Does COVID19 Infect the Brain? If So, Smokers Might Be at a Higher Risk.
Identifieur interne : 000717 ( 2020/Analysis ); précédent : 000716; suivant : 000718Does COVID19 Infect the Brain? If So, Smokers Might Be at a Higher Risk.
Auteurs : Nadine Kabbani [États-Unis] ; James L. OldsSource :
- Molecular pharmacology [ 1521-0111 ] ; 2020.
Abstract
COVID19 is a devastating global pandemic with epicenters in China, Italy, Spain, and now the United States. While the majority of infected cases appear mild, in some cases, individuals present serious cardiorespiratory complications with possible long-term lung damage. Infected individuals report a range of symptoms from headaches to shortness of breath to taste and smell loss. To that end, less is known about how the virus may impact different organ systems. The SARS-CoV2 virus, which is responsible for COVID19, is highly similar to SARS-CoV. Both viruses have evolved an ability to enter host cells through direct interaction with the angiotensin converting enzyme (ACE) 2 protein at the surface of many cells. Published findings indicate that SARS-CoV can enter the human nervous system with evidence from both postmortem brains and detection in cerebrospinal fluid of infected individuals. Here, we consider the ability of SARS-CoV2 to enter and infect the human nervous system based on the strong expression of the ACE2 target throughout the brain. Moreover, we predict that nicotine exposure through various kinds of smoking (cigarettes, electronic cigarettes, or vape) can increase the risk for COVID19 neuroinfection based on known functional interactions between the nicotinic receptor and ACE2. We advocate for higher surveillance and analysis of neurocomplications in infected cases. SIGNIFICANCE STATEMENT: The COVID19 epidemic has spurred a global public health crisis. While many of the cases requiring hospitalization and intensive medical care center on cardiorespiratory treatment, a growing number of cases present neurological symptoms. Viral entry into the brain now appears a strong possibility with deleterious consequences and an urgent need for addressing.
DOI: 10.1124/molpharm.120.000014
PubMed: 32238438
Affiliations:
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pubmed:32238438Le document en format XML
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If So, Smokers Might Be at a Higher Risk.</title><author><name sortKey="Kabbani, Nadine" sort="Kabbani, Nadine" uniqKey="Kabbani N" first="Nadine" last="Kabbani">Nadine Kabbani</name><affiliation wicri:level="1"><nlm:affiliation>School of Systems Biology, George Mason University, Fairfax, Virginia (N.K.) and Schar School of Policy and Government, George Mason University, Arlington, Virginia (J.L.O.) nkabbani@gmu.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country></affiliation></author><author><name sortKey="Olds, James L" sort="Olds, James L" uniqKey="Olds J" first="James L" last="Olds">James L. Olds</name><affiliation><nlm:affiliation>School of Systems Biology, George Mason University, Fairfax, Virginia (N.K.) and Schar School of Policy and Government, George Mason University, Arlington, Virginia (J.L.O.).</nlm:affiliation><wicri:noCountry code="subField">Virginia (J.L.O.).</wicri:noCountry></affiliation></author></analytic><series><title level="j">Molecular pharmacology</title><idno type="eISSN">1521-0111</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">COVID19 is a devastating global pandemic with epicenters in China, Italy, Spain, and now the United States. While the majority of infected cases appear mild, in some cases, individuals present serious cardiorespiratory complications with possible long-term lung damage. Infected individuals report a range of symptoms from headaches to shortness of breath to taste and smell loss. To that end, less is known about how the virus may impact different organ systems. The SARS-CoV2 virus, which is responsible for COVID19, is highly similar to SARS-CoV. Both viruses have evolved an ability to enter host cells through direct interaction with the angiotensin converting enzyme (ACE) 2 protein at the surface of many cells. Published findings indicate that SARS-CoV can enter the human nervous system with evidence from both postmortem brains and detection in cerebrospinal fluid of infected individuals. Here, we consider the ability of SARS-CoV2 to enter and infect the human nervous system based on the strong expression of the ACE2 target throughout the brain. Moreover, we predict that nicotine exposure through various kinds of smoking (cigarettes, electronic cigarettes, or vape) can increase the risk for COVID19 neuroinfection based on known functional interactions between the nicotinic receptor and ACE2. We advocate for higher surveillance and analysis of neurocomplications in infected cases. SIGNIFICANCE STATEMENT: The COVID19 epidemic has spurred a global public health crisis. While many of the cases requiring hospitalization and intensive medical care center on cardiorespiratory treatment, a growing number of cases present neurological symptoms. Viral entry into the brain now appears a strong possibility with deleterious consequences and an urgent need for addressing.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Olds, James L" sort="Olds, James L" uniqKey="Olds J" first="James L" last="Olds">James L. 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