During the 2016/17 influenza season 532 clinical samples were tested with the VIASURE assay on the BD MAX™ system versus an in-house real time RT-PCR assay with discrepant results resolved by a real time RT-PCR assay at a national reference laboratory.
To further characterize the role of CD31 in the neonatal CTL response, 3-d and 7-d-old murine neonates were infected with influenza virus and compared to adults.
SJL genetic content affected enhancer elements, gene regulation, protein expression, and amino acid content in CD4<sup>+</sup> T helper 1 cells, and mice infected with influenza showed reduced expression of Cxcr4 on B6.SJL-CD45.1 T follicular helper cells.
To date, numerous biomarkers have been identified for the diagnostic or prognostic purpose; for instance, miR-182, miR-486, and miR15a in sepsis; miR-320 and miR505 in inflammatory bowel disease; miR-155 and miR-1260 in influenza; miR-12, miRVP-3p, and miR-184 in arboviruses; and miR-29b and miR-125 in hepatitis infection.
Unc-93 homolog B1 (UNC93B1), a transmembrane protein, is correlated with immune diseases, such as influenza, herpes simplex encephalitis, and the pathogenesis of systemic lupus erythematosus; however, the role of UNC93B1 in cancers including human oral squamous cell carcinomas (OSCCs) remains unknown.
Targeting of antigens to the dendritic cell (DC) molecule Clec9A has been shown to enhance antibody affinity and titers for model antigens, and influenza and enterovirus antigens, and may be advantageous for immunogens that otherwise fail to elicit antibodies with sufficient titers and breadth for broad protection, such as the envelope protein (Env) of HIV.
Through adoptive transfer, CD8<sup>+</sup> lung T cells but not CD4<sup>+</sup> T cells from virosomes plus PAR-2AP-primed mice protected from lethal influenza virus challenge and enhanced survival with less weight loss and faster recovery.
Previous studies have shown that circulating EV miR-451a regulates innate immune responses, and miR-451a levels in serum EVs are negatively correlated with the pro-inflammatory cytokine expression levels in response to the influenza vaccine.
By integrating knockout and reconstitution models with system-wide transcriptomics, we provide evidence that influenza virus-triggered loss of SUMO-modified TRIM28 leads to derepression of endogenous retroviral (ERV) elements, unmasking this cellular source of "self" double-stranded (ds)RNA.
This Japanese, single-center, prospective, observational study (UMIN-CTR: UMIN000024650) enrolled index patients with confirmed influenza who were treated with an NAI during 6 influenza seasons (2010-2016).
Wild-type mice or mice lacking the ability to respond to Type 1 IFN were infected with influenza prior to the transfusion of transgenic murine RBCs (K1) expressing the human KEL glycoprotein or the triple fusion HOD protein.
To date, numerous biomarkers have been identified for the diagnostic or prognostic purpose; for instance, miR-182, miR-486, and miR15a in sepsis; miR-320 and miR505 in inflammatory bowel disease; miR-155 and miR-1260 in influenza; miR-12, miRVP-3p, and miR-184 in arboviruses; and miR-29b and miR-125 in hepatitis infection.
We showed that NTHi infection drove Th 17-mediated pulmonary neutrophilic inflammation, aggravated airway hyper-responsiveness, and upset the balance of MUC5AC and MUC5B expression.
While MUC15 did not interact directly with influenza virus, we showed that its increase coincides with the peak of immune activation and thus MUC15 may serve an immunomodulatory role during influenza infection.
In this prospective, 45-day study, in young women (n=46; age 18-49 years) with or without IDA, we compared iron and inflammation markers, serum hepcidin and erythrocyte iron incorporation from <sup>57</sup>Fe-labeled test meals, before and 8, 24 and 36 hours (h) after influenza/DPT vaccination as an acute inflammatory stimulus.