Coinfection with blood-stage plasmodium promotes systemic type I interferon production during pneumovirus infection but impairs inflammation and viral control in the lung

Edwards, Chelsea L., Zhang, Vivian, Werder, Rhiannon B., Best, Shannon E., Sebina, Ismail, James, Kylie R., Faleiro, Rebecca J., Rivera, Fabian de Labastida, Amante, Fiona H., Engwerda, Christian R., Phipps, Simon and Haque, Ashraful (2015) Coinfection with blood-stage plasmodium promotes systemic type I interferon production during pneumovirus infection but impairs inflammation and viral control in the lung. Clinical and Vaccine Immunology, 22 5: 477-483. doi:10.1128/CVI.00051-15


Author Edwards, Chelsea L.
Zhang, Vivian
Werder, Rhiannon B.
Best, Shannon E.
Sebina, Ismail
James, Kylie R.
Faleiro, Rebecca J.
Rivera, Fabian de Labastida
Amante, Fiona H.
Engwerda, Christian R.
Phipps, Simon
Haque, Ashraful
Title Coinfection with blood-stage plasmodium promotes systemic type I interferon production during pneumovirus infection but impairs inflammation and viral control in the lung
Journal name Clinical and Vaccine Immunology   Check publisher's open access policy
ISSN 1556-6811
1556-679X
Publication date 2015-05
Year available 2015
Sub-type Article (original research)
DOI 10.1128/CVI.00051-15
Volume 22
Issue 5
Start page 477
End page 483
Total pages 7
Place of publication Washington, DC United States
Publisher American Society for Microbiology
Collection year 2016
Language eng
Formatted abstract
Acute lower respiratory tract infections (ALRTI) are the leading cause of global childhood mortality, with human respiratory syncytial virus (hRSV) being a major cause of viral ALRTI in young children worldwide. In sub-Saharan Africa, many young children experience severe illnesses due to hRSV or Plasmodium infection. Although the incidence of malaria in this region has decreased in recent years, there remains a significant opportunity for coinfection. Recent data show that febrile young children infected with Plasmodium are often concurrently infected with respiratory viral pathogens but are less likely to suffer from pneumonia than are non-Plasmodium-infected children. Here, we hypothesized that blood-stage Plasmodium infection modulates pulmonary inflammatory responses to a viral pathogen but does not aid its control in the lung. To test this, we established a novel coinfection model in which mice were simultaneously infected with pneumovirus of mice (PVM) (to model hRSV) and blood-stage Plasmodium chabaudi chabaudi AS (PcAS) parasites. We found that PcAS infection was unaffected by coinfection with PVM. In contrast, PVM-associated weight loss, pulmonary cytokine responses, and immune cell recruitment to the airways were substantially reduced by coinfection with PcAS. Importantly, PcAS coinfection facilitated greater viral dissemination throughout the lung. Although Plasmodium coinfection induced low levels of systemic interleukin-10 (IL-10), this regulatory cytokine played no role in the modulation of lung inflammation or viral dissemination. Instead, we found that Plasmodium coinfection drove an early systemic beta interferon (IFN-β) response. Therefore, we propose that blood-stage Plasmodium coinfection may exacerbate viral dissemination and impair inflammation in the lung by dysregulating type I IFN-dependent responses to respiratory viruses.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

 
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