KI and WU Polyomavirus in Respiratory Samples of SARS-CoV-2 Infected Patients.

Carla Prezioso,Guido Antonelli,Alessandra Pierangeli,Mirko Scordio,Giuliana Guerrizio,Giuseppe Oliveto,Ugo Moens,Agnese Viscido,Donatella Maria Rodio,Carolina Scagnolari,Valeria Pietropaolo,Ombretta Turriziani,Federica Frasca,Gabriella D’Ettorre,Gabriele Brazzini,Francesca Piacentini

doi:10.3390/microorganisms9061259

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.

Highlights

In late December 2019, several cases of pneumonia of unknown origin were reported in Wuhan, China, and in early January 2020, a novel coronavirus denominated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was identified and defined as the etiological agent of coronavirus disease 2019 (COVID-19) [1,2]
SARS-CoV-2 infection during the early outbreak period of COVID-19 has not emerged, our goal was to determine whether co-infections with Karolinska Institutet polyomavirus (KIPyV) and Washington University polyomavirus (WUPyV) occur in a significant subset of SARS-CoV-2 infected patients
Oropharyngeal swabs collected from 150 individuals, 112 symptomatic COVID-19 patients and 38 healthcare workers not infected by SARS-CoV-2, were tested for KIPyV and

Summary

Introduction

In late December 2019, several cases of pneumonia of unknown origin were reported in Wuhan, China, and in early January 2020, a novel coronavirus denominated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was identified and defined as the etiological agent of coronavirus disease 2019 (COVID-19) [1,2]. Co-infection with several viruses has been documented in patients with severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). Among patients infected by SARS-CoV-2, the knowledge remains limited. In this regard, it has been established that the prevalence of co-infection with respiratory pathogens was variable among COVID-19 patients and could be up to 50% among non-survivors [6]. To date, there is no data on the relationship between human polyomavirus (HPyVs)/SARSCoV-2 co-infection and clinical and epidemiological profile of COVID-19 patients

Objectives

Methods

Results