{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T05:02:39Z","timestamp":1791435759775,"version":"4.3.3"},"reference-count":51,"publisher":"American Society for Microbiology","issue":"22","license":[{"start":{"date-parts":[[2012,11,15]],"date-time":"2012-11-15T00:00:00Z","timestamp":1352937600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2012,11,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    The majority of deaths following influenza virus infection result from secondary bacterial superinfection, most commonly caused by\n                    <jats:named-content content-type=\"genus-species\">Streptococcus pneumoniae<\/jats:named-content>\n                    . Several models have been proposed to explain how primary respiratory viral infections exacerbate secondary bacterial disease, but the mechanistic explanations have been contradictory. In this study, mice were infected with\n                    <jats:named-content content-type=\"genus-species\">S. pneumoniae<\/jats:named-content>\n                    at different days after primary influenza A (X31) virus infection. Our findings show that the induction of type I interferons (IFNs) during a primary nonlethal influenza virus infection is sufficient to promote a deadly\n                    <jats:named-content content-type=\"genus-species\">S. pneumoniae<\/jats:named-content>\n                    secondary infection. Moreover, mice deficient in type I interferon receptor (IFNAR knockout [KO] mice) effectively cleared the secondary bacterial infection from their lungs, increased the recruitment of neutrophils, and demonstrated an enhanced innate expression of interleukin-17 (IL-17) relative to wild-type (WT) mice. Lung \u03b3\u03b4 T cells were responsible for almost all IL-17 production, and their function is compromised during secondary\n                    <jats:named-content content-type=\"genus-species\">S. pneumoniae<\/jats:named-content>\n                    infection of WT but not IFNAR KO mice. Adoptive transfer of \u03b3\u03b4 T cells from IFNAR KO mice reduced the susceptibility to secondary\n                    <jats:named-content content-type=\"genus-species\">S. pneumoniae<\/jats:named-content>\n                    infection in the lung of WT mice. Altogether, our study highlights the importance of type I interferon as a key master regulator that is exploited by opportunistic pathogens such as\n                    <jats:named-content content-type=\"genus-species\">S. pneumoniae<\/jats:named-content>\n                    . Our findings may be utilized to design effective preventive and therapeutic strategies that may be beneficial for coinfected patients during influenza epidemics.\n                  <\/jats:p>","DOI":"10.1128\/jvi.01269-12","type":"journal-article","created":{"date-parts":[[2012,9,6]],"date-time":"2012-09-06T00:41:50Z","timestamp":1346892110000},"page":"12304-12312","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":192,"title":["Type I Interferon Induction during Influenza Virus Infection Increases Susceptibility to Secondary Streptococcus pneumoniae Infection by Negative Regulation of \u03b3\u03b4 T Cells"],"prefix":"10.1128","volume":"86","author":[{"given":"Wenjing","family":"Li","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology Institute, Mount Sinai School of Medicine, New York, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruno","family":"Moltedo","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology Institute, Mount Sinai School of Medicine, New York, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas M.","family":"Moran","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology Institute, Mount Sinai School of Medicine, New York, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20040976"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.80.4.1629-1636.2006"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1089\/jir.2010.0049"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20030266"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1473-3099(06)70466-2"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.3201\/eid1408.071313"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijantimicag.2009.10.002"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20040769"},{"key":"e_1_3_2_10_2","first-page":"1071","article-title":"Bacterial coinfections in lung tissue specimens from fatal cases of 2009 pandemic influenza A (H1N1)\u2014United States, May-August 2009","volume":"58","author":"Centers for Disease Control and Prevention","year":"2009","unstructured":"Centers for Disease Control and Prevention. 2009. 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