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1.
Sci Rep ; 12(1): 1357, 2022 01 25.
Article in English | MEDLINE | ID: covidwho-1655613

ABSTRACT

SARS-CoV-2, a novel coronavirus and an etiologic agent for the current global health emergency, causes acute infection of the respiratory tract leading to severe disease and significant mortality. Ever since the start of SARS-CoV-2, also known as the COVID-19 pandemic, countless uncertainties have been revolving around the pathogenesis and epidemiology of the SARS-CoV-2 infection. While air pollution has been shown to be strongly correlated to increased SARS-CoV-2 morbidity and mortality, whether environmental pollutants such as ground-level ozone affects the susceptibility of individuals to SARS-CoV-2 is not yet established. To investigate the impact of ozone inhalation on the expression levels of signatures associated with host susceptibility to SARS-CoV-2, we analyzed lung tissues collected from mice that were sub-chronically exposed to air or 0.8 ppm ozone for three weeks (4 h/night, 5 nights/week), and analyzed the expression of signatures associated with host susceptibility to SARS-CoV-2. SARS-CoV-2 entry into the host cells is dependent on the binding of the virus to the host cellular receptor, angiotensin-converting enzyme (ACE2), and its subsequent proteolytic priming by the host-derived protease, transmembrane protease serine 2 (TMPRSS2). The Ace2 transcripts were significantly elevated in the parenchyma, but not in the extrapulmonary airways and alveolar macrophages, from ozone-exposed mice. The TMPRSS2 protein and Tmprss2 transcripts were significantly elevated in the extrapulmonary airways, parenchyma, and alveolar macrophages from ozone-exposed mice. A significant proportion of additional known SARS-CoV-2 host susceptibility genes were upregulated in alveolar macrophages and parenchyma from ozone-exposed mice. Our data indicate that the unhealthy levels of ozone in the environment may predispose individuals to severe SARS-CoV-2 infection. Given the severity of this pandemic and the challenges associated with direct testing of host-environment interactions in clinical settings, we believe that this ozone exposure-based study informs the scientific community of the potentially detrimental effects of the ambient ozone levels in determining the host susceptibility to SARS-CoV-2.


Subject(s)
COVID-19/metabolism , Macrophages, Alveolar/metabolism , Ozone/toxicity , SARS-CoV-2/metabolism , Serine Endopeptidases/metabolism , Up-Regulation/drug effects , Animals , COVID-19/chemically induced , Disease Susceptibility/chemically induced , Disease Susceptibility/metabolism , Mice
2.
Zool Res ; 42(3): 335-338, 2021 May 18.
Article in English | MEDLINE | ID: covidwho-1231642

ABSTRACT

The global outbreak of coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as of 8 May 2021, has surpassed 150 700 000 infections and 3 279 000 deaths worldwide. Evidence indicates that SARS-CoV-2 RNA can be detected on particulate matter (PM), and COVID-19 cases are correlated with levels of air pollutants. However, the mechanisms of PM involvement in the spread of SARS-CoV-2 remain poorly understood. Here, we found that PM exposure increased the expression level of angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) in several epithelial cells and increased the adsorption of the SARS-CoV-2 spike protein. Instillation of PM in a hACE2 mouse model significantly increased the expression of ACE2 and Tmprss2 and viral replication in the lungs. Furthermore, PM exacerbated the pulmonary lesions caused by SARS-CoV-2 infection in the hACE2 mice. In conclusion, our study demonstrated that PM is an epidemiological factor of COVID-19, emphasizing the necessity of wearing anti-PM masks to cope with this global pandemic.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/chemically induced , COVID-19/immunology , Particulate Matter/adverse effects , SARS-CoV-2 , Adsorption/drug effects , Animals , Disease Susceptibility/chemically induced , Disease Susceptibility/immunology , Epithelial Cells/metabolism , Mice , Mice, Inbred Strains , Particulate Matter/chemistry , RNA, Viral/analysis , SARS-CoV-2/genetics , Serine Endopeptidases/metabolism , Spike Glycoprotein, Coronavirus/metabolism , Virus Internalization/drug effects
3.
Am J Physiol Lung Cell Mol Physiol ; 319(4): L585-L595, 2020 10 01.
Article in English | MEDLINE | ID: covidwho-991951

ABSTRACT

In 2019, the United States experienced the emergence of the vaping-associated lung injury (VALI) epidemic. Vaping is now known to result in the development and progression of severe lung disease in the young and healthy. Lack of regulation on electronic cigarettes in the United States has resulted in over 2,000 patients and 68 deaths. We examine the clinical representation of VALI and the delve into the scientific evidence of how deadly exposure to electronic cigarettes can be. E-cigarette vapor is shown to affect numerous cellular processes, cellular metabolism, and cause DNA damage (which has implications for cancer). E-cigarette use is associated with a higher risk of developing crippling lung conditions such as chronic obstructive pulmonary disease (COPD), which would develop several years from now, increasing the already existent smoking-related burden. The role of vaping and virus susceptibility is yet to be determined; however, vaping can increase the virulence and inflammatory potential of several lung pathogens and is also linked to an increased risk of pneumonia. As it has emerged for cigarette smoking, great caution should also be given to vaping in relation to SARS-CoV-2 infection and the COVID-19 pandemic. Sadly, e-cigarettes are continually promoted and perceived as a safer alternative to cigarette smoking. E-cigarettes and their modifiable nature are harmful, as the lungs are not designed for the chronic inhalation of e-cigarette vapor. It is of interest that e-cigarettes have been shown to be of no help with smoking cessation. A true danger lies in vaping, which, if ignored, will lead to disastrous future costs.


Subject(s)
E-Cigarette Vapor/toxicity , Lung Diseases, Interstitial/epidemiology , Lung Injury/epidemiology , Pulmonary Disease, Chronic Obstructive/epidemiology , Vaping/adverse effects , Adolescent , Betacoronavirus , COVID-19 , Coronavirus Infections/pathology , Disease Susceptibility/chemically induced , Electronic Nicotine Delivery Systems/statistics & numerical data , Female , Humans , Lung Diseases, Interstitial/chemically induced , Lung Injury/chemically induced , Lung Injury/mortality , Male , Middle Aged , Pandemics , Pneumonia/epidemiology , Pneumonia, Viral/pathology , Pulmonary Disease, Chronic Obstructive/chemically induced , Pulmonary Disease, Chronic Obstructive/mortality , SARS-CoV-2 , Smoking Cessation/methods , United States/epidemiology , Vaping/epidemiology , Vaping/mortality
4.
Neurologia (Engl Ed) ; 35(9): 628-632, 2020.
Article in English, Spanish | MEDLINE | ID: covidwho-747866

ABSTRACT

INTRODUCTION: In recent months, doubts have arisen among patients, general practitioners, and neurologists as to whether some drugs commonly used in patients with headaches and neuralgia may favour or complicate the disease caused by SARS-CoV-2. MATERIAL AND METHODS: We collected information on the opinions of scientific societies and medicines agencies (American, European, and Spanish) to clarify doubts regarding the use of drugs such as lisinopril, candesartan, ibuprofen, corticosteroids, carbamazepine, and monoclonal antibodies targeting the calcitonin gene-related peptide in the context of the COVID-19 pandemic. RESULTS: We make recommendations about the use of standard headache treatments in the context of the COVID-19 pandemic, based on the current scientific evidence. CONCLUSIONS: At present, there is no robust scientific argument to formally contraindicate any of the standard treatments employed for headaches and neuralgias.


Subject(s)
Analgesics/adverse effects , Coronavirus Infections/complications , Headache/drug therapy , Neuralgia/drug therapy , Pneumonia, Viral/complications , Adrenal Cortex Hormones/adverse effects , Adrenal Cortex Hormones/therapeutic use , Analgesics/pharmacology , Analgesics/therapeutic use , Angiotensin-Converting Enzyme 2 , Antibodies, Monoclonal/adverse effects , Antibodies, Monoclonal/therapeutic use , Anticonvulsants/adverse effects , Anticonvulsants/therapeutic use , Antihypertensive Agents/adverse effects , Antihypertensive Agents/therapeutic use , Antiviral Agents/pharmacology , Benzimidazoles/adverse effects , Benzimidazoles/therapeutic use , Betacoronavirus , Biphenyl Compounds , COVID-19 , Calcitonin Gene-Related Peptide Receptor Antagonists/adverse effects , Calcitonin Gene-Related Peptide Receptor Antagonists/therapeutic use , Carbamazepine/adverse effects , Carbamazepine/therapeutic use , Coronavirus Infections/drug therapy , Disease Susceptibility/chemically induced , Drug Interactions , Enzyme Induction/drug effects , Headache/complications , Headache/prevention & control , Humans , Ibuprofen/adverse effects , Ibuprofen/pharmacology , Ibuprofen/therapeutic use , Lisinopril/adverse effects , Lisinopril/therapeutic use , Neuralgia/complications , Pandemics , Peptidyl-Dipeptidase A/biosynthesis , Peptidyl-Dipeptidase A/genetics , Receptors, Virus/biosynthesis , Receptors, Virus/genetics , Risk Factors , SARS-CoV-2 , Tetrazoles/adverse effects , Tetrazoles/therapeutic use
5.
Headache ; 60(8): 1558-1568, 2020 09.
Article in English | MEDLINE | ID: covidwho-638748

ABSTRACT

OBJECTIVE: To summarize the current literature on non-steroidal anti-inflammatory drug and corticosteroid use during the coronavirus disease 2019 (COVID-19) pandemic, recognizing that these are commonly used treatments in the field of headache medicine. BACKGROUND: The use of non-steroidal anti-inflammatory drugs and corticosteroids in patients during the COVID-19 pandemic has been a controversial topic within the medical community and international and national health organizations. Lay press and social media outlets have circulated opinions on this topic despite the fact that the evidence for or against the use of these medications is sparse. In the field of headache medicine, these medications are used commonly and both patients and clinicians may have questions or hesitations pertaining to their use during the COVID-19 pandemic. METHODS: A detailed search of the scientific and popular literature was performed. RESULTS: There is limited literature pertaining to the safety of non-steroidal anti-inflammatory drugs and corticosteroids during the COVID-19 pandemic. To date, there are no clear scientific data that preclude the use of non-steroidal anti-inflammatory drugs in the general population who may acquire COVID-19 or in those acutely infected with the virus. Several health organizations have concluded that treatment with corticosteroids during active infection should be avoided due to concerns of prolonged viral shedding in the respiratory tract and the lack of survival benefit based on the data from past coronaviruses and influenza virus; specific exceptions exist including treatment for underlying asthma or chronic obstructive pulmonary disease, septic shock, and acute respiratory distress syndrome. CONCLUSION: Scientific information regarding the COVID-19 pandemic is constantly evolving, and limited or contradictory information can lead to confusion for both patients and clinicians. It is recommended that prior to prescribing non-steroidal anti-inflammatory drugs and steroids for the treatment of headache, clinicians have open discussions with their patients about the potential risks and benefits of using these medications during the COVID-19 pandemic. This manuscript summarizes the currently available evidence and understanding about these risks and benefits to help clinicians navigate such discussions.


Subject(s)
Adrenal Cortex Hormones/adverse effects , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , COVID-19/epidemiology , Headache/drug therapy , Pandemics , SARS-CoV-2/drug effects , Adrenal Cortex Hormones/therapeutic use , Angiotensin-Converting Enzyme 2/biosynthesis , Angiotensin-Converting Enzyme 2/genetics , Animals , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , COVID-19/etiology , COVID-19/prevention & control , Contraindications, Drug , Disease Susceptibility/chemically induced , Dogs , Humans , Hypernatremia/chemically induced , Immunosuppressive Agents/adverse effects , Immunosuppressive Agents/therapeutic use , Mass Media , Models, Animal , Neutrophils/drug effects , Practice Guidelines as Topic , Pulmonary Edema/chemically induced , Rats , Receptors, Virus/biosynthesis , Receptors, Virus/genetics , Risk Assessment , SARS-CoV-2/growth & development , SARS-CoV-2/physiology , Up-Regulation/drug effects , Virus Shedding/drug effects
6.
Int J Dermatol ; 59(9): 1043-1056, 2020 Sep.
Article in English | MEDLINE | ID: covidwho-625433

ABSTRACT

Recommendations were made recently to limit or stop the use of oral and systemic immunotherapies for skin diseases due to potential risks to the patients during the current severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) COVID-19 pandemic. Herein, we attempt to identify potentially safe immunotherapies that may be used in the treatment of cutaneous diseases during the current COVID-19 pandemic. We performed a literature review to approximate the risk of SARS-CoV-2 infection, including available data on the roles of relevant cytokines, cell subsets, and their mediators in eliciting an optimal immune response against respiratory viruses in murine gene deletion models and humans with congenital deficiencies were reviewed for viral infections risk and if possible coronaviruses specifically. Furthermore, reported risk of infections of biologic and non-biologic therapeutics for skin diseases from clinical trials and drug data registries were evaluated. Many of the immunotherapies used in dermatology have data to support their safe use during the COVID-19 pandemic including the biologics that target IgE, IL-4/13, TNF-α, IL-17, IL-12, and IL-23. Furthermore, we provide evidence to show that oral immunosuppressive medications such as methotrexate and cyclosporine do not significantly increase the risk to patients. Most biologic and conventional immunotherapies, based on doses and indications in dermatology, do not appear to increase risk of viral susceptibility and are most likely safe for use during the COVID-19 pandemic. The limitation of this study is availability of data on COVID-19.


Subject(s)
Coronavirus Infections/epidemiology , Cytokine Release Syndrome/immunology , Dermatologic Agents/adverse effects , Disease Susceptibility/chemically induced , Pneumonia, Viral/epidemiology , Skin Diseases/drug therapy , Animals , Betacoronavirus/immunology , Biological Products/adverse effects , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/diagnosis , Coronavirus Infections/immunology , Cytokine Release Syndrome/virology , Dermatology/methods , Dermatology/statistics & numerical data , Disease Models, Animal , Disease Susceptibility/immunology , Evidence-Based Medicine/methods , Evidence-Based Medicine/statistics & numerical data , Humans , Immunologic Factors/adverse effects , Mice , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/diagnosis , Pneumonia, Viral/immunology , Randomized Controlled Trials as Topic , Risk Assessment , SARS-CoV-2 , Severity of Illness Index , Skin Diseases/immunology
7.
Neurol Neuroimmunol Neuroinflamm ; 7(4)2020 07.
Article in English | MEDLINE | ID: covidwho-273239

ABSTRACT

OBJECTIVE: To address concerns regarding the effect of MS disease-modifying therapies (DMTs) on the expression of coronavirus 2019 (COVID-19). METHODS: Review of the current state of knowledge regarding the viral etiology of COVID-19, mechanisms of injury by SARS-CoV-2 infection, and the effect of individual DMTs on the risk of infection and COVID-19 disease expression. RESULTS: Although data are limited, MS DMTs do not obviously increase the risk of acquiring symptomatic SARS-CoV-2 infection. The severe morbidity and mortality of SARS-CoV-2 appear to be largely the consequence of an overly robust immune response rather than the consequence of unchecked viral replication. The effects of specific MS DMTs on the immune response that may increase the risk of impaired viral clearance and their potential counterbalancing beneficial effects on the development of COVID-19-associated acute respiratory distress syndrome are reviewed. CONCLUSION: Although there is currently insufficient real-world experience to definitively answer the question of the effect of a specific MS DMT on COVID-19, registries presently in nascent form should provide these answers. This review provides an approach to addressing these concerns while the data are being accumulated. Early insights suggest that the risk of infection and associated morbidity of COVID-19 in this population is little different than that of the population at large.


Subject(s)
Coronavirus Infections/physiopathology , Immunosuppressive Agents/adverse effects , Pneumonia, Viral/physiopathology , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/immunology , Disease Susceptibility/chemically induced , Humans , Immunosuppressive Agents/therapeutic use , Multiple Sclerosis/drug therapy , Pandemics , Pneumonia, Viral/immunology , Risk Assessment , SARS-CoV-2
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