-
Annual Review of Virology Sep 2020The seasonal cycle of respiratory viral diseases has been widely recognized for thousands of years, as annual epidemics of the common cold and influenza disease hit the... (Review)
Review
The seasonal cycle of respiratory viral diseases has been widely recognized for thousands of years, as annual epidemics of the common cold and influenza disease hit the human population like clockwork in the winter season in temperate regions. Moreover, epidemics caused by viruses such as severe acute respiratory syndrome coronavirus (SARS-CoV) and the newly emerging SARS-CoV-2 occur during the winter months. The mechanisms underlying the seasonal nature of respiratory viral infections have been examined and debated for many years. The two major contributing factors are the changes in environmental parameters and human behavior. Studies have revealed the effect of temperature and humidity on respiratory virus stability and transmission rates. More recent research highlights the importance of the environmental factors, especially temperature and humidity, in modulating host intrinsic, innate, and adaptive immune responses to viral infections in the respiratory tract. Here we review evidence of how outdoor and indoor climates are linked to the seasonality of viral respiratory infections. We further discuss determinants of host response in the seasonality of respiratory viruses by highlighting recent studies in the field.
Topics: Betacoronavirus; COVID-19; Coronavirus Infections; Humans; Humidity; Infectious Disease Incubation Period; Influenza, Human; Orthomyxoviridae; Pandemics; Picornaviridae Infections; Pneumonia, Viral; Respiratory Tract Infections; Rhinovirus; Severe acute respiratory syndrome-related coronavirus; SARS-CoV-2; Seasons; Severe Acute Respiratory Syndrome; Severity of Illness Index; Temperature
PubMed: 32196426
DOI: 10.1146/annurev-virology-012420-022445 -
Le Infezioni in MedicinaThe recent outbreak of SARS-CoV-2 that started in Wuhan, China, has now spread to several other countries and is in its exponential phase of spread. Although less... (Comparative Study)
Comparative Study Review
The recent outbreak of SARS-CoV-2 that started in Wuhan, China, has now spread to several other countries and is in its exponential phase of spread. Although less pathogenic than SARS-CoV, it has taken several lives and taken down the economies of many countries. Before this outbreak, the most recent coronavirus outbreaks were the SARS-CoV and the MERS-CoV outbreaks that happened in China and Saudi Arabia, respectively. Since the SARS-CoV-2 belongs to the same family as of SARS-CoV and MERS-CoV, they share several similarities. So, this review aims at understanding the new scenario of SARS-CoV-2 outbreak and compares the epidemiology, clinical presentations, and the genetics of these coronaviruses. Studies reveal that SARS-CoV-2 is very similar in structure and pathogenicity with SARS-CoV, but the most important structural protein, i.e., the spike protein (S), is slightly different in these viruses. The presence of a furin-like cleavage site in SARS-CoV-2 facilitates the S protein priming and might increase the efficiency of the spread of SARS-CoV-2 as compared to other beta coronaviruses. So, furin inhibitors can be targeted as potential drug therapies for SARS-CoV.
Topics: Betacoronavirus; Coronavirus Infections; Humans; Middle East Respiratory Syndrome Coronavirus; Pandemics; Severe acute respiratory syndrome-related coronavirus; SARS-CoV-2; Severe Acute Respiratory Syndrome
PubMed: 32275259
DOI: No ID Found -
Infection, Genetics and Evolution :... Nov 2020Human Coronaviruses (HCoV), periodically emerging across the world, are potential threat to humans such as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) -... (Review)
Review
Human Coronaviruses (HCoV), periodically emerging across the world, are potential threat to humans such as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) - diseases termed as COVID-19. Current SARS-CoV-2 outbreak have fueled ongoing efforts to exploit various viral target proteins for therapy, but strategies aimed at blocking the viral proteins as in drug and vaccine development have largely failed. In fact, evidence has now shown that coronaviruses undergoes rapid recombination to generate new strains of altered virulence; additionally, escaped the host antiviral defense system and target humoral immune system which further results in severe deterioration of the body such as by cytokine storm. This demands the understanding of phenotypic and genotypic classification, and pathogenesis of SARS-CoV-2 for the production of potential therapy. In lack of clear clinical evidences for the pathogenesis of COVID-19, comparative analysis of previous pandemic HCoVs associated immunological responses can provide insights into COVID-19 pathogenesis. In this review, we summarize the possible origin and transmission mode of CoVs and the current understanding on the viral genome integrity of known pandemic virus against SARS-CoV-2. We also consider the host immune response and viral evasion based on available clinical evidences which would be helpful to remodel COVID-19 pathogenesis; and hence, development of therapeutics against broad spectrum of coronaviruses.
Topics: Animals; Coronavirus Infections; Genome, Viral; Humans; Pandemics; Phylogeny; Severe acute respiratory syndrome-related coronavirus; SARS-CoV-2; Virulence
PubMed: 32798769
DOI: 10.1016/j.meegid.2020.104502 -
Nature Mar 2020Since the outbreak of severe acute respiratory syndrome (SARS) 18 years ago, a large number of SARS-related coronaviruses (SARSr-CoVs) have been discovered in their...
Since the outbreak of severe acute respiratory syndrome (SARS) 18 years ago, a large number of SARS-related coronaviruses (SARSr-CoVs) have been discovered in their natural reservoir host, bats. Previous studies have shown that some bat SARSr-CoVs have the potential to infect humans. Here we report the identification and characterization of a new coronavirus (2019-nCoV), which caused an epidemic of acute respiratory syndrome in humans in Wuhan, China. The epidemic, which started on 12 December 2019, had caused 2,794 laboratory-confirmed infections including 80 deaths by 26 January 2020. Full-length genome sequences were obtained from five patients at an early stage of the outbreak. The sequences are almost identical and share 79.6% sequence identity to SARS-CoV. Furthermore, we show that 2019-nCoV is 96% identical at the whole-genome level to a bat coronavirus. Pairwise protein sequence analysis of seven conserved non-structural proteins domains show that this virus belongs to the species of SARSr-CoV. In addition, 2019-nCoV virus isolated from the bronchoalveolar lavage fluid of a critically ill patient could be neutralized by sera from several patients. Notably, we confirmed that 2019-nCoV uses the same cell entry receptor-angiotensin converting enzyme II (ACE2)-as SARS-CoV.
Topics: Angiotensin-Converting Enzyme 2; Animals; Antibodies, Viral; Betacoronavirus; COVID-19; Cell Line; China; Chiroptera; Chlorocebus aethiops; Coronavirus Infections; Disease Outbreaks; Female; Genome, Viral; Humans; Male; Peptidyl-Dipeptidase A; Phylogeny; Pneumonia, Viral; Severe acute respiratory syndrome-related coronavirus; SARS-CoV-2; Sequence Homology, Nucleic Acid; Severe Acute Respiratory Syndrome; Vero Cells
PubMed: 32015507
DOI: 10.1038/s41586-020-2012-7 -
Nature Microbiology Apr 2020The present outbreak of a coronavirus-associated acute respiratory disease called coronavirus disease 19 (COVID-19) is the third documented spillover of an animal...
The present outbreak of a coronavirus-associated acute respiratory disease called coronavirus disease 19 (COVID-19) is the third documented spillover of an animal coronavirus to humans in only two decades that has resulted in a major epidemic. The Study Group (CSG) of the International Committee on Taxonomy of Viruses, which is responsible for developing the classification of viruses and taxon nomenclature of the family , has assessed the placement of the human pathogen, tentatively named 2019-nCoV, within the . Based on phylogeny, taxonomy and established practice, the CSG recognizes this virus as forming a sister clade to the prototype human and bat severe acute respiratory syndrome coronaviruses (SARS-CoVs) of the species , and designates it as SARS-CoV-2. In order to facilitate communication, the CSG proposes to use the following naming convention for individual isolates: SARS-CoV-2/host/location/isolate/date. While the full spectrum of clinical manifestations associated with SARS-CoV-2 infections in humans remains to be determined, the independent zoonotic transmission of SARS-CoV and SARS-CoV-2 highlights the need for studying viruses at the species level to complement research focused on individual pathogenic viruses of immediate significance. This will improve our understanding of virus–host interactions in an ever-changing environment and enhance our preparedness for future outbreaks.
Topics: Animals; Betacoronavirus; COVID-19; Classification; Coronaviridae; Coronavirus Infections; Genetic Variation; Genome, Viral; Humans; Nidovirales; Open Reading Frames; Pandemics; Phylogeny; Pneumonia, Viral; Severe acute respiratory syndrome-related coronavirus; SARS-CoV-2; Severe Acute Respiratory Syndrome; Terminology as Topic; World Health Organization; Zoonoses
PubMed: 32123347
DOI: 10.1038/s41564-020-0695-z -
Nature Reviews. Immunology Oct 2020Antibody-dependent enhancement (ADE) is a mechanism by which the pathogenesis of certain viral infections is enhanced in the presence of sub-neutralizing or... (Review)
Review
Antibody-dependent enhancement (ADE) is a mechanism by which the pathogenesis of certain viral infections is enhanced in the presence of sub-neutralizing or cross-reactive non-neutralizing antiviral antibodies. In vitro modelling of ADE has attributed enhanced pathogenesis to Fcγ receptor (FcγR)-mediated viral entry, rather than canonical viral receptor-mediated entry. However, the putative FcγR-dependent mechanisms of ADE overlap with the role of these receptors in mediating antiviral protection in various viral infections, necessitating a detailed understanding of how this diverse family of receptors functions in protection and pathogenesis. Here, we discuss the diversity of immune responses mediated upon FcγR engagement and review the available experimental evidence supporting the role of FcγRs in antiviral protection and pathogenesis through ADE. We explore FcγR engagement in the context of a range of different viral infections, including dengue virus and SARS-CoV, and consider ADE in the context of the ongoing SARS-CoV-2 pandemic.
Topics: Antibodies, Monoclonal; Antibodies, Neutralizing; Antibodies, Viral; Antibody-Dependent Enhancement; Betacoronavirus; COVID-19; Coronavirus Infections; Dengue; Dengue Virus; Gene Expression Regulation; Host-Pathogen Interactions; Humans; Leukocytes; Pandemics; Pneumonia, Viral; Receptors, IgG; Severe acute respiratory syndrome-related coronavirus; SARS-CoV-2; Severe Acute Respiratory Syndrome; Signal Transduction; Virus Internalization
PubMed: 32782358
DOI: 10.1038/s41577-020-00410-0 -
Science (New York, N.Y.) Mar 2020The outbreak of a novel coronavirus (2019-nCoV) represents a pandemic threat that has been declared a public health emergency of international concern. The CoV spike (S)...
The outbreak of a novel coronavirus (2019-nCoV) represents a pandemic threat that has been declared a public health emergency of international concern. The CoV spike (S) glycoprotein is a key target for vaccines, therapeutic antibodies, and diagnostics. To facilitate medical countermeasure development, we determined a 3.5-angstrom-resolution cryo-electron microscopy structure of the 2019-nCoV S trimer in the prefusion conformation. The predominant state of the trimer has one of the three receptor-binding domains (RBDs) rotated up in a receptor-accessible conformation. We also provide biophysical and structural evidence that the 2019-nCoV S protein binds angiotensin-converting enzyme 2 (ACE2) with higher affinity than does severe acute respiratory syndrome (SARS)-CoV S. Additionally, we tested several published SARS-CoV RBD-specific monoclonal antibodies and found that they do not have appreciable binding to 2019-nCoV S, suggesting that antibody cross-reactivity may be limited between the two RBDs. The structure of 2019-nCoV S should enable the rapid development and evaluation of medical countermeasures to address the ongoing public health crisis.
Topics: Angiotensin-Converting Enzyme 2; Antibodies, Monoclonal; Antibodies, Viral; Betacoronavirus; Cross Reactions; Cryoelectron Microscopy; Image Processing, Computer-Assisted; Models, Molecular; Peptidyl-Dipeptidase A; Protein Binding; Protein Conformation; Protein Domains; Protein Multimerization; Receptors, Coronavirus; Receptors, Virus; Severe acute respiratory syndrome-related coronavirus; SARS-CoV-2; Spike Glycoprotein, Coronavirus
PubMed: 32075877
DOI: 10.1126/science.abb2507 -
Journal of Translational Medicine Dec 2021Pulmonary fibrosis is the end stage of a broad range of heterogeneous interstitial lung diseases and more than 200 factors contribute to it. In recent years, the... (Review)
Review
Pulmonary fibrosis is the end stage of a broad range of heterogeneous interstitial lung diseases and more than 200 factors contribute to it. In recent years, the relationship between virus infection and pulmonary fibrosis is getting more and more attention, especially after the outbreak of SARS-CoV-2 in 2019, however, the mechanisms underlying the virus-induced pulmonary fibrosis are not fully understood. Here, we review the relationship between pulmonary fibrosis and several viruses such as Human T-cell leukemia virus (HTLV), Human immunodeficiency virus (HIV), Cytomegalovirus (CMV), Epstein-Barr virus (EBV), Murine γ-herpesvirus 68 (MHV-68), Influenza virus, Avian influenza virus, Middle East Respiratory Syndrome (MERS)-CoV, Severe acute respiratory syndrome (SARS)-CoV and SARS-CoV-2 as well as the mechanisms underlying the virus infection induced pulmonary fibrosis. This may shed new light on the potential targets for anti-fibrotic therapy to treat pulmonary fibrosis induced by viruses including SARS-CoV-2.
Topics: Animals; COVID-19; Epstein-Barr Virus Infections; Herpesvirus 4, Human; Humans; Mice; Pulmonary Fibrosis; Severe acute respiratory syndrome-related coronavirus; SARS-CoV-2; Virus Diseases
PubMed: 34876129
DOI: 10.1186/s12967-021-03159-9 -
Proceedings of the National Academy of... May 2020A novel severe acute respiratory syndrome (SARS)-like coronavirus (SARS-CoV-2) is causing the global coronavirus disease 2019 (COVID-19) pandemic. Understanding how...
A novel severe acute respiratory syndrome (SARS)-like coronavirus (SARS-CoV-2) is causing the global coronavirus disease 2019 (COVID-19) pandemic. Understanding how SARS-CoV-2 enters human cells is a high priority for deciphering its mystery and curbing its spread. A virus surface spike protein mediates SARS-CoV-2 entry into cells. To fulfill its function, SARS-CoV-2 spike binds to its receptor human ACE2 (hACE2) through its receptor-binding domain (RBD) and is proteolytically activated by human proteases. Here we investigated receptor binding and protease activation of SARS-CoV-2 spike using biochemical and pseudovirus entry assays. Our findings have identified key cell entry mechanisms of SARS-CoV-2. First, SARS-CoV-2 RBD has higher hACE2 binding affinity than SARS-CoV RBD, supporting efficient cell entry. Second, paradoxically, the hACE2 binding affinity of the entire SARS-CoV-2 spike is comparable to or lower than that of SARS-CoV spike, suggesting that SARS-CoV-2 RBD, albeit more potent, is less exposed than SARS-CoV RBD. Third, unlike SARS-CoV, cell entry of SARS-CoV-2 is preactivated by proprotein convertase furin, reducing its dependence on target cell proteases for entry. The high hACE2 binding affinity of the RBD, furin preactivation of the spike, and hidden RBD in the spike potentially allow SARS-CoV-2 to maintain efficient cell entry while evading immune surveillance. These features may contribute to the wide spread of the virus. Successful intervention strategies must target both the potency of SARS-CoV-2 and its evasiveness.
Topics: Angiotensin-Converting Enzyme 2; Cell Line; Humans; Immune Evasion; Peptidyl-Dipeptidase A; Protein Domains; Receptors, Coronavirus; Receptors, Virus; Severe acute respiratory syndrome-related coronavirus; Spike Glycoprotein, Coronavirus; Virus Activation; Virus Internalization
PubMed: 32376634
DOI: 10.1073/pnas.2003138117 -
Frontiers in Immunology 2020The 2019 novel coronavirus (SARS-CoV-2) pandemic has caused a global health emergency. The outbreak of this virus has raised a number of questions: What is SARS-CoV-2?... (Comparative Study)
Comparative Study Review
The 2019 novel coronavirus (SARS-CoV-2) pandemic has caused a global health emergency. The outbreak of this virus has raised a number of questions: What is SARS-CoV-2? How transmissible is SARS-CoV-2? How severely affected are patients infected with SARS-CoV-2? What are the risk factors for viral infection? What are the differences between this novel coronavirus and other coronaviruses? To answer these questions, we performed a comparative study of four pathogenic viruses that primarily attack the respiratory system and may cause death, namely, SARS-CoV-2, severe acute respiratory syndrome (SARS-CoV), Middle East respiratory syndrome (MERS-CoV), and influenza A viruses (H1N1 and H3N2 strains). This comparative study provides a critical evaluation of the origin, genomic features, transmission, and pathogenicity of these viruses. Because the coronavirus disease 2019 (COVID-19) pandemic caused by SARS-CoV-2 is ongoing, this evaluation may inform public health administrators and medical experts to aid in curbing the pandemic's progression.
Topics: Animals; Betacoronavirus; Birds; COVID-19; Coronavirus Infections; Genome, Viral; Humans; Influenza A Virus, H1N1 Subtype; Influenza A Virus, H3N2 Subtype; Influenza in Birds; Influenza, Human; Middle East Respiratory Syndrome Coronavirus; Pandemics; Pneumonia, Viral; Severe acute respiratory syndrome-related coronavirus; SARS-CoV-2; Severe Acute Respiratory Syndrome; Virulence
PubMed: 33013925
DOI: 10.3389/fimmu.2020.552909