Human Influenza Virus Infections

Peteranderl, Christin; Herold, Susanne; Schmoldt, Carole

doi:10.1055/s-0036-1584801

Cited by 172 publications

(137 citation statements)

References 201 publications

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“…Patients infected with influenza may exhibit a broad spectrum of clinical symptoms, ranging from self-limited upper respiratory tract illness to severe pneumonia [8,9]. Influenza-related pneumonia (Flu-p), including primary viral pneumonia and secondary bacterial pneumonia, is the major cause of influenza-associated hospitalizations and deaths [10].…”

Section: Introductionmentioning

confidence: 99%

FluA-p score: a novel prediction rule for mortality in influenza A-related pneumonia patients

Liang

Han

et al. 2020

Respir Res

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Background: The pneumonia severity index (PSI) and the CURB-65 (confusion, urea, respiratory rate, blood pressure, age ≥ 65 years) score have been shown to predict mortality in community-acquired pneumonia. Their ability to predict influenza-related pneumonia, however, is less well-established. Methods: A total of 693 laboratory-confirmed FluA-p patients diagnosed between Jan 2013 and Dec 2018 and recruited from five teaching hospitals in China were included in the study. The sample included 494 patients in the derivation cohort and 199 patients in the validation cohort. The prediction rule was established based on independent risk factors for 30-day mortality in FluA-p patients from the derivation cohort. Results: The 30-day mortality of FluA-p patients was 19.6% (136/693). The FluA-p score was based on a multivariate logistic regression model designed to predict mortality. Results indicated the following significant predictors (regression statistics and point contributions toward total score in parentheses): blood urea nitrogen > 7 mmol/L (OR 1.604, 95% CI 1.150-4.492, p = 0.040; 1 points), pO 2 /F i O 2 ≤ 250 mmHg (OR 2.649, 95% CI 1.103-5.142, p = 0.022; 2 points), cardiovascular disease (OR 3.967, 95% CI 1.269-7.322, p < 0.001; 3 points), arterial PH < 7.35 (OR 3.959, 95% CI 1.393-7.332, p < 0.001; 3 points), smoking history (OR 5.176, 95% CI 2.604-11.838, p = 0.001; 4 points), lymphocytes < 0.8 × 10 9 /L (OR 8.391, 95% CI 3.271-16.212, p < 0.001; 5 points), and early neurominidase inhibitor therapy (OR 0.567, 95% CI 0.202-0.833, p = 0.005; − 2 points). Seven points was used as the cut-off value for mortality risk stratification. The model showed a sensitivity of 0.941, a specificity of 0.762, and overall better predictive performance than the PSI risk class (AUROC = 0.908 vs 0.560, p < 0.001) and the CURB-65 score (AUROC = 0.908 vs 0.777, p < 0.001). Conclusions: Our results showed that a FluA-p score was easy to derive and that it served as a reliable prediction rule for 30-day mortality in FluA-p patients. The score could also effectively stratify FluA-p patients into relevant risk categories and thereby help treatment providers to make more rational clinical decisions.

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Section: Introductionmentioning

confidence: 99%

FluA-p score: a novel prediction rule for mortality in influenza A-related pneumonia patients

Liang

Han

et al. 2020

Respir Res

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“…Mucosal surfaces are prone to infection by many pathogens, and adequate protection of mucosal surfaces require the presence of effective local immune response [1][2][3][4][5][6]. Previous reports suggest that immunization by mucosal route (such as intranasal or oral immunization) can achieve superior mucosal immune response compared to the parenteral route (such as intradermal or intramuscular immunization) [7].…”

Section: Introductionmentioning

confidence: 99%

Preclinical Efficacy of a Trivalent Human FcγRI-Targeted Adjuvant-Free Subunit Mucosal Vaccine against Pulmonary Pneumococcal Infection

Kumar

Sunagar²,

Gosselin

2020

Vaccines

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Lack of safe and effective mucosal adjuvants has severely hampered the development of mucosal subunit vaccines. In this regard, we have previously shown that immunogenicity of vaccine antigens can be improved by targeting the antigens to the antigen-presenting cells. Specifically, groups of mice immunized intranasally with a fusion protein (Bivalent-FP) containing a fragment of pneumococcal-surface-protein-A (PspA) as antigen and a single-chain bivalent antibody raised against the anti-human Fc-gamma-receptor-I (hFcγRI) elicited protective immunity to pulmonary Streptococcus pneumoniae infection. In order to further enhance the immunogenicity, an additional hFcγRI-binding moiety of the single chain antibody was incorporated. The modified vaccine (Trivalent-FP) induced significantly improved protection against lethal pulmonary S. pneumoniae challenge compared to Bivalent-FP. In addition, the modified vaccine exhibited over 85% protection with only two immunizations. Trivalent-FP also induced S. pneumoniae-specific systemic and mucosal antibodies. Moreover, Trivalent-FP also induced IL-17-and IL-22-producing CD4 + T cells. Furthermore, it was found that the hFcγRI facilitated uptake and presentation of Trivalent-FP. In addition, Trivalent-FP also induced IL-1α, MIP-1α, and TNF-α; modulated recruitment of dendritic cells and macrophages; and induced CD80/86 and MHC-II expression on antigen presenting cells.With over 90 known serotypes, Streptococcus pneumoniae remains the leading cause of community acquired pneumoniae. In addition, younger and immunocompromised populations are more vulnerable to infection. Furthermore, S. pneumoniae causes over 1 million deaths per year in children aged less than 5 years [10]. To date, two polysaccharide-based subunit vaccines are available to combat select serotypes. However, use of these 13 and 23 serotype vaccines cause serotype replacement in the vaccinated population [11]. This results in a surge of non-vaccine serotypes within the vaccinated population. Thus, new approaches to pneumococcal vaccines are required, which can generate protection over multiple serotypes. The pneumococcal surface protein A (PspA) has been known to induce cross-serotype protection against S. pneumoniae [12]. Thus, not only is S. pneumoniae a significant global health problem, it also expresses a well-defined protective protein antigen, making it a particularly suitable model to test and optimize our mucosal subunit vaccine platform.Previously we have shown that targeting vaccine antigens to antigen-presenting cells (APCs) eliminates the need for adjuvants.By genetically fusing a bivalent single-chain variable fragment-based antibody (Bivalent anti-human-Fc-gamma-receptor-I (FcγRI)), which specifically recognizes human-FcγRI, to a pneumococcal antigen (PspA), a fusion protein named Bivalent-FP was obtained ( Figure 1A). Bivalent-FP induces systemic and mucosal antibodies and protection against pulmonary S. pneumoniae infection by intranasal immunization. However, this vaccine requires at least three i...

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“…In patients not immunocompromised, the immune system sufficiently controls infection, and clinical symptoms are limited to 2 to 8 days. 4 Histologically, acute influenza infection involves widespread epithelial damage. Multifocal destruction and desquamation of tracheal, bronchial, and alveolar epithelium were reported.…”

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confidence: 99%

Epigenetic and Transcriptomic Regulation of Lung Repair during Recovery from Influenza Infection

Pociask

Robinson

Chen

et al. 2017

The American Journal of Pathology

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Seasonal and pandemic influenza is a cause of morbidity and mortality worldwide. Most people infected with influenza virus display mild-to-moderate disease phenotypes and recover within a few weeks. Influenza is known to cause persistent alveolitis in animal models; however, little is known about the molecular pathways involved in this phenotype. We challenged C57BL/6 mice with influenza A/PR/8/34 and examined lung pathologic processes and inflammation, as well as transcriptomic and epigenetic changes at 21 to 60 days after infection. Influenza induced persistent parenchymal lung inflammation, alveolar epithelial metaplasia, and epithelial endoplasmic reticulum stress that were evident after the clearance of virus and resolution of morbidity. Influenza infection induced robust changes in the lung transcriptome, including a significant impact on inflammatory and extracellular matrix protein expression. Despite the robust changes in lung gene expression, preceding influenza (21 days) did not exacerbate secondary Staphylococcus aureus infection. Finally, we examined the impact of influenza on miRNA expression in the lung and found an increase in miR-155. miR-155 knockout mice recovered from influenza infection faster than controls and had decreased lung inflammation and endoplasmic reticulum stress. These data illuminate the dynamic molecular changes in the lung in the weeks after influenza infection and characterize the repair process, identifying a novel role for miR-155. (Am J Pathol 2017, 187: 851e863; http://dx

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Human Influenza Virus Infections

Cited by 172 publications

References 201 publications

FluA-p score: a novel prediction rule for mortality in influenza A-related pneumonia patients

FluA-p score: a novel prediction rule for mortality in influenza A-related pneumonia patients

Preclinical Efficacy of a Trivalent Human FcγRI-Targeted Adjuvant-Free Subunit Mucosal Vaccine against Pulmonary Pneumococcal Infection

Epigenetic and Transcriptomic Regulation of Lung Repair during Recovery from Influenza Infection

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