KI and WU Polyomavirus in Respiratory Samples of SARS-CoV-2 Infected Patients
0301 basic medicine
NCCR sequencing
Washington University polyomavirus
Karolinska Institutet polyomavirus
SARS-CoV-2
QH301-705.5
Communication
VDP::Medisinske Fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710
VDP::Medical disciplines: 700::Basic medical, dental and veterinary science disciplines: 710
3. Good health
03 medical and health sciences
co-infection
oropharyngeal swab
Biology (General)
co‐infection; karolinska institutet polyomavirus; nccr sequencing; oropharyngeal swab; sars‐cov‐2; washington university polyomavirus
DOI:
10.3390/microorganisms9061259
Publication Date:
2021-06-09T18:16:04Z
AUTHORS (16)
ABSTRACT
Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has been declared a global pandemic. Our goal was to determine whether co-infections with respiratory polyomaviruses, such as Karolinska Institutet polyomavirus (KIPyV) and Washington University polyomavirus (WUPyV) occur in SARS-CoV-2 infected patients. Oropharyngeal swabs from 150 individuals, 112 symptomatic COVID-19 patients and 38 healthcare workers not infected by SARS-CoV-2, were collected from March 2020 through May 2020 and tested for KIPyV and WUPyV DNA presence. Of the 112 SARS-CoV-2 positive patients, 27 (24.1%) were co-infected with KIPyV, 5 (4.5%) were positive for WUPyV, and 3 (2.7%) were infected simultaneously by KIPyV and WUPyV. Neither KIPyV nor WUPyV DNA was detected in samples of healthcare workers. Significant correlations were found in patients co-infected with SARS-CoV-2 and KIPyV (p < 0.05) and between SARS-CoV-2 cycle threshold values and KIPyV, WUPyV and KIPyV and WUPyV concurrently detected (p < 0.05). These results suggest that KIPyV and WUPyV may behave as opportunistic respiratory pathogens. Additional investigations are needed to understand the epidemiology and the prevalence of respiratory polyomavirus in COVID-19 patients and whether KIPyV and WUPyV could potentially drive viral interference or influence disease outcomes by upregulating SARS-CoV-2 replicative potential.
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