scholarly journals Novel influenza A antibodies reduce severity of secondary pneumococcal pneumonia after influenza infection in mice

Critical Care ◽  
2015 ◽  
Vol 19 (Suppl 1) ◽  
pp. P103
Author(s):  
KF Van der Sluijs ◽  
F Van Someren Greve ◽  
MD Jong ◽  
MJ Schultz ◽  
NP Juffermans
Keyword(s):  
Influenza A ◽  
Pneumococcal Pneumonia ◽  
Influenza Infection ◽  
Novel Influenza A

scholarly journals Frequency of Positive Aspergillus Tests in COVID-19 Patients in Comparison to Other Patients with Pulmonary Infections Admitted to the ICU

2020 ◽  
Author(s):  
Erlangga Yusuf ◽  
Alieke Vonk ◽  
Johannes P.C. van den Akker ◽  
Lonneke Bode ◽  
Gregorius J. Sips ◽  
...  
Keyword(s):  
Influenza A ◽  
Pneumococcal Pneumonia ◽  
Bronchoalveolar Lavage Fluid ◽  
Influenza Infection ◽  
Positive Culture ◽  
Lavage Fluid ◽  
Positive Control ◽  
Community Acquired Pneumonia ◽  
Respiratory Sample ◽  
Test Result

The aim of this study was to describe the frequency of positive Aspergillus tests in COVID-19 patients and investigate the association between COVID-19 and a positive Aspergillus test result. We compared the proportion of positive Aspergillus tests in COVID-19 patients admitted to the ICU for > 24 hours with two control groups; patients with community acquired pneumonia with 1. a PCR confirmed influenza infection (considered as ‘positive’ control since the link between influenza and invasive aspergillosis has been established), and 2. Streptococcus pneumoniae pneumonia (in whom positive Aspergillus tests are mostly considered as colonisation). During the study period, 92 COVID-19 patients (mean age (SD) 62(14) years, 76.1% males), 48 influenza (55(14), 56.2% males), and 65 pneumococcal pneumonia (58 (15), 63,1% males) patients were identified. Any positive Aspergillus test from any respiratory sample was found in 10.9% of the COVID-19 patients, 6.2% of the patients with pneumococcal pneumonia and 22.9% of those infected with influenza. A positive culture or PCR or galactomannan test on bronchoalveolar lavage fluid (BAL) only was found in 5.4% of COVID-19 patients, which was lower than in patients with influenza (18.8%) and comparable to pneumococcal pneumonia group (4.6%). Using logistic regression analysis, the odds ratio, OR (95% CI) for a positive Aspergillus test on BAL fluid for COVID19 patients was 1.2 (0.3 to 5.1, p=0.8) compared to the pneumococcal pneumonia group while it was 0.2 (0.1 to 0.8, p=0.02) compared with influenza group. This difference remained significant when corrected for age and sex. In conclusion, in COVID19 patients, the prevalence of a positive aspergillus test was comparable to patients with admitted for pneumococcal pneumonia but substantially lower than what we observed in patients with influenza.

Streptococcus pneumoniae purulent pericarditis secondary to influenza A infection and pneumococcal pneumonia in an immunocompetent woman

2021 ◽  
Vol 14 (3) ◽  
pp. e240763
Author(s):  
Elaine Houlihan ◽  
Raymond McLoughlin ◽  
Ruth Waldron
Keyword(s):  
Streptococcus Pneumoniae ◽  
Bloodstream Infection ◽  
Influenza A ◽  
Pneumococcal Pneumonia ◽  
Influenza Infection ◽  
Community Acquired Pneumonia ◽  
Nasopharyngeal Swab ◽  
Purulent Pericarditis ◽  
Productive Cough ◽  
Concurrent Treatment

A 44-year-old previously well woman presented with features of respiratory sepsis including a productive cough and fevers, with a recent preceding influenza-like illness. She was diagnosed with community-acquired pneumonia on chest radiograph, influenza infection via nasopharyngeal swab and Streptococcus pneumoniae bloodstream infection with associated purulent pericarditis. She was managed with pericardial drainage and concurrent treatment with antibiotics and made an excellent recovery. This case highlights the complications of both influenza and S. pneumoniae infections, and the importance of prevention via vaccination.

Diagnostic Wrinkles Anticipated in Novel Influenza A (H1N1) Pandemic

2009 ◽  
Vol 39 (15) ◽  
pp. 22
Author(s):  
BRUCE JANCIN
Keyword(s):  
Influenza A ◽  
H1n1 Pandemic ◽  
Influenza A H1n1 ◽  
Novel Influenza A

scholarly journals Thin-section Computed Tomography Detects Long-term Pulmonary Sequelae 3 Years after Novel Influenza A Virus-associated Pneumonia

2015 ◽  
Vol 128 (7) ◽  
pp. 902-908 ◽  
Author(s):  
Zhi-Heng Xing ◽  
Xin Sun ◽  
Long Xu ◽  
Qi Wu ◽  
Li Li ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Influenza A Virus ◽  
Thin Section ◽  
Influenza A ◽  
Novel Influenza A

scholarly journals Differential Expression of Serum Exosome microRNAs and Cytokines in Influenza A and B Patients Collected in the 2016 and 2017 Influenza Seasons

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 149
Author(s):  
Sreekumar Othumpangat ◽  
William G. Lindsley ◽  
Donald H. Beezhold ◽  
Michael L. Kashon ◽  
Carmen N. Burrell ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Influenza A ◽  
Influenza Infection ◽  
Cell Types ◽  
Airway Epithelial Cells ◽  
Differentially Expressed ◽  
Influenza B ◽  
Airway Epithelial ◽  
Monocyte Chemoattractant Protein 1 ◽  
Novel Approach

MicroRNAs (miRNAs) have remarkable stability and are key regulators of mRNA transcripts for several essential proteins required for the survival of cells and replication of the virus. Exosomes are thought to play an essential role in intercellular communications by transporting proteins and miRNAs, making them ideal in the search for biomarkers. Evidence suggests that miRNAs are involved in the regulation of influenza virus replication in many cell types. During the 2016 and 2017 influenza season, we collected blood samples from 54 patients infected with influenza and from 30 healthy volunteers to identify the potential role of circulating serum miRNAs and cytokines in influenza infection. Data comparing the exosomal miRNAs in patients with influenza B to healthy volunteers showed 76 miRNAs that were differentially expressed (p < 0.05). In contrast, 26 miRNAs were differentially expressed between patients with influenza A (p < 0.05) and the controls. Of these miRNAs, 11 were commonly expressed in both the influenza A and B patients. Interferon (IFN)-inducing protein 10 (IP-10), which is involved in IFN synthesis during influenza infection, showed the highest level of expression in both influenza A and B patients. Influenza A patients showed increased expression of IFNα, GM-CSF, interleukin (IL)-13, IL-17A, IL-1β, IL-6 and TNFα, while influenza B induced increased levels of EGF, G-CSF, IL-1α, MIP-1α, and TNF-β. In addition, hsa-miR-326, hsa-miR-15b-5p, hsa-miR-885, hsa-miR-122-5p, hsa-miR-133a-3p, and hsa-miR-150-5p showed high correlations to IL-6, IL-15, IL-17A, IL-1β, and monocyte chemoattractant protein-1 (MCP-1) with both strains of influenza. Next-generation sequencing studies of H1N1-infected human lung small airway epithelial cells also showed similar pattern of expression of miR-375-5p, miR-143-3p, 199a-3p, and miR-199a-5p compared to influenza A patients. In summary, this study provides insights into the miRNA profiling in both influenza A and B virus in circulation and a novel approach to identify the early infections through a combination of cytokines and miRNA expression.

Absence of SP-A modulates innate and adaptive defense responses to pulmonary influenza infection

2002 ◽  
Vol 282 (3) ◽  
pp. L563-L572 ◽  
Author(s):  
Ann Marie LeVine ◽  
Kevan Hartshorn ◽  
James Elliott ◽  
Jeffrey Whitsett ◽  
Thomas Korfhagen
Keyword(s):  
Lung Inflammation ◽  
Influenza A ◽  
Influenza Infection ◽  
Pulmonary Inflammation ◽  
Defense Responses ◽  
Interferon Γ ◽  
Viral Clearance ◽  
Myeloperoxidase Activity ◽  
Respiratory Pathogens ◽  
Innate Defense

Mice lacking surfactant protein SP-A [SP-A(−/−)] and wild type SP-A(+/+) mice were infected with influenza A virus (IAV) by intranasal instillation. Decreased clearance of IAV was observed in SP-A(−/−) mice and was associated with increased pulmonary inflammation. Treatment of SP-A(−/−) mice with exogenous SP-A enhanced viral clearance and decreased lung inflammation. Uptake of IAV by alveolar macrophages was similar in SP-A(−/−) and SP-A(+/+) mice. Myeloperoxidase activity was reduced in isolated bronchoalveolar lavage neutrophils from SP-A(−/−) mice. B lymphocytes and activated T lymphocytes were increased in the lung and spleen, whereas T helper (Th) 1 responses were increased [interferon-γ, interleukin (IL)-2, and IgG2a] and Th2 responses were decreased (IL-4, and IL-10, and IgG1) in the lungs of SP-A(−/−) mice 7 days after IAV infection. In the absence of SP-A, impaired viral clearance was associated with increased lung inflammation, decreased neutrophil myeloperoxidase activity, and increased Th1 responses. Because the airway is the usual portal of entry for IAV and other respiratory pathogens, SP-A is likely to play a role in innate defense and adaptive immune responses to IAV.

Amphotericin b effect on the sensitivity to influenza infection of WI-38 VA-13 cells with IFITM3 gene knockout

2021 ◽  
Vol 21 (3) ◽  
pp. 109-112
Author(s):  
Kira S. Koryabina ◽  
Mariya V. Sergeeva ◽  
Andrey B. Komissarov ◽  
Nataliya V. Eshchenko ◽  
Grigoriy A. Stepanov
Keyword(s):  
Amphotericin B ◽  
Influenza A Virus ◽  
Influenza A ◽  
Gene Knockout ◽  
Influenza Infection ◽  
Restriction Factors ◽  
Host Restriction ◽  
Host Restriction Factors ◽  
Infected Cells ◽  
The Difference

BACKGROUND: The application of CRISPR/Cas9 is one of the most rapidly developing areas in biotechnology. This method was used to obtain clones of а human origin cell line with knockout of one or more genes of the IFITM family, representing host restriction factors for influenza infection. Amphotericin B has previously been shown to promote influenza infection by blocking IFITM3 function. AIM: The aim of this study was to evaluate the effect of amphotericin B on the sensitivity of IFITM knockout cells to influenza A virus infection. MATERIALS AND METHODS: WI-38 VA-13 cells and mutant clones with IFITM3 knockout (F3 clone) or IFITM1, IFITM3 knockout (clone E12) were infected with influenza virus A/PR/8/34 (H1N1) in the presence or absence of amphotericin B. Forty-four hours after infection, the culture medium was taken to determine the infectious activity of the virus by titration in the MDCK cell culture, as well as the hemagglutinating activity of the virus. The infected cells were stained with fluorescently labeled antibodies against the viral NP protein, and the number of NP-positive cells was determined by flow cytometry. RESULTS: The addition of amphotericin B increased the hemagglutinating and infectious activity of the virus in WI-38 VA-13cells, while the difference was insignificant for clones with IFITM gene knockout. A similar dependency was obtained for the percent of infected cells. CONCLUSIONS: Mutant cells with a knockout of one or several genes of the IFITM family were equally susceptible to influenza infection regardless of the addition of amphotericin B, which confirms the crucial importance of a defect in the IFITM3 protein in increasing the permissiveness of cells to influenza A virus.

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