ScholarWorksIndianapolis
  • Communities & Collections
  • Browse ScholarWorks
  • English
  • Català
  • Čeština
  • Deutsch
  • Español
  • Français
  • Gàidhlig
  • Italiano
  • Latviešu
  • Magyar
  • Nederlands
  • Polski
  • Português
  • Português do Brasil
  • Suomi
  • Svenska
  • Türkçe
  • Tiếng Việt
  • Қазақ
  • বাংলা
  • हिंदी
  • Ελληνικά
  • Yкраї́нська
  • Log In
    or
    New user? Click here to register.Have you forgotten your password?
  1. Home
  2. Browse by Subject

Browsing by Subject "bacterial"

Now showing 1 - 2 of 2
Results Per Page
Sort Options
  • Loading...
    Thumbnail Image
    Item
    Coinfections with Bacteria, Fungi, and Respiratory Viruses in Patients with SARS-CoV-2: A Systematic Review and Meta-Analysis
    (MDPI, 2021-06) Alhumaid, Saad; Al Mutair, Abbas; Al Alawi, Zainab; Alshawi, Abeer M.; Alomran, Salamah A.; Almuhanna, Mohammed S.; Almuslim, Anwar A.; Bu Shafia, Ahmed H.; Alotaibi, Abdullah M.; Ahmed, Gasmelseed Y.; Rabaan, Ali A.; Al-Tawfiq, Jaffar A.; Al-Omari, Awad; Medicine, School of Medicine
    Background: Coinfection with bacteria, fungi, and respiratory viruses in SARS-CoV-2 is of particular importance due to the possibility of increased morbidity and mortality. In this meta-analysis, we calculated the prevalence of such coinfections. Methods: Electronic databases were searched from 1 December 2019 to 31 March 2021. Effect sizes of prevalence were pooled with 95% confidence intervals (CIs). To minimize heterogeneity, we performed sub-group analyses. Results: Of the 6189 papers that were identified, 72 articles were included in the systematic review (40 case series and 32 cohort studies) and 68 articles (38 case series and 30 cohort studies) were included in the meta-analysis. Of the 31,953 SARS-CoV-2 patients included in the meta-analysis, the overall pooled proportion who had a laboratory-confirmed bacterial infection was 15.9% (95% CI 13.6–18.2, n = 1940, 49 studies, I2 = 99%, p < 0.00001), while 3.7% (95% CI 2.6–4.8, n = 177, 16 studies, I2 = 93%, p < 0.00001) had fungal infections and 6.6% (95% CI 5.5–7.6, n = 737, 44 studies, I2 = 96%, p < 0.00001) had other respiratory viruses. SARS-CoV-2 patients in the ICU had higher co-infections compared to ICU and non-ICU patients as follows: bacterial (22.2%, 95% CI 16.1–28.4, I2 = 88% versus 14.8%, 95% CI 12.4–17.3, I2 = 99%), and fungal (9.6%, 95% CI 6.8–12.4, I2 = 74% versus 2.7%, 95% CI 0.0–3.8, I2 = 95%); however, there was an identical other respiratory viral co-infection proportion between all SARS-CoV-2 patients [(ICU and non-ICU) and the ICU only] (6.6%, 95% CI 0.0–11.3, I2 = 58% versus 6.6%, 95% CI 5.5–7.7, I2 = 96%). Funnel plots for possible publication bias for the pooled effect sizes of the prevalence of coinfections was asymmetrical on visual inspection, and Egger’s tests confirmed asymmetry (p values < 0.05). Conclusion: Bacterial co-infection is relatively high in hospitalized patients with SARS-CoV-2, with little evidence of S. aureus playing a major role. Knowledge of the prevalence and type of co-infections in SARS-CoV-2 patients may have diagnostic and management implications.
  • Loading...
    Thumbnail Image
    Item
    The Toll-like receptor 9 signalling pathway regulates MR1-mediated bacterial antigen presentation in B cells
    (Wiley, 2017) Liu, Jianyun; Brutkiewicz, Randy R.; Department of Microbiology and Immunology, IU School of Medicine
    Mucosal-associated invariant T (MAIT) cells are conserved T cells that express a semi-invariant T-cell receptor (Vα7.2 in humans and Vα19 in mice). The development of MAIT cells requires the antigen-presenting MHC-related protein 1 (MR1), as well as commensal bacteria. The mechanisms that regulate the functional expression of MR1 molecules and their loading with bacterial antigen in antigen-presenting cells are largely unknown. We have found that treating B cells with the Toll-like receptor 9 (TLR9) agonist CpG increases MR1 surface expression. Interestingly, activation of TLR9 by CpG-A (but not CpG-B) enhances MR1 surface expression. This is limited to B cells and not other types of cells such as monocytes, T or natural killer cells. Knocking-down TLR9 expression by short hairpin RNA reduces MR1 surface expression and MR1-mediated bacterial antigen presentation. CpG-A triggers early endosomal TLR9 activation, whereas CpG-B is responsible for late endosomal/lysosomal activation of TLR9. Consistently, blocking endoplasmic reticulum to Golgi protein transport, rather than lysosomal acidification, suppressed MR1 antigen presentation. Overall, our results indicate that early endosomal TLR9 activation is important for MR1-mediated bacterial antigen presentation.
About IU Indianapolis ScholarWorks
  • Accessibility
  • Privacy Notice
  • Copyright © 2025 The Trustees of Indiana University