Time-Dependent Increase in Susceptibility and Severity of Secondary Bacterial Infections During SARS-CoV-2.

Autor:	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.; Department of Acute and Tertiary Care, University of Tennessee Health Science Center, Memphis, TN, United States.; Institute for the Study of Host-Pathogen Systems, University of Tennessee Health Science Center, Memphis, TN, United States., Jonsson CB; Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.; Institute for the Study of Host-Pathogen Systems, University of Tennessee Health Science Center, Memphis, TN, United States., Smith AM; Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN, United States.; Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.; Institute for the Study of Host-Pathogen Systems, University of Tennessee Health Science Center, Memphis, TN, United States.
Jazyk:	angličtina
Zdroj:	Frontiers in immunology [Front Immunol] 2022 May 12; Vol. 13, pp. 894534. Date of Electronic Publication: 2022 May 12 (Print Publication: 2022).
DOI:	10.3389/fimmu.2022.894534
Abstrakt:	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. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2022 Smith, Williams, Plunkett, Selvaraj, Lane, Zalduondo, Xue, Vogel, Channappanavar, Jonsson and Smith.)
Databáze:	MEDLINE
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