scholarly journals The immune system view of the coronavirus SARS-CoV-2

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Ivana Celardo ◽  
Luigia Pace ◽  
Loredana Cifaldi ◽  
Carlo Gaudio ◽  
Vincenzo Barnaba
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Virus Infection ◽  
Severe Acute Respiratory Syndrome ◽  
Protective Immune Response ◽  
Point Of View ◽  
Clinical Infection ◽  
System View ◽  
Host Pathogen

AbstractKnowing the “point of view” of the immune system is essential to understand the characteristic of a pandemic, such as that generated by the Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV)-2, responsible for the Coronavirus Disease (COVID)-19. In this review, we will discuss the general host/pathogen interactions dictating protective immune response or immunopathology, addressing the role of immunity or immunopathology in influencing the clinical infection outcome, and debate the potential immunoprophylactic and immunotherapy strategies required to fight the virus infection.

CORONAVIRUS: Pathology, Immunology and Therapies.

2020 ◽  
pp. 1-17
Keyword(s):  
Immune System ◽  
Virus Infection ◽  
Severe Acute Respiratory Syndrome ◽  
Effective Treatment ◽  
Common Cold ◽  
Rna Virus ◽  
Clinical Protocols ◽  
Biochemical Mechanism ◽  
The Family

Abstract Coronavirus is a family of positive single-stranded RNA virus belonging to the family of coronaviridae. Coronavirus-19 infection (COVID-19) has appeared in 2019 and so there is no effective treatment that can eradicate it. The objective of this review is to present data on cellular and molecular characteristic of virus infection and also elucidate all molecular associated events with covid-19 infection in patients. The infection in humans can cause diseases ranging from a common cold to more serious diseases such as severe acute respiratory syndrome (SARS). The disease that it transmits (Covid-19) cannot be cured with conventional treatments. However, a large number of protocols have been implemented based on the sequels that it produces. In this review we summarize 1) the role of immune system against this pathogen as well as the biochemical mechanism by which squealed is responsible for disease progression 2) the possibility or not that patients who have suffered the disease have antibodies against the virus and 3) the clinical protocols used in order to mitigate induced-damage by virus.

scholarly journals Modelling the effects of phylogeny and body size on within-host pathogen replication and immune response

2017 ◽  
Vol 14 (136) ◽  
pp. 20170479 ◽  
Author(s):  
Soumya Banerjee ◽  
Alan S. Perelson ◽  
Melanie Moses
Keyword(s):  
Infectious Disease ◽  
Immune Response ◽  
Immune System ◽  
Body Size ◽  
Zoonotic Diseases ◽  
Passerine Species ◽  
Host Pathogen ◽  
Host Phylogeny ◽  
Multiple Species

Understanding how quickly pathogens replicate and how quickly the immune system responds is important for predicting the epidemic spread of emerging pathogens. Host body size, through its correlation with metabolic rates, is theoretically predicted to impact pathogen replication rates and immune system response rates. Here, we use mathematical models of viral time courses from multiple species of birds infected by a generalist pathogen (West Nile Virus; WNV) to test more thoroughly how disease progression and immune response depend on mass and host phylogeny. We use hierarchical Bayesian models coupled with nonlinear dynamical models of disease dynamics to incorporate the hierarchical nature of host phylogeny. Our analysis suggests an important role for both host phylogeny and species mass in determining factors important for viral spread such as the basic reproductive number, WNV production rate, peak viraemia in blood and competency of a host to infect mosquitoes. Our model is based on a principled analysis and gives a quantitative prediction for key epidemiological determinants and how they vary with species mass and phylogeny. This leads to new hypotheses about the mechanisms that cause certain taxonomic groups to have higher viraemia. For example, our models suggest that higher viral burst sizes cause corvids to have higher levels of viraemia and that the cellular rate of virus production is lower in larger species. We derive a metric of competency of a host to infect disease vectors and thereby sustain the disease between hosts. This suggests that smaller passerine species are highly competent at spreading the disease compared with larger non-passerine species. Our models lend mechanistic insight into why some species (smaller passerine species) are pathogen reservoirs and some (larger non-passerine species) are potentially dead-end hosts for WNV. Our techniques give insights into the role of body mass and host phylogeny in the spread of WNV and potentially other zoonotic diseases. The major contribution of this work is a computational framework for infectious disease modelling at the within-host level that leverages data from multiple species. This is likely to be of interest to modellers of infectious diseases that jump species barriers and infect multiple species. Our method can be used to computationally determine the competency of a host to infect mosquitoes that will sustain WNV and other zoonotic diseases. We find that smaller passerine species are more competent in spreading the disease than larger non-passerine species. This suggests the role of host phylogeny as an important determinant of within-host pathogen replication. Ultimately, we view our work as an important step in linking within-host viral dynamics models to between-host models that determine spread of infectious disease between different hosts.

scholarly journals Thromboses and Hemostasis Disorders Associated with Coronavirus Disease 2019: The Possible Causal Role of Cross-Reactivity and Immunological Imprinting

2021 ◽  
Author(s):  
Darja Kanduc
Keyword(s):  
Immune System ◽  
Severe Acute Respiratory Syndrome ◽  
Natural Infection ◽  
Vascular Diseases ◽  
Cross Reactivity ◽  
Active Immunization ◽  
Thromboembolic Complications ◽  
Human Proteins ◽  
Almost All

AbstractBy examining the issue of the thromboses and hemostasis disorders associated with severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) through the lens of cross-reactivity, it was found that 60 pentapeptides are shared by SARS-CoV-2 spike glycoprotein (gp) and human proteins that— when altered, mutated, deficient or, however, improperly functioning— cause vascular diseases, thromboembolic complications, venous thrombosis, thrombocytopenia, coagulopathies, and bleeding, inter alia. The peptide commonality has a relevant immunological potential as almost all of the shared sequences are present in experimentally validated SARS-CoV-2 spike gp-derived epitopes, thus supporting the possibility of cross-reactions between the viral gp and the thromboses-related human proteins. Moreover, many of the shared peptide sequences are also present in pathogens to which individuals have previously been exposed following natural infection or vaccinal routes, and of which the immune system has stored imprint. Such an immunological memory might rapidly trigger anamnestic secondary cross-reactive responses of extreme affinity and avidity, in this way explaining the thromboembolic adverse events that can associate with SARS-CoV-2 infection or active immunization.

scholarly journals MITF induces escape from innate immunity in melanoma

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Luis Sánchez-del-Campo ◽  
Román Martí-Díaz ◽  
María F. Montenegro ◽  
Rebeca González-Guerrero ◽  
Trinidad Hernández-Caselles ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Nk Cells ◽  
Nk Cell ◽  
Luciferase Reporter ◽  
Damage Repair ◽  
Reporter Assays ◽  
Underlying Mechanisms ◽  
Nk Cytotoxicity

Abstract Background The application of immune-based therapies has revolutionized cancer treatment. Yet how the immune system responds to phenotypically heterogeneous populations within tumors is poorly understood. In melanoma, one of the major determinants of phenotypic identity is the lineage survival oncogene MITF that integrates diverse microenvironmental cues to coordinate melanoma survival, senescence bypass, differentiation, proliferation, invasion, metabolism and DNA damage repair. Whether MITF also controls the immune response is unknown. Methods By using several mouse melanoma models, we examine the potential role of MITF to modulate the anti-melanoma immune response. ChIP-seq data analysis, ChIP-qPCR, CRISPR-Cas9 genome editing, and luciferase reporter assays were utilized to identify ADAM10 as a direct MITF target gene. Western blotting, confocal microscopy, flow cytometry, and natural killer (NK) cytotoxicity assays were used to determine the underlying mechanisms by which MITF-driven phenotypic plasticity modulates melanoma NK cell-mediated killing. Results Here we show that MITF regulates expression of ADAM10, a key sheddase that cleaves the MICA/B family of ligands for NK cells. By controlling melanoma recognition by NK-cells MITF thereby controls the melanoma response to the innate immune system. Consequently, while melanoma MITFLow cells can be effectively suppressed by NK-mediated killing, MITF-expressing cells escape NK cell surveillance. Conclusion Our results reveal how modulation of MITF activity can impact the anti-melanoma immune response with implications for the application of anti-melanoma immunotherapies.

Immunotherapy: New insights in breast cancer treatment

2021 ◽  
pp. 1-10
Author(s):  
Bader Alshehri
Keyword(s):  
Breast Cancer ◽  
Immune Response ◽  
Immune System ◽  
Cancer Treatment ◽  
Immune Evasion ◽  
Breast Tumor ◽  
Parp Inhibitor ◽  
Breast Cancer Treatment ◽  
New Treatment

Breast cancer being the most malignant and lethal disease persistent among women globally. Immunotherapy as a new treatment modality has emerged in understanding the loopholes in the treatment of breast cancer which is mainly attributed to the potential of tumor cells to evade and survive the immune response by developing various strategies. Therefore, improved understanding of the immune evasion by cancer cells and the monoclonal antibodies against PD- and PD-L1 can help us in the diagnosis of this malignancy. Here in this article, I have highlighted that in addition to focusing on other strategies for breast cancer treatment, the involvement of immune system in breast cancer is vital for the understanding of this malignancy. Further, the complete involvement of immune system in the relapse or recurrence of the breast tumor and have also highlighted the role of vaccines, PD-1 and CTLA-4 with the recent advances in the field. Moreover, in addition to the application of immunotherapy as a sole therapy, combinations of immunotherapy with various strategies like targeting it with MEK inhibitors, Vaccines, chemotherapy and PARP inhibitor has shown to have significant benefits is also discussed in this article.

scholarly journals Haptoglobin and Its Related Protein, Zonulin—What Is Their Role in Spondyloarthropathy?

2021 ◽  
Vol 10 (5) ◽  
pp. 1131
Author(s):  
Magdalena Chmielińska ◽  
Marzena Olesińska ◽  
Katarzyna Romanowska-Próchnicka ◽  
Dariusz Szukiewicz
Keyword(s):  
Immune Response ◽  
Free Radicals ◽  
Immune System ◽  
Potential Role ◽  
Acute Phase Protein ◽  
Related Protein ◽  
Functional Differences ◽  
Phase Protein ◽  
Its Polymorphism

Haptoglobin (Hp) is an acute phase protein which supports the immune response and protects tissues from free radicals. Its concentration correlates with disease activity in spondyloarthropathies (SpAs). The Hp polymorphism determines the functional differences between Hp1 and Hp2 protein products. The role of the Hp polymorphism has been demonstrated in many diseases. In particular, the Hp 2-2 phenotype has been associated with the unfavorable course of some inflammatory and autoimmune disorders. Its potential role in modulating the immune system in SpA is still unknown. This article contains pathophysiological considerations on the potential relationship between Hp, its polymorphism and SpA.

Looking into a New Challenge, DKA and Covid-19 A Review on Pediatric DKA Cases during New Coronavirus Pandemic Who is to Blame, the Virus or Health System?

2021 ◽  
Vol 5 (7) ◽  
pp. 01-04
Author(s):  
Vida Tajiknia ◽  
Maryam Ghandali ◽  
Ardavan Ahmadvand ◽  
Ali Afrasiabi ◽  
Reza Pirdehghan ◽  
...  
Keyword(s):  
Immune System ◽  
Virus Infection ◽  
Pediatric Patients ◽  
Strong Association ◽  
Diabetes Type ◽  
Diabetes Type 1 ◽  
The World ◽  
Existing Data

Since the first month of this new pandemic situation, all around the world healthcare system has been facing different challenges and difficulties; patients with chronic diseases such as cancer or diabetes with impaired immune system were at greater risk of infections and complications. It goes without saying that this issue was extremely important among pediatric clinicians dealing with diabetic pediatrics. Diabetes is the number one chronic illness among pediatric patients and the most dangerous and frightened complication of it is Diabetic Ketoacidosis (DKA). Studies have shown a strong association between pandemic and increase in new diabetes type 1 cases and its lethal complication called DKA. Here we are going to take a look at existing data and report about cases with this condition trying to find the missing piece of a big puzzle; what is the role of Covid-19 in causing Diabetes in previously healthy kids and what is the real association between SARS-COV2 virus infection and DKA? We are going to review different studies, possible mechanism, new t1dm cases and old cases, with or without covid infection, DKA cases and its severity.

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