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Time-Dependent Increase in Susceptibility and Severity of Secondary Bacterial Infections During SARS-CoV-2.
Smith, Amanda P; Williams, Evan P; Plunkett, Taylor R; Selvaraj, Muneeswaran; Lane, Lindey C; Zalduondo, Lillian; Xue, Yi; Vogel, Peter; Channappanavar, Rudragouda; Jonsson, Colleen B; Smith, Amber M.
  • Smith AP; Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN, United States.
  • Williams EP; Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
  • Plunkett TR; Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
  • Selvaraj M; Department of Acute and Tertiary Care, University of Tennessee Health Science Center, Memphis, TN, United States.
  • Lane LC; College of Pharmacy, University of Tennessee Health Science Center, Memphis, TN, United States.
  • Zalduondo L; Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
  • Xue Y; Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
  • Vogel P; Animal Resources Center and Veterinary Pathology Core, St. Jude Children's Research Hospital, Memphis, TN, United States.
  • Channappanavar R; Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
  • Jonsson CB; Department of Acute and Tertiary Care, University of Tennessee Health Science Center, Memphis, TN, United States.
  • Smith AM; Institute for the Study of Host-Pathogen Systems, University of Tennessee Health Science Center, Memphis, TN, United States.
Front Immunol ; 13: 894534, 2022.
Article in English | MEDLINE | ID: covidwho-1933683
ABSTRACT
Secondary bacterial infections can exacerbate SARS-CoV-2 infection, but their prevalence and impact remain poorly understood. Here, we established that a mild to moderate infection with the SARS-CoV-2 USA-WA1/2020 strain increased the risk of pneumococcal (type 2 strain D39) coinfection in a time-dependent, but sex-independent, manner in the transgenic K18-hACE2 mouse model of COVID-19. Bacterial coinfection increased lethality when the bacteria was initiated at 5 or 7 d post-virus infection (pvi) but not at 3 d pvi. Bacterial outgrowth was accompanied by neutrophilia in the groups coinfected at 7 d pvi and reductions in B cells, T cells, IL-6, IL-15, IL-18, and LIF were present in groups coinfected at 5 d pvi. However, viral burden, lung pathology, cytokines, chemokines, and immune cell activation were largely unchanged after bacterial coinfection. Examining surviving animals more than a week after infection resolution suggested that immune cell activation remained high and was exacerbated in the lungs of coinfected animals compared with SARS-CoV-2 infection alone. These data suggest that SARS-CoV-2 increases susceptibility and pathogenicity to bacterial coinfection, and further studies are needed to understand and combat disease associated with bacterial pneumonia in COVID-19 patients.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Bacterial Infections / Coinfection / COVID-19 Type of study: Experimental Studies / Observational study / Prognostic study / Randomized controlled trials Limits: Animals / Humans Language: English Journal: Front Immunol Year: 2022 Document Type: Article Affiliation country: Fimmu.2022.894534

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Bacterial Infections / Coinfection / COVID-19 Type of study: Experimental Studies / Observational study / Prognostic study / Randomized controlled trials Limits: Animals / Humans Language: English Journal: Front Immunol Year: 2022 Document Type: Article Affiliation country: Fimmu.2022.894534