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Article

COVID-19 and Genetic Variants of Protein Involved in the SARS-CoV-2 Entry into the Host Cells

1
Department of Biomedicine and Prevention, Tor Vergata University Hospital, 00133 Rome, Italy
2
Laboratory of Medical Genetics, Bambino Gesù Children’s Hospital, IRCCS, 00165 Rome, Italy
3
Medical Genetics Laboratory, Tor Vergata University Hospital, Rome, 00133 Rome, Italy
4
UOC Pediatria, Bambino Gesù Children’s Hospital, IRCCS, 00165 Rome, Italy
5
Department of Clinical Sciences and Translational Medicine, Tor Vergata University Hospital, 00133 Rome, Italy
6
Department of Systems Medicine, Tor Vergata University Hospital, 00133 Rome, Italy
7
Infectious Diseases Clinic, Tor Vergata University Hospital, 00133 Rome, Italy
8
Unit of Respiratory Medicine, Department of Experimental Medicine, Tor Vergata University Hospital, 00133 Rome, Italy
9
Department of Experimental Medicine and Biochemical Sciences, Tor Vergata University Hospital, 00133 Rome, Italy
10
Department of Biology, Tor Vergata University Hospital, 00133 Rome, Italy
11
IRCCS Neuromed, 86077 Pozzilli, Italy
12
Department of Pharmacology, School of Medicine, University of Nevada, Reno, NV 89557, USA
*
Author to whom correspondence should be addressed.
Received: 13 July 2020 / Revised: 22 August 2020 / Accepted: 26 August 2020 / Published: 27 August 2020
(This article belongs to the Special Issue Host Genetics in Susceptibility to Infectious Diseases)
The recent global COVID-19 public health emergency is caused by SARS-CoV-2 infections and can manifest extremely variable clinical symptoms. Host human genetic variability could influence susceptibility and response to infection. It is known that ACE2 acts as a receptor for this pathogen, but the viral entry into the target cell also depends on other proteins. The aim of this study was to investigate the variability of genes coding for these proteins involved in the SARS-CoV-2 entry into the cells. We analyzed 131 COVID-19 patients by exome sequencing and examined the genetic variants of TMPRSS2, PCSK3, DPP4, and BSG genes. In total we identified seventeen variants. In PCSK3 gene, we observed a missense variant (c.893G>A) statistically more frequent compared to the EUR GnomAD reference population and a missense mutation (c.1906A>G) not found in the GnomAD database. In TMPRSS2 gene, we observed a significant difference in the frequency of c.331G>A, c.23G>T, and c.589G>A variant alleles in COVID-19 patients, compared to the corresponding allelic frequency in GnomAD. Genetic variants in these genes could influence the entry of the SARS-CoV-2. These data also support the hypothesis that host genetic variability may contribute to the variability in infection susceptibility and severity. View Full-Text
Keywords: COVID-19; SARS-CoV-2; genetic variants; host genetic variability; TMPRSS2; PCSK3 COVID-19; SARS-CoV-2; genetic variants; host genetic variability; TMPRSS2; PCSK3
MDPI and ACS Style

Latini, A.; Agolini, E.; Novelli, A.; Borgiani, P.; Giannini, R.; Gravina, P.; Smarrazzo, A.; Dauri, M.; Andreoni, M.; Rogliani, P.; Bernardini, S.; Helmer-Citterich, M.; Biancolella, M.; Novelli, G. COVID-19 and Genetic Variants of Protein Involved in the SARS-CoV-2 Entry into the Host Cells. Genes 2020, 11, 1010. https://0-doi-org.brum.beds.ac.uk/10.3390/genes11091010

AMA Style

Latini A, Agolini E, Novelli A, Borgiani P, Giannini R, Gravina P, Smarrazzo A, Dauri M, Andreoni M, Rogliani P, Bernardini S, Helmer-Citterich M, Biancolella M, Novelli G. COVID-19 and Genetic Variants of Protein Involved in the SARS-CoV-2 Entry into the Host Cells. Genes. 2020; 11(9):1010. https://0-doi-org.brum.beds.ac.uk/10.3390/genes11091010

Chicago/Turabian Style

Latini, Andrea, Emanuele Agolini, Antonio Novelli, Paola Borgiani, Rosalinda Giannini, Paolo Gravina, Andrea Smarrazzo, Mario Dauri, Massimo Andreoni, Paola Rogliani, Sergio Bernardini, Manuela Helmer-Citterich, Michela Biancolella, and Giuseppe Novelli. 2020. "COVID-19 and Genetic Variants of Protein Involved in the SARS-CoV-2 Entry into the Host Cells" Genes 11, no. 9: 1010. https://0-doi-org.brum.beds.ac.uk/10.3390/genes11091010

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