scholarly journals Why did the COVID-19 Epidemic Stop in China and does not Stop in the Rest of the World? (Application of the Two-Component Model)

2021 ◽  
Vol 3 (2) ◽  
pp. 88-99
Author(s):  
Juri Dimaschko ◽  
Vladimir Shlyakhover ◽  
Mykola Iabluchanskyi
Keyword(s):  
Innate Immunity ◽  
Adaptive Immunity ◽  
Pathogenic Strain ◽  
Spread Rate ◽  
Single Wave ◽  
Innate And Adaptive Immunity ◽  
First Case ◽  
Pathogenic Virus ◽  
Two Component ◽  
The World

The vastly different courses of the COVID-19 epidemic in China and the rest of the world are investigated and explained within two-component epidemic model. The model is based on separate accounting for the contribution to the epidemic from two types of immune response to a viral infection - innate and adaptive immunity. Any infected person becomes asymptomatic with probability (1−𝑝) or symptomatic with probability 𝑝. In the first case, innate immunity is sufficient to protect a person. In the second case, innate immunity is insufficient, and adaptive immunity comes into play. In the asymptomatic state, the person remains outwardly healthy, mobile and can spread the infection. In the symptomatic state, the person becomes ill, isolated and cannot spread the infection. We assume that the contribution to the epidemic process from asymptomatic carriers is dominant in comparison with the contribution from the usual incubation period in the symptomatic state. The key parameters of the model are the virus lifetime 𝑇 in the asymptomatic state and the spread rate 𝛽. At moderate 𝛽𝑇 values, the model describes a long, slowly decreasing morbidity plateau, which transforms into wave-like solution at 𝛽𝑇. In the case of 𝛽𝑇→∞, which corresponds to a stable non-pathogenic strain, the model solution is limited to single wave only. We believe that the spread of such a non-pathogenic strain and its subsequent dominance is responsible for ending the epidemic after the single wave of incidence in China. A way to stop the epidemic in the rest of the world may consist in displacing the circulating pathogenic virus with its stable non-pathogenic strain. Doi: 10.28991/SciMedJ-2021-0302-2 Full Text: PDF

scholarly journals Immune Status Creative Analysis in Patients after Coronary Artery Bypass Surgery (CABS) With the use of Cardiopulmonary Bypass (CPB) Machine

2020 ◽  
pp. 19-32
Author(s):  
Barsukov A.A. ◽  
Zemskov V.M. ◽  
Pronko K.N. ◽  
Kozlova M.N. ◽  
Shishkina N.S. ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Coronary Artery ◽  
Coronary Artery Bypass ◽  
Adaptive Immunity ◽  
Coronary Artery Bypass Surgery ◽  
Immune Status ◽  
Artery Bypass ◽  
Innate And Adaptive Immunity ◽  
First Case ◽  
Hla Dr

An analysis of the immune status in 53 patients that underwent coronary artery bypass grafting under cardiopulmonary bypass was carried out in the preoperative period and on day 1 and 7 after the surgical intervention. Significant changes in innate and adaptive immunity were revealed. In the first case, they were expressed as an inflammatory process developed throughout the postoperative period; it was confirmed with an increase in leukocytes, total and stab granulocytes, monocytes, oxidative stress of phagocytes, CD64+ and CD40+ granulocytes, endogenous intoxication with the developed significant deficiency in CD4+ monocytes, and regulatory NK cells; while immediately after the surgery, it was confirmed by IgG and IgM levels.Some changes in adaptive immunity manifested through its activation, confirmed by an increased CD4+, CD11b+, HLA-DR+, and CD4+CD25+lymphocyte content, together with a deficiency noted in total lymphocytes and CD8+ lymphocytes.

scholarly journals Modulation of the Complement System by Neoplastic Disease of the Central Nervous System

2021 ◽  
Vol 12 ◽  
Author(s):  
Steven K. Yarmoska ◽  
Ali M. Alawieh ◽  
Stephen Tomlinson ◽  
Kimberly B. Hoang
Keyword(s):  
Central Nervous System ◽  
Innate Immunity ◽  
Nervous System ◽  
Adaptive Immunity ◽  
Complement System ◽  
Neoplastic Disease ◽  
Innate And Adaptive Immunity ◽  
Neoplastic Diseases ◽  
The Central Nervous System ◽  
The Complement System

The complement system is a highly conserved component of innate immunity that is involved in recognizing and responding to pathogens. The system serves as a bridge between innate and adaptive immunity, and modulation of the complement system can affect the entire host immune response to a foreign insult. Neoplastic diseases have been shown to engage the complement system in order to evade the immune system, gain a selective growth advantage, and co-opt the surrounding environment for tumor proliferation. Historically, the central nervous system has been considered to be an immune-privileged environment, but it is now clear that there are active roles for both innate and adaptive immunity within the central nervous system. Much of the research on the role of immunological modulation of neoplastic disease within the central nervous system has focused on adaptive immunity, even though innate immunity still plays a critical role in the natural history of central nervous system neoplasms. Here, we review the modulation of the complement system by a variety of neoplastic diseases of the central nervous system. We also discuss gaps in the current body of knowledge and comment on future directions for investigation.

scholarly journals Simultaneous activation of innate and adaptive immunity participates in the development of renal injury in a model of heavy proteinuria

2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Viviane Dias Faustino ◽  
Simone Costa Alarcon Arias ◽  
Victor Ferreira Ávila ◽  
Orestes Foresto-Neto ◽  
Fernanda Florencia Fregnan Zambom ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Innate Immunity ◽  
Adaptive Immunity ◽  
Renal Injury ◽  
Prolonged Exposure ◽  
Interstitial Fibrosis ◽  
Innate And Adaptive Immunity ◽  
Tubular Cells ◽  
Proximal Tubular ◽  
Simultaneous Activation

Protein overload of proximal tubular cells (PTCs) can promote interstitial injury by unclear mechanisms that may involve activation of innate immunity. We investigated whether prolonged exposure of tubular cells to high protein concentrations stimulates innate immunity, triggering progressive interstitial inflammation and renal injury, and whether specific inhibition of innate or adaptive immunity would provide renoprotection in an established model of massive proteinuria, adriamycin nephropathy (ADR). Adult male Munich–Wistar rats received a single dose of ADR (5 mg/kg, iv), being followed for 2, 4, or 20 weeks. Massive albuminuria was associated with early activation of both the NF-κB and NLRP3 innate immunity pathways, whose intensity correlated strongly with the density of lymphocyte infiltration. In addition, ADR rats exhibited clear signs of renal oxidative stress. Twenty weeks after ADR administration, marked interstitial fibrosis, glomerulosclerosis, and renal functional loss were observed. Administration of mycophenolate mofetil (MMF), 10 mg/kg/day, prevented activation of both innate and adaptive immunity, as well as renal oxidative stress and renal fibrosis. Moreover, MMF treatment was associated with shifting of M from the M1 to the M2 phenotype. In cultivated NRK52-E cells, excess albumin increased the protein content of Toll-like receptor (TLR) 4 (TLR4), NLRP3, MCP-1, IL6, IL-1β, Caspase-1, α-actin, and collagen-1. Silencing of TLR4 and/or NLRP3 mRNA abrogated this proinflammatory/profibrotic behavior. Simultaneous activation of innate and adaptive immunity may be key to the development of renal injury in heavy proteinuric disease. Inhibition of specific components of innate and/or adaptive immunity may be the basis for future strategies to prevent chronic kidney disease (CKD) in this setting.

scholarly journals Innate Resistance to Babesia Infection Is Influenced by Genetic Background and Gender

2001 ◽  
Vol 69 (12) ◽  
pp. 7955-7958 ◽  
Author(s):  
Irma Aguilar-Delfin ◽  
Mary J. Homer ◽  
Peter J. Wettstein ◽  
David H. Persing
Keyword(s):  
Innate Immunity ◽  
Adaptive Immunity ◽  
Genetic Background ◽  
Acquired Immunity ◽  
Male Mice ◽  
Innate And Adaptive Immunity ◽  
Innate Resistance ◽  
Immunodeficient Mice ◽  
C3h Mice ◽  
And Gender

ABSTRACT Infection of severe combined immunodeficient mice withBabesia sp. strain WA1 was studied to assess the contributions of innate and adaptive immunity in resistance to acute babesiosis. The scid mutation showed little effect in genetically susceptible C3H mice and did not decrease the inherent resistance of C57BL/6 mice to the infection, suggesting that innate immunity plays a central role in determining the course ofBabesia infection in these strains. In contrast, thescid mutation dramatically impaired resistance in moderately susceptible BALB/c mice, suggesting that acquired immunity may play an important secondary role. In comparison to their female counterparts, male mice of different genetic backgrounds showed increased resistance to the infection, indicating that the gender of the host may influence protection against babesiosis.

scholarly journals Roles of Innate and Adaptive Immunity in Respiratory Mycoplasmosis

1998 ◽  
Vol 66 (8) ◽  
pp. 3485-3491 ◽  
Author(s):  
Samuel C. Cartner ◽  
J. Russell Lindsey ◽  
Julie Gibbs-Erwin ◽  
Gail H. Cassell ◽  
Jerry W. Simecka
Keyword(s):  
Innate Immunity ◽  
Immune Responses ◽  
Adaptive Immunity ◽  
Humoral Immunity ◽  
Lung Lesion ◽  
Scid Mice ◽  
Current Evidence ◽  
Innate And Adaptive Immunity ◽  
Lung Lesions ◽  
Multiple Organs

ABSTRACT Current evidence suggests that host defense in respiratory mycoplasmosis is dependent on both innate and humoral immunity. To further delineate the roles of innate and adaptive immunity in antimycoplasmal defenses, we intranasally infected C3H/HeSnJ-scid/scid (C3H-SCID), C3H/HeSnJ (C3H), C57BL/6J-scid/scid (C57-SCID), and C57BL/6N (C57BL) mice with Mycoplasma pulmonis and at 14 and 21 days postinfection performed quantitative cultures of lungs and spleens, quantification of lung lesions, and histopathologic assessments of all other major organs. We found that numbers of mycoplasmas in lungs were associated with genetic background (C3H susceptible, C57BL resistant) rather than functional state of adaptive immunity, indicating that innate immunity is the main contributor to antimycoplasmal defense of the lungs. Extrapulmonary dissemination of mycoplasmas with colonization of spleens and histologic lesions in multiple organs was a common occurrence in all mice. The absence of adaptive immune responses in severe combined immunodeficient (SCID) mice resulted in increased mycoplasmal colonization of spleens and lesions in extrapulmonary sites, particularly spleens, hearts, and joints, and also reduced lung lesion severity. The transfer of anti-M. pulmonis serum to infected C3H-SCID mice prevented extrapulmonary infection and disease, while the severity of lung lesions was restored by transfer of naive spleen cells to infected C3H-SCID mice. Collectively, our results strongly support the conclusions that innate immunity provides antimycoplasmal defense of the lungs and humoral immunity has the major role in defense against systemic dissemination of mycoplasmal infection, but cellular immune responses may be important in exacerbation of mycoplasmal lung disease.

scholarly journals Innate immunity and adjuvants

2011 ◽  
Vol 366 (1579) ◽  
pp. 2748-2755 ◽  
Author(s):  
Shizuo Akira
Keyword(s):  
Innate Immunity ◽  
Adaptive Immunity ◽  
Crucial Role ◽  
Paradigm Shift ◽  
Allergic Diseases ◽  
Acquired Immunity ◽  
Innate And Adaptive Immunity ◽  
Major Function ◽  
Evolutionarily Conserved ◽  
Long Time

Innate immunity was for a long time considered to be non-specific because the major function of this system is to digest pathogens and present antigens to the cells involved in acquired immunity. However, recent studies have shown that innate immunity is not non-specific, but is instead sufficiently specific to discriminate self from pathogens through evolutionarily conserved receptors, designated Toll-like receptors (TLRs). Indeed, innate immunity has a crucial role in early host defence against invading pathogens. Furthermore, TLRs were found to act as adjuvant receptors that create a bridge between innate and adaptive immunity, and to have important roles in the induction of adaptive immunity. This paradigm shift is now changing our thinking on the pathogenesis and treatment of infectious, immune and allergic diseases, as well as cancers. Besides TLRs, recent findings have revealed the presence of a cytosolic detector system for invading pathogens. I will review the mechanisms of pathogen recognition by TLRs and cytoplasmic receptors, and then discuss the roles of these receptors in the development of adaptive immunity in response to viral infection.

The wave front spread rate of Chinese ferret-badger rabies in eastern Taiwan

2021 ◽  
Vol 2 (1) ◽  
pp. 057-062
Author(s):  
Wen-Jane Tu ◽  
Satoshi Inoue ◽  
Kwong-Chung Tung ◽  
Tien-Huan Hsu ◽  
Cheng-Yao Yang ◽  
...  
Keyword(s):  
Linear Regression ◽  
Wave Front ◽  
Rabies Virus ◽  
Epidemiological Data ◽  
Simple Linear Regression ◽  
Spread Rate ◽  
First Case ◽  
The World ◽  
The Mean

This study used epidemiological data of Chinese ferret-badger (CFB) rabies in eastern Taiwan, the Hualien County, from July 2013 to December 2020 to estimate its wave front spread rate. The first case of the CFB rabies virus in eastern Taiwan was detected in Zhuoxi Township in Hualien County on July 31, 2013. Our technique regressed TIME (months elapsed from the first case in Zhuoxi and the first case in each infected township invaded by the first case of CFB rabies) on DISTANCE (kilometers between locations of the first case in Zhuoxi and centroids of each infected township invaded by the first case of CFB rabies), using simple linear regression. The mean rate of wave front spread was 10.698 kilometers/year. The correlation between TIME and DISTANCE was R = 0.9273 at p = 0.0001. As CFB rabies has only occurred in China and Taiwan, studies on its epidemiology are extremely rare. This paper is the first study to estimate the wave front spread rate of CFB rabies in the world.

scholarly journals Genetic models of latent tuberculosis in mice reveal differential control by innate and adaptive immunity

2021 ◽  
Author(s):  
Hongwei Su ◽  
Kan Lin ◽  
Divya Tiwari ◽  
Claire Healy ◽  
Carolina Trujillo ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Adaptive Immunity ◽  
High Frequency ◽  
Latent Infection ◽  
Latent Tuberculosis ◽  
Thioredoxin Reductase ◽  
Therapeutic Strategies ◽  
Innate And Adaptive Immunity ◽  
Biotin Ligase ◽  
Differential Control

AbstractStudying latent Mycobacterium tuberculosis (Mtb) infection has been limited by the lack of a suitable mouse model. We discovered that transient depletion of protein biotin ligase (BPL) and thioredoxin reductase (TrxB2) results in latent infections during which Mtb cannot be detected but that relapse in a subset of mice. The immune requirements for Mtb control during latency, and the frequency of relapse, were strikingly different depending on how latency was established. TrxB2 depletion resulted in a latent infection that required adaptive immunity for control and reactivated with high frequency, whereas latent infection after BPL depletion was dependent on innate immunity and rarely reactivated. We identified immune signatures of T cells indicative of relapse and demonstrated that BCG vaccination failed to protect mice from TB relapse. These reproducible genetic latency models allow investigating the host immunological determinants that control the latent state and offer opportunities to evaluate therapeutic strategies in settings that mimic aspects of latency and TB relapse in humans.

scholarly journals Blurring Borders: Innate Immunity with Adaptive Features

2007 ◽  
Vol 2007 ◽  
pp. 1-10 ◽  
Author(s):  
K. Kvell ◽  
EL. Cooper ◽  
P. Engelmann ◽  
J. Bovari ◽  
P. Nemeth
Keyword(s):  
Innate Immunity ◽  
Animal Models ◽  
Adaptive Immunity ◽  
Innate And Adaptive Immunity ◽  
C Elegans ◽  
Chordate Evolution ◽  
Effector Activity

Adaptive immunity has often been considered the penultimate of immune capacities. That system is now being deconstructed to encompass less stringent rules that govern its initiation, actual effector activity, and ambivalent results. Expanding the repertoire of innate immunity found in all invertebrates has greatly facilitated the relaxation of convictions concerning what actually constitutes innate and adaptive immunity. Two animal models, incidentally not on the line of chordate evolution (C. elegansandDrosophila), have contributed enormously to defining homology. The characteristics of specificity and memory and whether the antigen is pathogenic or nonpathogenic reveal considerable information on homology, thus deconstructing the more fundamentalist view. Senescence, cancer, and immunosuppression often associated with mammals that possess both innate and adaptive immunity also exist in invertebrates that only possess innate immunity. Strict definitions become blurred casting skepticism on the utility of creating rigid definitions of what innate and adaptive immunity are without considering overlaps.

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