keywords: Human respiratory syncytial virus, Central Nervous System, Inflammation, Astrocytes, Learning

Conference: IMMUNOCOLOMBIA2015 - 11th Congress of the Latin American Association of Immunology - 10o. Congreso de la Asociación Colombiana de Alergia, Asma e Inmunología, Medellin, Colombia, 13 Oct - 16 Oct, 2015.

Presentation Type: Poster Presentation

Topic: Infectious and parasitic diseases

Citation: Bohmwald K, Espinoza JA, Bueno SM, Riedel CA and Kalergis AM (2015). Central Nervous System inflammation due to respiratory syncytial virus infection.. Front. Immunol. Conference Abstract: IMMUNOCOLOMBIA2015 - 11th Congress of the Latin American Association of Immunology - 10o. Congreso de la Asociación Colombiana de Alergia, Asma e Inmunología. doi: 10.3389/conf.fimmu.2015.05.00178

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Received: 02 May 2015; Published Online: 14 Sep 2015.

* Correspondence: PhD. Alexis M Kalergis, Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Santiago, Chile, akalergis@bio.puc.cl