Androgen sensitivity gateway to COVID‐19 disease severity
In this communication, we present arguments for androgen sensitivity as a likely determinant of COVID‐19 disease severity. The androgen sensitivity model explains why males are more likely to develop severe symptoms while children are ostensibly resistant to infection. Further, the model explains th...
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| Veröffentlicht in: | Drug development research 2020-11, Vol.81 (7), p.771-776 |
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| creator | Wambier, Carlos Gustavo Goren, Andy Vaño‐Galván, Sergio Ramos, Paulo Müller Ossimetha, Angelina Nau, Gerard Herrera, Sabina McCoy, John |
| description | In this communication, we present arguments for androgen sensitivity as a likely determinant of COVID‐19 disease severity. The androgen sensitivity model explains why males are more likely to develop severe symptoms while children are ostensibly resistant to infection. Further, the model explains the difference in COVID‐19 mortality rates among different ethnicities. Androgen sensitivity is determined by genetic variants of the androgen receptor. The androgen receptor regulates transcription of the transmembrane protease, serine 2 (TMPRSS2), which is required for SARS‐CoV‐2 infectivity. TMPRSS2 primes the Spike protein of the virus, which has two consequences: diminishing viral recognition by neutralizing antibodies and activating SARS‐CoV‐2 for virus‐cell fusion. Genetic variants that have been associated with androgenetic alopecia, prostate cancer, benign prostatic hyperplasia and polycystic ovary syndrome could be associated with host susceptibility. In addition to theoretical epidemiological and molecular mechanisms, there are reports of high rates of androgenetic alopecia of from hospitalized COVID‐19 patients due to severe symptoms. Androgen sensitivity is a likely determinant of COVID‐19 disease severity. We believe that the evidence presented in this communication warrants the initiation of trials using anti‐androgen agents. |
| doi_str_mv | 10.1002/ddr.21688 |
| format | Article |
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The androgen sensitivity model explains why males are more likely to develop severe symptoms while children are ostensibly resistant to infection. Further, the model explains the difference in COVID‐19 mortality rates among different ethnicities. Androgen sensitivity is determined by genetic variants of the androgen receptor. The androgen receptor regulates transcription of the transmembrane protease, serine 2 (TMPRSS2), which is required for SARS‐CoV‐2 infectivity. TMPRSS2 primes the Spike protein of the virus, which has two consequences: diminishing viral recognition by neutralizing antibodies and activating SARS‐CoV‐2 for virus‐cell fusion. Genetic variants that have been associated with androgenetic alopecia, prostate cancer, benign prostatic hyperplasia and polycystic ovary syndrome could be associated with host susceptibility. In addition to theoretical epidemiological and molecular mechanisms, there are reports of high rates of androgenetic alopecia of from hospitalized COVID‐19 patients due to severe symptoms. Androgen sensitivity is a likely determinant of COVID‐19 disease severity. We believe that the evidence presented in this communication warrants the initiation of trials using anti‐androgen agents.</description><identifier>ISSN: 0272-4391</identifier><identifier>EISSN: 1098-2299</identifier><identifier>DOI: 10.1002/ddr.21688</identifier><identifier>PMID: 32412125</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>Alopecia ; Alopecia - etiology ; Alopecia - genetics ; Alopecia - metabolism ; Androgen receptors ; Androgens ; Antibodies ; anti‐androgen ; Baldness ; Cell fusion ; clinical trial ; Clinical trials ; Commentaries ; COVID-19 ; COVID-19 - complications ; COVID-19 - genetics ; COVID-19 - metabolism ; Epidemiology ; Genetic diversity ; Genetic variance ; Humans ; Hyperplasia ; Infectivity ; Male ; Models, Theoretical ; Molecular modelling ; pandemic ; Pandemics ; Polycystic ovary syndrome ; Prostate cancer ; Receptors ; Receptors, Androgen - genetics ; Receptors, Androgen - metabolism ; SARS-CoV-2 - physiology ; SARS‐CoV‐2 ; Sensitivity ; Serine ; Serine Endopeptidases - metabolism ; Severe acute respiratory syndrome ; Severe acute respiratory syndrome coronavirus 2 ; Severity of Illness Index ; Signs and symptoms ; Spike Glycoprotein, Coronavirus - metabolism ; Spike protein ; TMPRSS2 ; Transcription ; Viral diseases ; Virus Internalization ; Viruses</subject><ispartof>Drug development research, 2020-11, Vol.81 (7), p.771-776</ispartof><rights>2020 Wiley Periodicals, Inc.</rights><rights>2020 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5778-6a65e673a33dc2402518b8bbf7c8e2f13da2e33e8a289e487c412f146d18d5593</citedby><cites>FETCH-LOGICAL-c5778-6a65e673a33dc2402518b8bbf7c8e2f13da2e33e8a289e487c412f146d18d5593</cites><orcidid>0000-0002-8190-2289 ; 0000-0003-2773-7494 ; 0000-0001-7921-8317 ; 0000-0002-1561-414X ; 0000-0002-4636-4489</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fddr.21688$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fddr.21688$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32412125$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wambier, Carlos Gustavo</creatorcontrib><creatorcontrib>Goren, Andy</creatorcontrib><creatorcontrib>Vaño‐Galván, Sergio</creatorcontrib><creatorcontrib>Ramos, Paulo Müller</creatorcontrib><creatorcontrib>Ossimetha, Angelina</creatorcontrib><creatorcontrib>Nau, Gerard</creatorcontrib><creatorcontrib>Herrera, Sabina</creatorcontrib><creatorcontrib>McCoy, John</creatorcontrib><title>Androgen sensitivity gateway to COVID‐19 disease severity</title><title>Drug development research</title><addtitle>Drug Dev Res</addtitle><description>In this communication, we present arguments for androgen sensitivity as a likely determinant of COVID‐19 disease severity. The androgen sensitivity model explains why males are more likely to develop severe symptoms while children are ostensibly resistant to infection. Further, the model explains the difference in COVID‐19 mortality rates among different ethnicities. Androgen sensitivity is determined by genetic variants of the androgen receptor. The androgen receptor regulates transcription of the transmembrane protease, serine 2 (TMPRSS2), which is required for SARS‐CoV‐2 infectivity. TMPRSS2 primes the Spike protein of the virus, which has two consequences: diminishing viral recognition by neutralizing antibodies and activating SARS‐CoV‐2 for virus‐cell fusion. Genetic variants that have been associated with androgenetic alopecia, prostate cancer, benign prostatic hyperplasia and polycystic ovary syndrome could be associated with host susceptibility. In addition to theoretical epidemiological and molecular mechanisms, there are reports of high rates of androgenetic alopecia of from hospitalized COVID‐19 patients due to severe symptoms. Androgen sensitivity is a likely determinant of COVID‐19 disease severity. We believe that the evidence presented in this communication warrants the initiation of trials using anti‐androgen agents.</description><subject>Alopecia</subject><subject>Alopecia - etiology</subject><subject>Alopecia - genetics</subject><subject>Alopecia - metabolism</subject><subject>Androgen receptors</subject><subject>Androgens</subject><subject>Antibodies</subject><subject>anti‐androgen</subject><subject>Baldness</subject><subject>Cell fusion</subject><subject>clinical trial</subject><subject>Clinical trials</subject><subject>Commentaries</subject><subject>COVID-19</subject><subject>COVID-19 - complications</subject><subject>COVID-19 - genetics</subject><subject>COVID-19 - metabolism</subject><subject>Epidemiology</subject><subject>Genetic diversity</subject><subject>Genetic variance</subject><subject>Humans</subject><subject>Hyperplasia</subject><subject>Infectivity</subject><subject>Male</subject><subject>Models, Theoretical</subject><subject>Molecular modelling</subject><subject>pandemic</subject><subject>Pandemics</subject><subject>Polycystic ovary syndrome</subject><subject>Prostate cancer</subject><subject>Receptors</subject><subject>Receptors, Androgen - genetics</subject><subject>Receptors, Androgen - metabolism</subject><subject>SARS-CoV-2 - physiology</subject><subject>SARS‐CoV‐2</subject><subject>Sensitivity</subject><subject>Serine</subject><subject>Serine Endopeptidases - metabolism</subject><subject>Severe acute respiratory syndrome</subject><subject>Severe acute respiratory syndrome coronavirus 2</subject><subject>Severity of Illness Index</subject><subject>Signs and symptoms</subject><subject>Spike Glycoprotein, Coronavirus - metabolism</subject><subject>Spike protein</subject><subject>TMPRSS2</subject><subject>Transcription</subject><subject>Viral diseases</subject><subject>Virus Internalization</subject><subject>Viruses</subject><issn>0272-4391</issn><issn>1098-2299</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctKAzEYRoMoWqsLX0AG3Ohiai6TmQRBKK03EARRtyGd_FMj0xlNpi3d-Qg-o09i6lRRwVUW_-FwwofQHsE9gjE9Nsb1KEmFWEMdgqWIKZVyHXUwzWicMEm20Lb3TxgTkgixibYYTQgllHfQSb8yrh5DFXmovG3szDaLaKwbmOtF1NTR4Obhavj--kZkZKwH7SGQM3AB20EbhS497K7eLro_P7sbXMbXNxdXg_51nPMsE3GqUw5pxjRjJqcJppyIkRiNiiwXQAvCjKbAGAhNhYREZHmIK0iSGiIM55J10WnrfZ6OJmByqBqnS_Xs7ES7haq1Vb8vlX1U43qmMpoxLHkQHK4Ern6Zgm_UxPocylJXUE-9ClEJ5lhwGtCDP-hTPXVV-F6guJBYMrYUHrVU7mrvHRTfMQSr5SQqTKI-Jwns_s_6b_JrgwAct8DclrD436SGw9tW-QHXWZUj</recordid><startdate>202011</startdate><enddate>202011</enddate><creator>Wambier, Carlos Gustavo</creator><creator>Goren, Andy</creator><creator>Vaño‐Galván, Sergio</creator><creator>Ramos, Paulo Müller</creator><creator>Ossimetha, Angelina</creator><creator>Nau, Gerard</creator><creator>Herrera, Sabina</creator><creator>McCoy, John</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8190-2289</orcidid><orcidid>https://orcid.org/0000-0003-2773-7494</orcidid><orcidid>https://orcid.org/0000-0001-7921-8317</orcidid><orcidid>https://orcid.org/0000-0002-1561-414X</orcidid><orcidid>https://orcid.org/0000-0002-4636-4489</orcidid></search><sort><creationdate>202011</creationdate><title>Androgen sensitivity gateway to COVID‐19 disease severity</title><author>Wambier, Carlos Gustavo ; Goren, Andy ; Vaño‐Galván, Sergio ; Ramos, Paulo Müller ; Ossimetha, Angelina ; Nau, Gerard ; Herrera, Sabina ; McCoy, John</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5778-6a65e673a33dc2402518b8bbf7c8e2f13da2e33e8a289e487c412f146d18d5593</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Alopecia</topic><topic>Alopecia - etiology</topic><topic>Alopecia - genetics</topic><topic>Alopecia - metabolism</topic><topic>Androgen receptors</topic><topic>Androgens</topic><topic>Antibodies</topic><topic>anti‐androgen</topic><topic>Baldness</topic><topic>Cell fusion</topic><topic>clinical trial</topic><topic>Clinical trials</topic><topic>Commentaries</topic><topic>COVID-19</topic><topic>COVID-19 - complications</topic><topic>COVID-19 - genetics</topic><topic>COVID-19 - metabolism</topic><topic>Epidemiology</topic><topic>Genetic diversity</topic><topic>Genetic variance</topic><topic>Humans</topic><topic>Hyperplasia</topic><topic>Infectivity</topic><topic>Male</topic><topic>Models, Theoretical</topic><topic>Molecular modelling</topic><topic>pandemic</topic><topic>Pandemics</topic><topic>Polycystic ovary syndrome</topic><topic>Prostate cancer</topic><topic>Receptors</topic><topic>Receptors, Androgen - genetics</topic><topic>Receptors, Androgen - metabolism</topic><topic>SARS-CoV-2 - physiology</topic><topic>SARS‐CoV‐2</topic><topic>Sensitivity</topic><topic>Serine</topic><topic>Serine Endopeptidases - metabolism</topic><topic>Severe acute respiratory syndrome</topic><topic>Severe acute respiratory syndrome coronavirus 2</topic><topic>Severity of Illness Index</topic><topic>Signs and symptoms</topic><topic>Spike Glycoprotein, Coronavirus - metabolism</topic><topic>Spike protein</topic><topic>TMPRSS2</topic><topic>Transcription</topic><topic>Viral diseases</topic><topic>Virus Internalization</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wambier, Carlos Gustavo</creatorcontrib><creatorcontrib>Goren, Andy</creatorcontrib><creatorcontrib>Vaño‐Galván, Sergio</creatorcontrib><creatorcontrib>Ramos, Paulo Müller</creatorcontrib><creatorcontrib>Ossimetha, Angelina</creatorcontrib><creatorcontrib>Nau, Gerard</creatorcontrib><creatorcontrib>Herrera, Sabina</creatorcontrib><creatorcontrib>McCoy, John</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Drug development research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wambier, Carlos Gustavo</au><au>Goren, Andy</au><au>Vaño‐Galván, Sergio</au><au>Ramos, Paulo Müller</au><au>Ossimetha, Angelina</au><au>Nau, Gerard</au><au>Herrera, Sabina</au><au>McCoy, John</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Androgen sensitivity gateway to COVID‐19 disease severity</atitle><jtitle>Drug development research</jtitle><addtitle>Drug Dev Res</addtitle><date>2020-11</date><risdate>2020</risdate><volume>81</volume><issue>7</issue><spage>771</spage><epage>776</epage><pages>771-776</pages><issn>0272-4391</issn><eissn>1098-2299</eissn><abstract>In this communication, we present arguments for androgen sensitivity as a likely determinant of COVID‐19 disease severity. The androgen sensitivity model explains why males are more likely to develop severe symptoms while children are ostensibly resistant to infection. Further, the model explains the difference in COVID‐19 mortality rates among different ethnicities. Androgen sensitivity is determined by genetic variants of the androgen receptor. The androgen receptor regulates transcription of the transmembrane protease, serine 2 (TMPRSS2), which is required for SARS‐CoV‐2 infectivity. TMPRSS2 primes the Spike protein of the virus, which has two consequences: diminishing viral recognition by neutralizing antibodies and activating SARS‐CoV‐2 for virus‐cell fusion. Genetic variants that have been associated with androgenetic alopecia, prostate cancer, benign prostatic hyperplasia and polycystic ovary syndrome could be associated with host susceptibility. In addition to theoretical epidemiological and molecular mechanisms, there are reports of high rates of androgenetic alopecia of from hospitalized COVID‐19 patients due to severe symptoms. Androgen sensitivity is a likely determinant of COVID‐19 disease severity. We believe that the evidence presented in this communication warrants the initiation of trials using anti‐androgen agents.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>32412125</pmid><doi>10.1002/ddr.21688</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-8190-2289</orcidid><orcidid>https://orcid.org/0000-0003-2773-7494</orcidid><orcidid>https://orcid.org/0000-0001-7921-8317</orcidid><orcidid>https://orcid.org/0000-0002-1561-414X</orcidid><orcidid>https://orcid.org/0000-0002-4636-4489</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Alopecia Alopecia - etiology Alopecia - genetics Alopecia - metabolism Androgen receptors Androgens Antibodies anti‐androgen Baldness Cell fusion clinical trial Clinical trials Commentaries COVID-19 COVID-19 - complications COVID-19 - genetics COVID-19 - metabolism Epidemiology Genetic diversity Genetic variance Humans Hyperplasia Infectivity Male Models, Theoretical Molecular modelling pandemic Pandemics Polycystic ovary syndrome Prostate cancer Receptors Receptors, Androgen - genetics Receptors, Androgen - metabolism SARS-CoV-2 - physiology SARS‐CoV‐2 Sensitivity Serine Serine Endopeptidases - metabolism Severe acute respiratory syndrome Severe acute respiratory syndrome coronavirus 2 Severity of Illness Index Signs and symptoms Spike Glycoprotein, Coronavirus - metabolism Spike protein TMPRSS2 Transcription Viral diseases Virus Internalization Viruses |
| title | Androgen sensitivity gateway to COVID‐19 disease severity |
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