scholarly journals Coronavirus Disease 2019 (COVID-19): Pathogenesis, Immune Responses, and Treatment Options

2020 ◽  
Author(s):  
Nandini Eswaran ◽  
Shwetha Krishna
Keyword(s):  
Immune Responses ◽  
Immune Evasion ◽  
Defense Mechanisms ◽  
Current Knowledge ◽  
Treatment Options ◽  
Clinical Manifestations ◽  
Evolutionary Process ◽  
Effective Vaccine ◽  
Novel Coronavirus

Background: The emergence and the spread of the novel coronavirus or the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a devastating impact on the economy and has become a pressing issue globally. Due to the significant increase in the number of confirmed cases and death tolls worldwide, and certain countries reporting second waves, there is an immediate need for an effective vaccine or other therapeutic intervention to control the spread of the disease. Improving our understanding on the host’s anti-viral immune response on SARS-CoV-2 infection, the potential immune evasion mechanisms adopted by the virus, and the speculated role of antibody dependent enhancement (ADE) in coronavirus disease 2019 (COVID-19) pathogenesis will aid in identifying and designing effective therapeutics. Aim: This review aims to provide an in-depth view of the current knowledge available on the range of host defense mechanisms activated by SARS-CoV-2 infection and various immune evasion mechanisms utilized by the virus. In addition, it also highlights the postulated role of ADE in viral pathogenesis and covers the different preventive and therapeutic options available for the treatment of COVID-19 based on current literature. Discussion: The ongoing COVID-19 pandemic serves as a timely reminder on the constant evolutionary process the virus undergoes to emerge as a novel strain and to spread undetected within the population. Similar to other infectious diseases, the host defence mechanism is triggered, and it plays a central role in dampening viral replication by recruiting immune cells and activating anti-viral mechanisms to control the spread of infection by SARS-CoV-2. However, the virus has adopted different immune evasion mechanisms to circumvent host surveillance to successfully establish infection. Hence, understanding the host’s immune responses triggered by SARS-CoV-2 infection is critical for identifying and designing novel and effective therapeutics. Currently, over 70% of the population are either asymptomatic or they showcase mild to moderate symptoms and reasons for why some people can mount immune responses more quickly than others are unknown. However, a growing body of research speculates that the ADE mechanism may facilitate the SARS-CoV-2 entry and can contribute to severe clinical manifestations. With the constant rise in the number of confirmed cases, there is an immediate need for an effective vaccine to mitigate the spread of the virus. Presently, there is no treatment for COVID-19 although several vaccine candidates are in clinical trials. Therefore, preventive measures like social distancing, isolation, and travel restrictions, may be the key to controlling the rapid spread of COVID-19.

scholarly journals SeXX and COVID-19: Tussle between the Two

2020 ◽  
Author(s):  
Ashlesh Patil ◽  
Jaya Prasad Tripathy ◽  
Vishwajit Deshmukh ◽  
Bharat Sontakke ◽  
Satyendra C. Tripathi
Keyword(s):  
Immune Responses ◽  
Current Knowledge ◽  
Occupational Exposures ◽  
Point Of View ◽  
Host Immune Responses ◽  
Social Inequities ◽  
Biological Explanation ◽  
Novel Coronavirus ◽  
Biological Differences

Novel coronavirus disease (COVID-19) has affected nearly 7 million individuals and claimed more than 0.4 million lives to date. There are several reports of gender differences related to infection and death due to COVID-19. This raises important questions such as “Whether there are differences based on gender in risk and severity of infection or mortality rate?” and “What are the biological explanation and mechanisms underlying these differences?” Emerging evidence has proposed sex-based immunological, genetic, and hormonal differences to explain this ambiguity. Besides biological differences, women have also faced social inequities and economic hardships due to this pandemic. Several recent studies have shown that independent of age males are at higher risk for severity and mortality in COVID-19 patients. Although susceptibility to SARS-CoV-2 was found to be similar across both genders in several disease cohorts, a disproportionate death ratio in men can be partly explained by the higher burden of pre-existing diseases and occupational exposures among men. From an immunological point of view, females can engage a more active immune response, which may protect them and counter infectious diseases as compared to men. This attribute of better immune responses towards pathogens is thought to be due to high estrogen levels in females. Here we review the current knowledge about sex differences in susceptibility, the severity of infection and mortality, host immune responses, and the role of sex hormones in COVID-19 disease.

scholarly journals SeXX and COVID-19: tussle between the two

2020 ◽  
Vol 90 (4) ◽  
Author(s):  
Ashlesh Patil ◽  
Jaya Prasad Tripathy ◽  
Vishwajit Deshmukh ◽  
Bharat Sontakke ◽  
Satyendra C. Tripathi
Keyword(s):  
Immune Responses ◽  
Current Knowledge ◽  
Occupational Exposures ◽  
Point Of View ◽  
Host Immune Responses ◽  
Social Inequities ◽  
Biological Explanation ◽  
Novel Coronavirus ◽  
Biological Differences

Novel coronavirus disease (COVID-19) has affected nearly 7 million individuals and claimed more than 0.4 million lives to date. There are several reports of gender differences related to infection and death due to COVID-19. This raises important questions such as “Whether there are differences based on gender in risk and severity of infection or mortality rate?” and “What are the biological explanation and mechanisms underlying these differences?” Emerging evidences have proposed sex-based immunological, genetic, and hormonal differences to explain this ambiguity. Besides biological differences, women have also faced social inequities and economic hardships due to this pandemic. Several recent studies have shown that independent of age males are at higher risk for severity and mortality in COVID-19 patients. Although susceptibility to SARS-CoV-2 was found to be similar across both genders in several disease cohorts, a disproportionate death ratio in men can be partly explained by the higher burden of pre-existing diseases and occupational exposures among men. At immunological point of view, females can engage a more active immune response, which may protect them and counter infectious diseases as compared to men. This attribute of better immune responses towards pathogens is thought to be due to high estrogen levels in females. Here we review the current knowledge about sex differences in susceptibility, the severity of infection and mortality, host immune responses, and the role of sex hormones in COVID-19 disease.

Treatment Options in COVID-19: The Role of Bioavailable Antiviral Ribonucleoside Analog on NHC in vitro

2020 ◽  
Author(s):  
Lara Bittmann
Keyword(s):  
World Health Organization ◽  
Clinical Picture ◽  
Treatment Options ◽  
World Health ◽  
Wuhan City ◽  
The World ◽  
Novel Coronavirus ◽  
Health Organization

On December 31, 2019, WHO was informed of cases of pneumonia of unknown cause in Wuhan City, China. A novel coronavirus was identified as the cause by Chinese authorities on January 7, 2020 and was provisionally named "2019-nCoV". This new Coronavirus causes a clinical picture which has received now the name COVID-19. The virus has spread subsequently worldwide and was explained on the 11th of March, 2020 by the World Health Organization to the pandemic.

scholarly journals Pathogenic Role of Immune Evasion and Integration of Human Papillomavirus in Oropharyngeal Cancer

2021 ◽  
Vol 9 (5) ◽  
pp. 891
Author(s):  
Takashi Hatano ◽  
Daisuke Sano ◽  
Hideaki Takahashi ◽  
Nobuhiko Oridate
Keyword(s):  
Human Papillomavirus ◽  
Immune Evasion ◽  
Oropharyngeal Cancer ◽  
Current Knowledge ◽  
Immune Evasion Mechanism ◽  
Cell Cycle Activation ◽  
Genome Integration ◽  
Integration Mechanisms ◽  
E6 And E7

The incidence of oropharyngeal cancer (OPC) is increasing remarkably among all head and neck cancers, mainly due to its association with the human papillomavirus (HPV). Most HPVs are eliminated by the host’s immune system; however, because HPV has developed an effective immune evasion mechanism to complete its replication cycle, a small number of HPVs are not eliminated, leading to persistent infection. Moreover, during the oncogenic process, the extrachromosomal HPV genome often becomes integrated into the host genome. Integration involves the induction and high expression of E6 and E7, leading to cell cycle activation and increased genomic instability in the host. Therefore, integration is an important event in oncogenesis, although the associated mechanism remains unclear, especially in HPV-OPC. In this review, we summarize the current knowledge on HPV-mediated carcinogenesis, with special emphasis on immune evasion and integration mechanisms, which are crucial for oncogenesis.

scholarly journals Role of PFKFB3 and PFKFB4 in Cancer: Genetic Basis, Impact on Disease Development/Progression, and Potential as Therapeutic Targets

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 909
Author(s):  
Krzysztof Kotowski ◽  
Jakub Rosik ◽  
Filip Machaj ◽  
Stanisław Supplitt ◽  
Daniel Wiczew ◽  
...  
Keyword(s):  
Current Knowledge ◽  
Treatment Options ◽  
Protein Structures ◽  
New Drugs ◽  
Proliferating Cells ◽  
Cancer Tissues ◽  
The Impact ◽  
Rate Limiting ◽  
Synthesis And Degradation

Glycolysis is a crucial metabolic process in rapidly proliferating cells such as cancer cells. Phosphofructokinase-1 (PFK-1) is a key rate-limiting enzyme of glycolysis. Its efficiency is allosterically regulated by numerous substances occurring in the cytoplasm. However, the most potent regulator of PFK-1 is fructose-2,6-bisphosphate (F-2,6-BP), the level of which is strongly associated with 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase activity (PFK-2/FBPase-2, PFKFB). PFK-2/FBPase-2 is a bifunctional enzyme responsible for F-2,6-BP synthesis and degradation. Four isozymes of PFKFB (PFKFB1, PFKFB2, PFKFB3, and PFKFB4) have been identified. Alterations in the levels of all PFK-2/FBPase-2 isozymes have been reported in different diseases. However, most recent studies have focused on an increased expression of PFKFB3 and PFKFB4 in cancer tissues and their role in carcinogenesis. In this review, we summarize our current knowledge on all PFKFB genes and protein structures, and emphasize important differences between the isoenzymes, which likely affect their kinase/phosphatase activities. The main focus is on the latest reports in this field of cancer research, and in particular the impact of PFKFB3 and PFKFB4 on tumor progression, metastasis, angiogenesis, and autophagy. We also present the most recent achievements in the development of new drugs targeting these isozymes. Finally, we discuss potential combination therapies using PFKFB3 inhibitors, which may represent important future cancer treatment options.

scholarly journals ATP Induces IL-1βSecretion inNeisseria gonorrhoeae-Infected Human Macrophages by a Mechanism Not Related to the NLRP3/ASC/Caspase-1 Axis

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Killen García ◽  
Gisselle Escobar ◽  
Pablo Mendoza ◽  
Caroll Beltran ◽  
Claudio Perez ◽  
...  
Keyword(s):  
Immune Responses ◽  
Immune Evasion ◽  
Transcriptional Activation ◽  
Pore Formation ◽  
Human Monocyte ◽  
Positive Staining ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Caspase 1

Neisseria gonorrhoeae(Ngo) has developed multiple immune evasion mechanisms involving the innate and adaptive immune responses. Recent findings have reported that Ngo reduces the IL-1βsecretion of infected human monocyte-derived macrophages (MDM). Here, we investigate the role of adenosine triphosphate (ATP) in production and release of IL-1βin Ngo-infected MDM. We found that the exposure of Ngo-infected MDM to ATP increases IL-1βlevels about ten times compared with unexposed Ngo-infected MDM (P<0.01). However, we did not observe any changes in inflammasome transcriptional activation of speck-like protein containing a caspase recruitment domain (CARD) (ASC,P>0.05) and caspase-1 (CASP1,P>0.05). In addition, ATP was not able to modify caspase-1 activity in Ngo-infected MDM but was able to increase pyroptosis (P>0.01). Notably ATP treatment defined an increase of positive staining for IL-1βwith a distinctive intracellular pattern of distribution. Collectively, these data demonstrate that ATP induces IL-1βsecretion by a mechanism not related to the NLRP3/ASC/caspase-1 axis and likely is acting at the level of vesicle trafficking or pore formation.

scholarly journals The complex functions of microRNA-150 in allergy, autoimmunity and immune tolerance

2021 ◽  
Vol 5 (4) ◽  
pp. 195-221
Author(s):  
Katarzyna Nazimek ◽  
Keyword(s):  
Immune Responses ◽  
Immune Tolerance ◽  
Therapeutic Potential ◽  
Current Knowledge ◽  
Signaling Cascades ◽  
Cell Functions ◽  
Regulatory Circuits ◽  
Complex Functions ◽  
Genetic Level

<abstract> <p>At present, special efforts are being made to develop the strategies allowing for activation of long-lasting antigen-specific immune tolerance in therapy of allergic and autoimmune diseases. Some of these therapeutic approaches are aimed at modulating cell functions at genetic level by using miRNA-based and miRNA-targeting treatments. Simultaneously, the crucial role of extracellular vesicles as natural miRNA conveyors is highlighted for induction of antigen-specific immune tolerance, especially that they appear to be easily manipulatable for therapeutic applications. Among other immune-related miRNAs, miR-150 is getting special attention as it is differently expressed by immune cells at various stages of their maturation and differentiation. In addition, miR-150 is involved in different signaling cascades orchestrating humoral and cell-mediated mechanisms of both innate and adaptive immune responses. Therefore, miR-150 is considered a master regulator of immunity in mammals. Currently, physiological miR-150-dependent regulatory circuits and causes of their malfunctioning that underlie the pathogenesis of allergic and autoimmune disorders are being unraveled. Thus, present review summarizes the current knowledge of the role of miR-150 in the pathogenesis and complications of these diseases. Furthermore, the involvement of miR-150 in regulation of immune responses to allergens and self-antigens and in induction of antigen-specific immune tolerance is discussed with the special emphasis on the therapeutic potential of this miRNA.</p> </abstract>

scholarly journals Regulatory Immune Cells in Idiopathic Pulmonary Fibrosis: Friends or Foes?

2021 ◽  
Vol 12 ◽  
Author(s):  
Chiel van Geffen ◽  
Astrid Deißler ◽  
Markus Quante ◽  
Harald Renz ◽  
Dominik Hartl ◽  
...  
Keyword(s):  
Immune System ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Immune Responses ◽  
Immune Cells ◽  
Current Knowledge ◽  
Suppressor Cells ◽  
Interstitial Lung Diseases ◽  
Stromal Stem Cells

The immune system is receiving increasing attention for interstitial lung diseases, as knowledge on its role in fibrosis development and response to therapies is expanding. Uncontrolled immune responses and unbalanced injury-inflammation-repair processes drive the initiation and progression of idiopathic pulmonary fibrosis. The regulatory immune system plays important roles in controlling pathogenic immune responses, regulating inflammation and modulating the transition of inflammation to fibrosis. This review aims to summarize and critically discuss the current knowledge on the potential role of regulatory immune cells, including mesenchymal stromal/stem cells, regulatory T cells, regulatory B cells, macrophages, dendritic cells and myeloid-derived suppressor cells in idiopathic pulmonary fibrosis. Furthermore, we review the emerging role of regulatory immune cells in anti-fibrotic therapy and lung transplantation. A comprehensive understanding of immune regulation could pave the way towards new therapeutic or preventive approaches in idiopathic pulmonary fibrosis.

Upper-Extremity Arteries

2018 ◽  
pp. 219-236
Author(s):  
Adam Zybulewski ◽  
Ilya Livshitz ◽  
Bhumika Patel ◽  
Aaron Fischman
Keyword(s):  
Upper Extremity ◽  
Upper Limb ◽  
Treatment Options ◽  
Clinical Manifestations ◽  
Limb Ischemia ◽  
Arterial Injury ◽  
Arterial Access ◽  
Imaging Characteristics ◽  
Ischemic Syndrome

This chapter evaluates the spectrum of pathologic diseases that affect the upper-extremity arteries, their clinical manifestations, imaging characteristics, and treatment options. We review the role of surgical and endovascular intervention for the treatment of acute upper limb ischemia (AULI) and chronic upper limb ischemia (CULI), the clinical and imaging findings associated with Raynaud’s phenomenon, hypothenar hammer syndrome, distal hypoperfusion ischemic syndrome (DHIS), thromboangittis obliterans (TOA), thoracic outlet syndrome (TOS), giant cell arteritis, Bechet’s disease, radiation arteritis, and traumatic arterial injury, including compartment syndrome and pseudoanuerysm formation. Finally, the evolution of upper-extremity arterial access and use of transradial access (TRA), including benefits and risks, technique, and complications, are discussed.

scholarly journals Phagocytosis: A Fundamental Process in Immunity

2017 ◽  
Vol 2017 ◽  
pp. 1-18 ◽  
Author(s):  
Carlos Rosales ◽  
Eileen Uribe-Querol
Keyword(s):  
Immune Responses ◽  
Host Response ◽  
Current Knowledge ◽  
General View ◽  
Cellular Mechanisms ◽  
Complex Process ◽  
Fundamental Process ◽  
Target Particle ◽  
Acquired Immune Responses

One hundred years have passed since the death of Élie Metchnikoff (1845–1916). He was the first to observe the uptake of particles by cells and realized the importance of this process for the host response to injury and infection. He also was a strong advocate of the role of phagocytosis in cellular immunity, and with this he gave us the basis for our modern understanding of inflammation and the innate and acquired immune responses. Phagocytosis is an elegant but complex process for the ingestion and elimination of pathogens, but it is also important for the elimination of apoptotic cells and hence fundamental for tissue homeostasis. Phagocytosis can be divided into four main steps: (i) recognition of the target particle, (ii) signaling to activate the internalization machinery, (iii) phagosome formation, and (iv) phagolysosome maturation. In recent years, the use of new tools of molecular biology and microscopy has provided new insights into the cellular mechanisms of phagocytosis. In this review, we present a general view of our current knowledge on phagocytosis. We emphasize novel molecular findings, particularly on phagosome formation and maturation, and discuss aspects that remain incompletely understood.

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