{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,17]],"date-time":"2026-01-17T09:26:37Z","timestamp":1768641997310,"version":"3.49.0"},"reference-count":25,"publisher":"American Society for Microbiology","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin. Vaccine Immunol."],"published-print":{"date-parts":[[2015,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>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<jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>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<jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>are often concurrently infected with respiratory viral pathogens but are less likely to suffer from pneumonia than are non-<jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>-infected children. Here, we hypothesized that blood-stage<jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>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<jats:named-content content-type=\"genus-species\">Plasmodium chabaudi chabaudi<\/jats:named-content>AS (<jats:italic>Pc<\/jats:italic>AS) parasites. We found that<jats:italic>Pc<\/jats:italic>AS 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<jats:italic>Pc<\/jats:italic>AS. Importantly,<jats:italic>Pc<\/jats:italic>AS coinfection facilitated greater viral dissemination throughout the lung. Although<jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>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<jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>coinfection drove an early systemic beta interferon (IFN-\u03b2) response. Therefore, we propose that blood-stage<jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>coinfection may exacerbate viral dissemination and impair inflammation in the lung by dysregulating type I IFN-dependent responses to respiratory viruses.<\/jats:p>","DOI":"10.1128\/cvi.00051-15","type":"journal-article","created":{"date-parts":[[2015,2,26]],"date-time":"2015-02-26T17:40:48Z","timestamp":1424972448000},"page":"477-483","source":"Crossref","is-referenced-by-count":24,"title":["Coinfection with Blood-Stage Plasmodium Promotes Systemic Type I Interferon Production during Pneumovirus Infection but Impairs Inflammation and Viral Control in the Lung"],"prefix":"10.1128","volume":"22","author":[{"given":"Chelsea 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