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Pathology, Research and Practice Sep 2020The novel coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), first appeared in December 2019, in Wuhan, China... (Review)
Review
The novel coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), first appeared in December 2019, in Wuhan, China and evolved into a pandemic. As Angiotensin-Converting Enzyme 2 (ACE2) is one of the potential target receptors for SARS-CoV-2 in human body, which is expressed in different tissues, multiple organs might become affected. In the initial phase of the current pandemic, a handful of post-mortem case-series revealed COVID-19-related pathological changes in various organs. Although pathological examination is not a feasible method of diagnosis, it can elucidate pathological changes, pathogenesis of the disease, and the cause of death in COVID-19 cases. Herein, we thoroughly reviewed multiple organs including lung, gastrointestinal tract, liver, kidney, skin, heart, blood, spleen, lymph nodes, brain, blood vessels, and placenta in terms of COVID-19-related pathological alterations. Also, these findings were compared with SARS and MERS infection, wherever applicable. We found a diverse range of pathological changes, some of which resemble those found in SARS and MERS.
Topics: Angiotensin-Converting Enzyme 2; Betacoronavirus; COVID-19; China; Coronavirus Infections; Humans; Lung; Pandemics; Peptidyl-Dipeptidase A; Pneumonia, Viral; SARS-CoV-2
PubMed: 32825963
DOI: 10.1016/j.prp.2020.153097 -
The Lancet. Respiratory Medicine Oct 2022Human papillomavirus (HPV) types 6 and 11 can infect the squamous epithelium of the respiratory tract. Up to 8·9% of patients with HPV-associated recurrent respiratory... (Review)
Review
Human papillomavirus (HPV) types 6 and 11 can infect the squamous epithelium of the respiratory tract. Up to 8·9% of patients with HPV-associated recurrent respiratory papillomatosis (RRP) have pulmonary involvement. Pulmonary manifestations of HPV infection are associated with considerable morbidity, in part because treatment options and management guidelines are lacking. Patients with pulmonary RRP have a 32-times increased lifetime risk of malignant transformation compared with the overall RRP population. We review the clinical and radiographic presentation, pathological features, and genetics of pulmonary RRP, and we provide management algorithms based on our clinical experience with this complex patient population. In patients with suspected pulmonary involvement, tissue-sparing procedures to address growing lesions might be warranted given the chronicity and multifocality of the disease over a patient's lifetime. However, malignant transformation of pulmonary lesion(s) warrants standard-of-care treatment for primary lung squamous cell carcinoma. Large cohort studies are needed to understand the clinical course of pulmonary RRP and to identify molecular markers of increased risk of malignant transformation in order to develop guidelines for optimal and standardised surveillance and treatment.
Topics: Cell Transformation, Neoplastic; Humans; Lung; Papillomavirus Infections; Respiratory Tract Infections
PubMed: 35863360
DOI: 10.1016/S2213-2600(22)00008-X -
Expert Review of Respiratory Medicine 2024Hypercapnia is developed in patients with acute and/or chronic respiratory conditions. Clinical data concerning hypercapnia and respiratory infections interaction is... (Review)
Review
INTRODUCTION
Hypercapnia is developed in patients with acute and/or chronic respiratory conditions. Clinical data concerning hypercapnia and respiratory infections interaction is limited.
AREAS COVERED
Currently, the relationship between hypercapnia and respiratory infections remains unclear. In this review, we summarize studies on the effects of hypercapnia on models of pulmonary infections to clarify the role of elevated CO2 in these pulmonary pathologies. Hypercapnia affects different cell types in the alveoli, leading to changes in the immune response. In vitro studies show that hypercapnia downregulates the NF-κβ pathway, reduces inflammation and impairs epithelial wound healing. While in vivo models show a dual role between short- and long-term effects of hypercapnia on lung infection. However, it is still controversial whether the effects observed under hypercapnia are pH dependent or not.
EXPERT OPINION
The role of hypercapnia is still a controversial debate. Hypercapnia could play a beneficial role in mechanically ventilated models, by lowering the inflammation produced by the stretch condition. But it could be detrimental in infectious scenarios, causing phagocyte dysfunction and lack of infection control. Further data concerning hypercapnia on respiratory infections is needed to elucidate this interaction.
Topics: Humans; Hypercapnia; Lung; Inflammation; Pulmonary Alveoli; Respiratory Tract Infections
PubMed: 38489161
DOI: 10.1080/17476348.2024.2331767 -
Radiologic Clinics of North America May 2022The chest radiograph is the most common imaging examination performed in most radiology departments, and one of the more common indications for these studies is... (Review)
Review
The chest radiograph is the most common imaging examination performed in most radiology departments, and one of the more common indications for these studies is suspected infection. Radiologists must therefore be aware of less common radiographic patterns of pulmonary infection if they are to add value in the interpretation of chest radiographs for this indication. This review uses a case-based format to illustrate a range of imaging findings that can be associated with acute pulmonary infection and highlight findings that should prompt investigation for diseases other than community-acquired pneumonia to prevent misdiagnosis and delays in appropriate management.
Topics: Community-Acquired Infections; Humans; Lung; Pneumonia; Radiography; Radiography, Thoracic
PubMed: 35534125
DOI: 10.1016/j.rcl.2022.01.011 -
Journal of Molecular Cell Biology Jul 2021The high infectivity and pathogenicity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have caused the COVID-19 outbreak, one of the most devastating... (Review)
Review
The high infectivity and pathogenicity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have caused the COVID-19 outbreak, one of the most devastating pandemics in more than a century. This pandemic has already left a trail of destruction, including enormous loss of life, a global economic slump, and widespread psychological damage. Despite assiduous world-wide endeavors, an effective cure for COVID-19 is still lacking. Surprisingly, infected neonates and children have relatively mild clinical manifestations and a much lower fatality rate than elderly adults. Recent studies have unambiguously demonstrated the vertical transmission of SARS-CoV-2 from infected pregnant women to fetuses, which creates yet another challenge for disease prevention. In this review, we will summarize the molecular mechanism for entry of SARS-CoV-2 into host cells, the basis for the failure of the lungs and other organs in severe acute cases, and the evidence for congenital transmission.
Topics: COVID-19; Female; Fetus; Humans; Infectious Disease Transmission, Vertical; Lung; Pandemics; Pregnancy; SARS-CoV-2; Virus Internalization
PubMed: 33677567
DOI: 10.1093/jmcb/mjab013 -
International Journal of Molecular... Apr 2024Despite the end of the pandemic, coronavirus disease 2019 (COVID-19) remains a major public health concern. The first waves of the virus led to a better understanding of... (Review)
Review
Despite the end of the pandemic, coronavirus disease 2019 (COVID-19) remains a major public health concern. The first waves of the virus led to a better understanding of its pathogenesis, highlighting the fact that there is a specific pulmonary vascular disorder. Indeed, COVID-19 may predispose patients to thrombotic disease in both venous and arterial circulation, and many cases of severe acute pulmonary embolism have been reported. The demonstrated presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) within the endothelial cells suggests that direct viral effects, in addition to indirect effects of perivascular inflammation and coagulopathy, may contribute to pulmonary vasculopathy in COVID-19. In this review, we discuss the pathological mechanisms leading to pulmonary vascular damage during acute infection, which appear to be mainly related to thromboembolic events, an impaired coagulation cascade, micro- and macrovascular thrombosis, endotheliitis and hypoxic pulmonary vasoconstriction. As many patients develop post-COVID symptoms, including dyspnea, we also discuss the hypothesis of pulmonary vascular damage and pulmonary hypertension as a sequela of the infection, which may be involved in the pathophysiology of long COVID.
Topics: Humans; COVID-19; SARS-CoV-2; Lung; Pulmonary Embolism; Hypertension, Pulmonary; Post-Acute COVID-19 Syndrome; Thrombosis
PubMed: 38732160
DOI: 10.3390/ijms25094941 -
Marine Drugs Dec 2020Compromised lung function is a feature of both infection driven and non-infective pathologies. Viral infections-including the current pandemic strain SARS-CoV-2-that... (Review)
Review
Compromised lung function is a feature of both infection driven and non-infective pathologies. Viral infections-including the current pandemic strain SARS-CoV-2-that affect lung function can cause both acute and long-term chronic damage. SARS-CoV-2 infection suppresses innate immunity and promotes an inflammatory response. Targeting these aspects of SARS-CoV-2 is important as the pandemic affects greater proportions of the population. In clinical and animal studies, fucoidans have been shown to increase innate immunity and decrease inflammation. In addition, dietary fucoidan has been shown to attenuate pulmonary damage in a model of acute viral infection. Direct inhibition of SARS-CoV-2 in vitro has been described, but is not universal. This short review summarizes the current research on fucoidan with regard to viral lung infections and lung damage.
Topics: Animals; COVID-19; Humans; Lung; Lung Diseases; Polysaccharides; SARS-CoV-2; Virus Diseases; COVID-19 Drug Treatment
PubMed: 33374149
DOI: 10.3390/md19010004 -
Viruses May 2020Respiratory syncytial virus (RSV) is often the first clinically relevant pathogen encountered in life, with nearly all children infected by two years of age. Many... (Review)
Review
Respiratory syncytial virus (RSV) is often the first clinically relevant pathogen encountered in life, with nearly all children infected by two years of age. Many studies have also linked early-life severe respiratory viral infection with more pathogenic immune responses later in life that lead to pulmonary diseases like childhood asthma. This phenomenon is thought to occur through long-term immune system alterations following early-life respiratory viral infection and may include local responses such as unresolved inflammation and/or direct structural or developmental modifications within the lung. Furthermore, systemic responses that could impact the bone marrow progenitors may be a significant cause of long-term alterations, through inflammatory mediators and shifts in metabolic profiles. Among these alterations may be changes in transcriptional and epigenetic programs that drive persistent modifications throughout life, leaving the immune system poised toward pathogenic responses upon secondary insult. This review will focus on early-life severe RSV infection and long-term alterations. Understanding these mechanisms will not only lead to better treatment options to limit initial RSV infection severity but also protect against the development of childhood asthma linked to severe respiratory viral infections.
Topics: Adaptive Immunity; Animals; Epigenomics; Humans; Lung; Lung Diseases; Respiratory Syncytial Virus Infections; Respiratory Syncytial Virus, Human
PubMed: 32375305
DOI: 10.3390/v12050505 -
Nature May 2021Recent studies have provided insights into the pathology of and immune response to COVID-19. However, a thorough investigation of the interplay between infected cells...
Recent studies have provided insights into the pathology of and immune response to COVID-19. However, a thorough investigation of the interplay between infected cells and the immune system at sites of infection has been lacking. Here we use high-parameter imaging mass cytometry that targets the expression of 36 proteins to investigate the cellular composition and spatial architecture of acute lung injury in humans (including injuries derived from SARS-CoV-2 infection) at single-cell resolution. These spatially resolved single-cell data unravel the disordered structure of the infected and injured lung, alongside the distribution of extensive immune infiltration. Neutrophil and macrophage infiltration are hallmarks of bacterial pneumonia and COVID-19, respectively. We provide evidence that SARS-CoV-2 infects predominantly alveolar epithelial cells and induces a localized hyperinflammatory cell state that is associated with lung damage. We leverage the temporal range of fatal outcomes of COVID-19 in relation to the onset of symptoms, which reveals increased macrophage extravasation and increased numbers of mesenchymal cells and fibroblasts concomitant with increased proximity between these cell types as the disease progresses-possibly as a result of attempts to repair the damaged lung tissue. Our data enable us to develop a biologically interpretable landscape of lung pathology from a structural, immunological and clinical standpoint. We use this landscape to characterize the pathophysiology of the human lung from its macroscopic presentation to the single-cell level, which provides an important basis for understanding COVID-19 and lung pathology in general.
Topics: Alveolar Epithelial Cells; COVID-19; Disease Progression; Humans; Inflammation; Lung; Macrophages; Neutrophils; SARS-CoV-2; Single-Cell Analysis; Time Factors; Viral Tropism
PubMed: 33780969
DOI: 10.1038/s41586-021-03475-6 -
American Journal of Physiology. Cell... Aug 2020The outbreak of COVID-19 pneumonia caused by a new coronavirus (severe acute respiratory syndrome coronavirus 2, SARS-CoV-2) is posing a global health emergency and has... (Review)
Review
The outbreak of COVID-19 pneumonia caused by a new coronavirus (severe acute respiratory syndrome coronavirus 2, SARS-CoV-2) is posing a global health emergency and has led to more than 380,000 deaths worldwide. The cell entry of SARS-CoV-2 depends on two host proteins angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). There is currently no vaccine available and also no effective drug for the treatment of COVID-19. Hydrogen sulfide (HS) as a novel gasotransmitter has been shown to protect against lung damage via its anti-inflammation, antioxidative stress, antiviral, prosurvival, and antiaging effects. In light of the research advances on HS signaling in biology and medicine, this review proposed HS as a potential defense against COVID-19. It is suggested that HS may block SARS-CoV-2 entry into host cells by interfering with ACE2 and TMPRSS2, inhibit SARS-CoV-2 replication by attenuating virus assembly/release, and protect SARS-CoV-2-induced lung damage by suppressing immune response and inflammation development. Preclinical studies and clinical trials with slow-releasing HS donor(s) or the activators of endogenous HS-generating enzymes should be considered as a preventative treatment or therapy for COVID-19.
Topics: Angiotensin-Converting Enzyme 2; Animals; Antiviral Agents; Betacoronavirus; COVID-19; Coronavirus Infections; Host-Pathogen Interactions; Humans; Hydrogen Sulfide; Lung; Pandemics; Peptidyl-Dipeptidase A; Pneumonia, Viral; SARS-CoV-2; Serine Endopeptidases; Signal Transduction; Virus Internalization; Virus Replication; COVID-19 Drug Treatment
PubMed: 32515982
DOI: 10.1152/ajpcell.00187.2020