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Article ; Online: Respiratory epithelial cell responses to SARS-CoV-2 in COVID-19.

Bridges, James P / Vladar, Eszter K / Huang, Hua / Mason, Robert J

2021 Volume 77, Issue 2, Page(s) 203–209

Abstract: ... for SARS-CoV-2 viral infection, replication and release. Infected cells shed their cilia, which disables ... COVID-19 has different clinical stages, and effective therapy depends on the location and extent ... can precipitate a hyperinflammatory state, which is the target of many therapies in severe COVID-19. Disease ...

Abstract	COVID-19 has different clinical stages, and effective therapy depends on the location and extent of the infection. The purpose of this review is to provide a background for understanding the progression of the disease throughout the pulmonary epithelium and discuss therapeutic options. The prime sites for infection that will be contrasted in this review are the conducting airways and the gas exchange portions of the lung. These two sites are characterised by distinct cellular composition and innate immune responses, which suggests the use of distinct therapeutic agents. In the nose, ciliated cells are the primary target cells for SARS-CoV-2 viral infection, replication and release. Infected cells shed their cilia, which disables mucociliary clearance. Evidence further points to a suppressed or incompletely activated innate immune response to SARS-CoV-2 infection in the upper airways. Asymptomatic individuals can still have a productive viral infection and infect others. In the gas exchange portion of the lung, the alveolar type II epithelial cell is the main target cell type. Cell death and marked innate immune response during infection likely contribute to alveolar damage and resultant acute respiratory distress syndrome. Alveolar infection can precipitate a hyperinflammatory state, which is the target of many therapies in severe COVID-19. Disease resolution in the lung is variable and may include scaring and long-term sequalae because the alveolar type II cells are also progenitor cells for the alveolar epithelium.
MeSH term(s)	COVID-19 ; Epithelial Cells ; Humans ; Lung ; Respiratory Mucosa ; SARS-CoV-2
Language	English
Publishing date	2021-08-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	204353-1
ISSN	1468-3296 ; 0040-6376
ISSN (online)	1468-3296
ISSN	0040-6376
DOI	10.1136/thoraxjnl-2021-217561
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Article ; Online: Viral Interference between Respiratory Viruses.

Piret, Jocelyne / Boivin, Guy

Emerging infectious diseases

2022 Volume 28, Issue 2, Page(s) 273–281

Abstract: ... the opportunity to study their interactions, notably with severe acute respiratory syndrome coronavirus 2. ... The mechanisms involved in viral interference have been evaluated in differentiated airway epithelial cells and ... in animal models susceptible to the respiratory viruses of interest. A likely mechanism is the interferon response ...

Abstract	Multiple respiratory viruses can concurrently or sequentially infect the respiratory tract and lead to virus‒virus interactions. Infection by a first virus could enhance or reduce infection and replication of a second virus, resulting in positive (additive or synergistic) or negative (antagonistic) interaction. The concept of viral interference has been demonstrated at the cellular, host, and population levels. The mechanisms involved in viral interference have been evaluated in differentiated airway epithelial cells and in animal models susceptible to the respiratory viruses of interest. A likely mechanism is the interferon response that could confer a temporary nonspecific immunity to the host. During the coronavirus disease pandemic, nonpharmacologic interventions have prevented the circulation of most respiratory viruses. Once the sanitary restrictions are lifted, circulation of seasonal respiratory viruses is expected to resume and will offer the opportunity to study their interactions, notably with severe acute respiratory syndrome coronavirus 2.
MeSH term(s)	Animals ; COVID-19 ; Humans ; Pandemics ; Respiratory Tract Infections/epidemiology ; SARS-CoV-2 ; Viral Interference ; Viruses
Language	English
Publishing date	2022-01-25
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1380686-5
ISSN	1080-6059 ; 1080-6040
ISSN (online)	1080-6059
ISSN	1080-6040
DOI	10.3201/eid2802.211727
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Article ; Online: Respiratory epithelium

Leštarević Snežana / Savić Slađana / Vitković Leonida / Mandić Predrag / Mijović Milica / Dejanović Mirjana / Marjanović Dragan / Rančić Ivan / Filipović Milan

Praxis Medica, Vol 50, Iss 1-2, Pp 35-

Place of entry and / or defense against SARS-CoV-2 virus

2021 Volume 43

Abstract: Coronavirus Disease (COVID-19) is caused by the RNA virus SARS-CoV-2. The primary ... to the virus, since prolonged and excessive SARS-CoV-2-induced activation of these cells leads to the secretion ... begin to synthesize various biologically active molecules. The pathophysiology of the COVID 19 is ...

Abstract	Coronavirus Disease (COVID-19) is caused by the RNA virus SARS-CoV-2. The primary receptor for the virus is most likely Angiotensin-converting enzyme 2 (ACE2), and the virus enters the body by infecting epithelial cells of the respiratory tract. Through the activation of Toll Like Receptors (TLRs), epithelial cells begin to synthesize various biologically active molecules. The pathophysiology of the COVID 19 is primarily attributed to the hyperactivation of host's immune system due to direct damage to the cells, with consequent release of proinflammatory substances, but also due to the activation of the innate immune response through the activation of alveolar macrophages and dendrite cells (DC). A strong proinflammatory reaction causes damage to alveolar epithelial cells and vascular endothelium. Respiratory epithelial cells, alveolar macrophages and DC are likely to be the most important cells involved in the innate immune response to the virus, since prolonged and excessive SARS-CoV-2-induced activation of these cells leads to the secretion of cytokines and chemokines that massively attract leukocytes and monocytes to the lungs and cause lung damage.
Keywords	sars-cov-2 virus ; respiratory system ; immune response ; cytokine storm ; Medicine ; R
Subject code	610 ; 570
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Medicinski fakultet Priština, Društvo lekara Kosova i Metohije Srpskog lekarskog društva
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Influenza A and Respiratory Syncytial Virus Trigger a Cellular Response That Blocks Severe Acute Respiratory Syndrome Virus 2 Infection in the Respiratory Tract.

Dee, Kieran / Schultz, Verena / Haney, Joanne / Bissett, Laura A / Magill, Callum / Murcia, Pablo R

The Journal of infectious diseases

2022 Volume 227, Issue 12, Page(s) 1396–1406

Abstract: ... severe acute respiratory syndrome virus 2 (SARS-CoV-2) and 2 major respiratory viruses: influenza A virus (IAV), and ... respiratory syncytial virus (RSV).: Methods: We performed single infections and coinfections with SARS-CoV-2 combined ... Infections with other respiratory viruses might provide transient resistance to SARS-CoV-2. It would therefore be expected ...

Abstract	Background: Multiple viruses cocirculate and contribute to the burden of respiratory disease. Virus-virus interactions can decrease susceptibility to infection and this interference can have an epidemiological impact. As humans are normally exposed to a community of cocirculating respiratory viruses, experimental coinfection studies are necessary to understand the disease mechanisms of multipathogen systems. We aimed to characterize interactions within the respiratory tract between severe acute respiratory syndrome virus 2 (SARS-CoV-2) and 2 major respiratory viruses: influenza A virus (IAV), and respiratory syncytial virus (RSV). Methods: We performed single infections and coinfections with SARS-CoV-2 combined with IAV or RSV in cultures of human bronchial epithelial cells. We combined microscopy with quantification of viral replication in the presence or absence of an innate immune inhibitor to determine changes in virus-induced pathology, virus spread, and virus replication. Results: SARS-CoV-2 replication is inhibited by both IAV and RSV. This inhibition is dependent on a functional antiviral response and the level of inhibition is proportional to the timing of secondary viral infection. Conclusions: Infections with other respiratory viruses might provide transient resistance to SARS-CoV-2. It would therefore be expected that the incidence of coronavirus disease 2019 (COVID-19) may decrease during periods of high circulation of IAV and RSV.
MeSH term(s)	Humans ; Influenza, Human/epidemiology ; Respiratory Syncytial Virus Infections ; COVID-19 ; SARS-CoV-2 ; Respiratory Syncytial Virus, Human ; Influenza A virus ; Respiratory Mucosa ; Coinfection/epidemiology
Language	English
Publishing date	2022-12-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiac494
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Article ; Online: Rethinking next-generation vaccines for coronaviruses, influenzaviruses, and other respiratory viruses.

Morens, David M / Taubenberger, Jeffery K / Fauci, Anthony S

Cell host & microbe

2023 Volume 31, Issue 1, Page(s) 146–157

Abstract: ... influenza A, SARS-CoV-2, endemic coronaviruses, RSV, and many other "common cold" viruses, cause significant ... window of time before adaptive immune responses are fully marshaled. We discuss possible approaches ... extremely rapidly in the surface epithelium and are quickly transmitted to other hosts, within a narrow ...

Abstract	Viruses that replicate in the human respiratory mucosa without infecting systemically, including influenza A, SARS-CoV-2, endemic coronaviruses, RSV, and many other "common cold" viruses, cause significant mortality and morbidity and are important public health concerns. Because these viruses generally do not elicit complete and durable protective immunity by themselves, they have not to date been effectively controlled by licensed or experimental vaccines. In this review, we examine challenges that have impeded development of effective mucosal respiratory vaccines, emphasizing that all of these viruses replicate extremely rapidly in the surface epithelium and are quickly transmitted to other hosts, within a narrow window of time before adaptive immune responses are fully marshaled. We discuss possible approaches to developing next-generation vaccines against these viruses, in consideration of several variables such as vaccine antigen configuration, dose and adjuventation, route and timing of vaccination, vaccine boosting, adjunctive therapies, and options for public health vaccination polices.
MeSH term(s)	Humans ; COVID-19/prevention & control ; SARS-CoV-2/genetics ; Orthomyxoviridae ; Influenza, Human ; Influenza Vaccines ; Antibodies, Viral
Chemical Substances	Influenza Vaccines ; Antibodies, Viral
Language	English
Publishing date	2023-01-27
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2022.11.016
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Article ; Online: Emergence and competition of virus variants in respiratory viral infections.

Bessonov, Nikolai / Neverova, Daria / Popov, Vladimir / Volpert, Vitaly

Frontiers in immunology

2023 Volume 13, Page(s) 945228

Abstract: The emergence of new variants of concern (VOCs) of the SARS-CoV-2 infection is one of the main ... of new variants and their progression in the epithelial tissue with a possible competition between ... of different variants for uninfected cells leads to the emergence of a single dominant variant and ...

Abstract	The emergence of new variants of concern (VOCs) of the SARS-CoV-2 infection is one of the main factors of epidemic progression. Their development can be characterized by three critical stages: virus mutation leading to the appearance of new viable variants; the competition of different variants leading to the production of a sufficiently large number of copies; and infection transmission between individuals and its spreading in the population. The first two stages take place at the individual level (infected individual), while the third one takes place at the population level with possible competition between different variants. This work is devoted to the mathematical modeling of the first two stages of this process: the emergence of new variants and their progression in the epithelial tissue with a possible competition between them. The emergence of new virus variants is modeled with non-local reaction-diffusion equations describing virus evolution and immune escape in the space of genotypes. The conditions of the emergence of new virus variants are determined by the mutation rate, the cross-reactivity of the immune response, and the rates of virus replication and death. Once different variants emerge, they spread in the infected tissue with a certain speed and viral load that can be determined through the parameters of the model. The competition of different variants for uninfected cells leads to the emergence of a single dominant variant and the elimination of the others due to competitive exclusion. The dominant variant is the one with the maximal individual spreading speed. Thus, the emergence of new variants at the individual level is determined by the immune escape and by the virus spreading speed in the infected tissue.
MeSH term(s)	Humans ; COVID-19 ; SARS-CoV-2 ; Cross Reactions ; Diffusion ; Epidemics
Language	English
Publishing date	2023-02-14
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.945228
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Article ; Online: How do deer respiratory epithelial cells weather the initial storm of SARS-CoV-2 WA1/2020 strain?

Sarlo Davila, Kaitlyn M / Nelli, Rahul K / Phadke, Kruttika S / Ruden, Rachel M / Sang, Yongming / Bellaire, Bryan H / Gimenez-Lirola, Luis G / Miller, Laura C

Microbiology spectrum

2024 Volume 12, Issue 2, Page(s) e0252423

Abstract: ... epithelial cells of human (HRECs) and WTD (Deer-RECs) infected with the SARS-CoV-2 WA1/2020 strain was assessed ... The potential infectivity of severe acute respiratory syndrome associated coronavirus-2 (SARS-CoV-2 ... have evaluated the innate immune factors responsible for the contrasting SARS-CoV-2-associated disease ...

Abstract	The potential infectivity of severe acute respiratory syndrome associated coronavirus-2 (SARS-CoV-2) in animals raises a public health and economic concern, particularly the high susceptibility of white-tailed deer (WTD) to SARS-CoV-2. The disparity in the disease outcome between humans and WTD is very intriguing, as the latter are often asymptomatic, subclinical carriers of SARS-CoV-2. To date, no studies have evaluated the innate immune factors responsible for the contrasting SARS-CoV-2-associated disease outcomes in these mammalian species. A comparative transcriptomic analysis in primary respiratory epithelial cells of human (HRECs) and WTD (Deer-RECs) infected with the SARS-CoV-2 WA1/2020 strain was assessed throughout 48 h post inoculation (hpi). Both HRECs and Deer-RECs were susceptible to virus infection, with significantly (
MeSH term(s)	Animals ; Humans ; SARS-CoV-2/metabolism ; COVID-19 ; Deer ; Interleukin-17 ; NF-kappa B/metabolism ; Cytokines/metabolism ; Epithelial Cells ; Cytokine Release Syndrome
Chemical Substances	Interleukin-17 ; NF-kappa B ; Cytokines
Language	English
Publishing date	2024-01-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2807133-5
ISSN	2165-0497 ; 2165-0497
ISSN (online)	2165-0497
ISSN	2165-0497
DOI	10.1128/spectrum.02524-23
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Article ; Online: Type I interferon signaling induces a delayed antiproliferative response in respiratory epithelial cells during SARS-CoV-2 infection.

Bragazzi Cunha, Juliana / Leix, Kyle / Sherman, Emily J / Mirabelli, Carmen / Frum, Tristan / Zhang, Charles J / Kennedy, Andrew A / Lauring, Adam S / Tai, Andrew W / Sexton, Jonathan Z / Spence, Jason R / Wobus, Christiane E / Emmer, Brian T

Journal of virology

2023 Volume 97, Issue 12, Page(s) e0127623

Abstract: ... epithelial cell death and proliferation during SARS-CoV-2 infection, however, remain unclear. We now report a high ... epithelial cells, with severe cases of COVID-19 characterized by direct injury of the alveolar epithelium and ... Abstract: Disease progression during SARS-CoV-2 infection is tightly linked to the fate of lung ...

Abstract	Abstract: Disease progression during SARS-CoV-2 infection is tightly linked to the fate of lung epithelial cells, with severe cases of COVID-19 characterized by direct injury of the alveolar epithelium and an impairment in its regeneration from progenitor cells. The molecular pathways that govern respiratory epithelial cell death and proliferation during SARS-CoV-2 infection, however, remain unclear. We now report a high-throughput CRISPR screen for host genetic modifiers of the survival and proliferation of SARS-CoV-2-infected Calu-3 respiratory epithelial cells. The top four genes identified in our screen encode components of the same type I interferon (IFN-I) signaling complex—
MeSH term(s)	Humans ; COVID-19/immunology ; COVID-19/pathology ; COVID-19/virology ; Epithelial Cells/pathology ; Epithelial Cells/virology ; Interferon Type I/immunology ; Lung/pathology ; Lung/virology ; SARS-CoV-2/immunology ; SARS-CoV-2/pathogenicity ; Cell Line ; Cell Proliferation
Chemical Substances	Interferon Type I
Language	English
Publishing date	2023-11-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/jvi.01276-23
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Article ; Online: Acute Respiratory Distress Syndrome: Diagnosis and Management.

Saguil, Aaron / Fargo, Matthew V

American family physician

2020 Volume 101, Issue 12, Page(s) 730–738

Abstract: ... promoting inflammatory cell accumulation in the alveoli and microcirculation of the lung. Inflammatory cells ... damage the vascular endothelium and alveolar epithelium, leading to pulmonary edema, hyaline membrane ... As patients with ARDS improve and the underlying illness resolves, a spontaneous breathing trial is indicated ...

Abstract	Acute respiratory distress syndrome (ARDS) is noncardiogenic pulmonary edema that manifests as rapidly progressive dyspnea, tachypnea, and hypoxemia. Diagnostic criteria include onset within one week of a known insult or new or worsening respiratory symptoms, profound hypoxemia, bilateral pulmonary opacities on radiography, and inability to explain respiratory failure by cardiac failure or fluid overload. ARDS is thought to occur when a pulmonary or extrapulmonary insult causes the release of inflammatory mediators, promoting inflammatory cell accumulation in the alveoli and microcirculation of the lung. Inflammatory cells damage the vascular endothelium and alveolar epithelium, leading to pulmonary edema, hyaline membrane formation, decreased lung compliance, and decreased gas exchange. Most cases are associated with pneumonia or sepsis. ARDS is responsible for one in 10 admissions to intensive care units and one in four mechanical ventilations. In-hospital mortality for patients with severe ARDS ranges from 46% to 60%. ARDS often must be differentiated from pneumonia and congestive heart failure, which typically has signs of fluid overload. Treatment of ARDS is supportive and includes mechanical ventilation, prophylaxis for stress ulcers and venous thromboembolism, nutritional support, and treatment of the underlying injury. Low tidal volume and high positive end-expiratory pressure improve outcomes. Prone positioning is recommended for some moderate and all severe cases. As patients with ARDS improve and the underlying illness resolves, a spontaneous breathing trial is indicated to assess eligibility for ventilator weaning. Patients who survive ARDS are at risk of diminished functional capacity, mental illness, and decreased quality of life; ongoing care by a primary care physician is beneficial for these patients.
MeSH term(s)	Adult ; COVID-19/complications ; Child ; Diagnosis, Differential ; Female ; Humans ; Hypoxia/diagnosis ; Male ; Patient Positioning/methods ; Pneumonia/diagnosis ; Respiration, Artificial/methods ; Respiratory Distress Syndrome/diagnosis ; Respiratory Distress Syndrome/etiology ; Respiratory Distress Syndrome/physiopathology ; Respiratory Distress Syndrome/therapy ; Risk Factors ; SARS-CoV-2
Language	English
Publishing date	2020-06-29
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	412694-4
ISSN	1532-0650 ; 0002-838X ; 0572-3612
ISSN (online)	1532-0650
ISSN	0002-838X ; 0572-3612
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Article ; Online: The seven constitutive respiratory defense barriers against SARS-CoV-2 infection.

Tosta, Eduardo

Revista da Sociedade Brasileira de Medicina Tropical

2021 Volume 54, Page(s) e04612021

Abstract: ... besides protecting the local microbiota against noxious agents, also inhibit SARS-CoV-2 cell invasion ... Before eliciting an adaptive immune response, SARS-CoV-2 must overcome seven constitutive ... immune cells' functions. The respiratory tract microbiota constitutes the third defense barrier against SARS-CoV ...

Abstract	Before eliciting an adaptive immune response, SARS-CoV-2 must overcome seven constitutive respiratory defense barriers. The first is the mucus covering the respiratory tract's luminal surface, which entraps inhaled particles, including infectious agents, and eliminates them by mucociliary clearance. The second barrier comprises various components present in the airway lining fluid, the surfactants. Besides providing low surface tension that allows efficient gas exchange at the alveoli, surfactants inhibit the invasion of epithelial cells by respiratory viruses, enhance pathogen uptake by phagocytes, and regulate immune cells' functions. The respiratory tract microbiota constitutes the third defense barrier against SARS-CoV-2. It activates the innate and adaptive immune cells and elicits anti-infectious molecules such as secretory IgA antibodies, defensins, and interferons. The fourth defense barrier comprises the antimicrobial peptides defensins, and lactoferrin. They show direct antiviral activity, inhibit viral fusion, and modulate the innate and adaptive immune responses. Secretory IgA antibodies, the fifth defense barrier, besides protecting the local microbiota against noxious agents, also inhibit SARS-CoV-2 cell invasion. If the virus overcomes this barrier, it reaches its target, the respiratory epithelial cells. However, these cells also act as a defense barrier, the sixth one, since they hinder the virus' access to receptors and produce antiviral and immunomodulatory molecules such as interferons, lactoferrin, and defensins. Finally, the sensing of the virus by the cells of innate immunity, the last constitutive defense barrier, elicits a cascade of signals that activate adaptive immune cells and may inhibit the development of productive infection. The subject of the present essay is discussing these mechanisms.
MeSH term(s)	Antibodies, Viral/immunology ; Antimicrobial Peptides/immunology ; COVID-19/immunology ; Humans ; Immunity, Innate ; Immunoglobulin A/immunology ; Interferons/immunology ; Lung/immunology ; Lung/virology ; SARS-CoV-2
Chemical Substances	Antibodies, Viral ; Antimicrobial Peptides ; Immunoglobulin A ; Interferons (9008-11-1)
Language	English
Publishing date	2021-12-17
Publishing country	Brazil
Document type	Journal Article ; Review
ZDB-ID	1038126-0
ISSN	1678-9849 ; 0037-8682
ISSN (online)	1678-9849
ISSN	0037-8682
DOI	10.1590/0037-8682-0461-2021
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