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Institute of Molecular Pathology and Immunology of the University of Porto, Porto, Portugal
Institute of Biomedical Sciences Abel Salazar, University of Porto, Porto, Portugal
Faculty of Medicine, University of Porto, Porto, Portugal
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Institute of Molecular Pathology and Immunology of the University of Porto, Porto, Portugal
Faculty of Medicine, University of Porto, Porto, Portugal
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Faculty of Medicine, University of Porto, Porto, Portugal
North Lisbon University Hospital Center, Lisbon, Portugal
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University Hospital Center of São João, Porto, Portugal
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University Hospital Center of São João, Porto, Portugal
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Institute of Molecular Pathology and Immunology of the University of Porto, Porto, Portugal
Faculty of Medicine, University of Porto, Porto, Portugal
University Hospital Center of São João, Porto, Portugal
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Faculty of Medicine, University of Porto, Porto, Portugal
University Hospital Center of São João, Porto, Portugal
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Institute of Molecular Pathology and Immunology of the University of Porto, Porto, Portugal
Faculty of Medicine, University of Porto, Porto, Portugal
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Objective
To understand whether thyroid cells can be directly infected by the SARS-CoV-2 virus and to establish a putative correlation with the expression of the host entry machinery: ACE-2, TMPRSS2, and furin.
Methods
We assessed the presence of SARS-CoV-2 virus at the gene level by RT-PCR, viral RNA transcripts localization by in situ hybridization, and by detecting viral proteins by immunohistochemistry for the nucleocapsid and the spike proteins. Furthermore, we also described the immunoexpression of key host factors for virus entry in the COVID-19 thyroid samples.
Results
We performed RT-PCR for SARS-CoV-2 in all autopsy specimens and detected viral genome positivity in 13 of 15 thyroid tissues and in a lung specimen. In 9 of the 14 positive samples, we were also able to confirm SARS-CoV-2 signal by in situ hybridization. Immunohistochemistry for the viral nucleocapsid and spike protein was also positive for ten and nine of the RT-PCR-positive cases, respectively, but revealed a lower sensitivity. We also described, for the first time in a COVID-19 series, the immunohistochemical expression of ACE-2, TMPRSS2, and furin in the thyroid.
Conclusions
Our results obtained in thyroid specimens from deceased COVID-19 patients indicate that thyrocytes can be directly infected by SARS-CoV-2 since we detected the presence of SARS-CoV-2 genome in follicular cells. Nevertheless, we did not find a clear correlation between the presence of viral genome and the expression of the host factors for virus entry, namely ACE-2, TMPRSS2, and furin.
