scholarly journals Global dynamics of a delayed latent virus model with both virus-to-cell and cell-to-cell transmissions and humoral immunity

2021 ◽  
Vol 2021 (1) ◽  
Author(s):  
Hui Miao ◽  
Rong Liu ◽  
Meiyan Jiao
Keyword(s):  
Humoral Immunity ◽  
Incidence Rates ◽  
Latent Virus ◽  
Global Dynamics ◽  
Nonlinear Functions ◽  
Cell Infection ◽  
Humoral Immune ◽  
Dynamical Behaviors ◽  
Threshold Conditions ◽  
Virus Model

AbstractIn this paper, the dynamical behaviors for multiple delayed latent virus model with virus-to-cell infection and cell-to-cell transmissions and humoral immunity are investigated. The virus-to-cell and cell-to-cell incidence rates are modeled by general nonlinear functions. The basic reproduction number $R_{0}$ R 0 and the humoral immune response number $R_{1}$ R 1 are calculated and proved to be threshold conditions determining the local and global properties of the virus model. The existence of Hopf bifurcation with immune delay as a bifurcation parameter is presented, and the effects of some key parameters on viral dynamics are revealed by numerical simulations.

Dynamical behaviors of a general humoral immunity viral infection model with distributed invasion and production

2017 ◽  
Vol 10 (03) ◽  
pp. 1750035 ◽  
Author(s):  
A. M. Ełaiw ◽  
N. H. AlShamrani ◽  
K. Hattaf
Keyword(s):  
Viral Infection ◽  
Humoral Immunity ◽  
Lyapunov Functions ◽  
Dynamical Behavior ◽  
Infection Model ◽  
Global Dynamics ◽  
Nonlinear Mathematical Model ◽  
Dynamical Behaviors ◽  
Number Formula ◽  
Viral Infection Model

A general nonlinear mathematical model for the viral infection with humoral immunity and two distributed delays is proposed and analyzed. Two bifurcation parameters, the basic reproduction number, [Formula: see text] and the humoral immunity number, [Formula: see text] are derived. We established a set of conditions on the general functions which are sufficient to determine the global dynamics of the model. Utilizing Lyapunov functions and LaSalle’s invariance principle, the global asymptotic stability of all equilibria of the model is obtained. An example is presented and some numerical simulations are conducted in order to illustrate the dynamical behavior.

GLOBAL STABILITY OF A GENERAL VIRUS DYNAMICS MODEL WITH MULTI-STAGED INFECTED PROGRESSION AND HUMORAL IMMUNITY

2016 ◽  
Vol 24 (04) ◽  
pp. 535-560 ◽  
Author(s):  
A. M. ELAIW ◽  
N. H. ALSHAMRANI
Keyword(s):  
Humoral Immunity ◽  
Lyapunov Functions ◽  
Dynamical Behavior ◽  
Target Cells ◽  
Global Dynamics ◽  
Virus Dynamics ◽  
Nonlinear Functions ◽  
Dynamics Model ◽  
Number Formula ◽  
Infected Cells

In this paper, we propose an [Formula: see text]-dimensional nonlinear virus dynamics model that describes the interactions of the virus, uninfected target cells, [Formula: see text]-stages of infected cells and B cells. We assume that the incidence rate of infection, the generation and removal rates of all compartments are given by general nonlinear functions. We derive two threshold parameters, the basic reproduction number, [Formula: see text] and the humoral immunity number, [Formula: see text] and establish a set of conditions on the general functions which are sufficient to determine the global dynamics of the model. Utilizing Lyapunov functions and LaSalle’s invariance principle, the global asymptotic stability of all steady states of the model is proved. Numerical simulations are conducted for specific forms of the general functions in order to illustrate the dynamical behavior.

Humoral Immunity in Heart Failure

2019 ◽  
Vol 19 (1) ◽  
pp. 14-18 ◽  
Author(s):  
Amrita Sarkar ◽  
Khadija Rafiq
Keyword(s):  
Heart Failure ◽  
Humoral Immunity ◽  
Treatment Strategies ◽  
Pathophysiological Mechanism ◽  
Peripheral Vascular ◽  
Cardiac Inflammation ◽  
Humoral Immune ◽  
Humoral Immune System ◽  
New Treatment ◽  
Immunity Function

Cardiovascular Disease (CVD) is a class of diseases that involve disorders of heart and blood vessels, including hypertension, coronary heart disease, cerebrovascular disease, peripheral vascular disease, which finally lead to Heart Failure (HF). There are several treatments available all over the world, but still, CVD and heart failure became the number one problem causing death every year worldwide. Both experimental and clinical studies have shown a role for inflammation in the pathogenesis of heart failure. This seems related to an imbalance between pro-inflammatory and anti-inflammatory cytokines. Cardiac inflammation is a major pathophysiological mechanism operating in the failing heart, regardless of HF aetiology. Disturbances of the cellular and humoral immune system are frequently observed in heart failure. This review describes how B-cells play a specific role in the heart failure states. There is an urgent need to identify novel therapeutic targets and develop advanced therapeutic strategies to combat the syndrome of HF. Understanding and describing the elements of the humoral immunity function are essential and may suggest potential new treatment strategies.

TLR4 regulates rabies virus-induced humoral immunity through recruitment of cDC2 to lymph organs

2021 ◽  
Author(s):  
Chen Chen ◽  
Chengguang Zhang ◽  
Haoqi Li ◽  
Zongmei Wang ◽  
Yueming Yuan ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Rabies Virus ◽  
Humoral Immunity ◽  
Humoral Immune Response ◽  
Critical Role ◽  
Wild Type ◽  
Humoral Immune ◽  
Specific Igg ◽  
Molecular Patterns

Rabies, caused by rabies virus (RABV), is fatal to both humans and animals around the world. Effective clinical therapy for rabies has not been achieved, and vaccination is the most effective means of preventing and controlling rabies. Although different vaccines, such as live attenuated and inactivated vaccines, can induce different immune responses, different expression of pattern recognition receptors (PRRs) also causes diverse immune responses. Toll-like receptor 4 (TLR4) is a pivotal PRR that induces cytokine production and bridges innate and adaptive immunity. Importantly, TLR4 recognizes various virus-derived pathogen-associated molecular patterns (PAMPs) and virus-induced damage-associated molecular patterns (DAMPs), usually leading to the activation of immune cells. However, the role of TLR4 in the humoral immune response induced by RABV has not been revealed yet. Based on TLR4-deficient ( TLR4 -/- ) and wild-type (WT) mouse models, we report that TLR4-dependent recruitment of the conventional type-2 dendritic cells (CD8α - CD11b + cDC2) into secondary lymph organs (SLOs) is critical for antigen presentation. cDC2-initiated differentiation of Tfh cells promotes the proliferation of germinal centre (GC) B cells, the formation of GCs, and the production of plasma cells (PCs), all of which contribute to the production of RABV-specific IgG and virus-neutralizing antibodies (VNAs). Collectively, our work demonstrates that TLR4 is necessary for the recruitment of cDC2 and for the induction of RABV-induced humoral immunity, which is regulated by the cDC2-Tfh-GC B axis. IMPORTANCE Vaccination is the most efficient method to prevent rabies. TLR4, a well-known immune sensor, plays a critical role in initiating innate immune response. Here, we found that TLR4 deficiency ( TLR4 -/- ) mice suppressed the induction of humoral immune response after immunization with rabies virus (RABV), including reduced production of VNAs and RABV-specific IgG, compared with that occurred in wild-type (WT) mice. As a consequence, TLR4 -/- mice exhibited higher mortality than WT mice after challenge with virulent RABV. Importantly, further investigation found that TLR4 signaling promoted the recruitment of cDC2 (CD8α + CD11b - ), a subset of cDCs known to induce CD4 + T cell immunity through their MHC-II presentation machinery. Our results imply that TLR4 is indispensable for an efficient humoral response to rabies vaccine, which provides new insight into the development of novel rabies vaccines.

scholarly journals Anti–4-1bb Monoclonal Antibodies Abrogate T Cell–Dependent Humoral Immune Responses in Vivo through the Induction of Helper T Cell Anergy

1999 ◽  
Vol 190 (10) ◽  
pp. 1535-1540 ◽  
Author(s):  
Robert S. Mittler ◽  
Tina S. Bailey ◽  
Kerry Klussman ◽  
Mark D. Trailsmith ◽  
Michael K. Hoffmann
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Monoclonal Antibodies ◽  
T Cell ◽  
B Cells ◽  
Humoral Immunity ◽  
Cd8 T Cells ◽  
Immunodeficient Mice ◽  
Humoral Immune

The 4-1BB receptor (CDw137), a member of the tumor necrosis factor receptor superfamily, has been shown to costimulate the activation of T cells. Here we show that anti–mouse 4-1BB monoclonal antibodies (mAbs) inhibit thymus-dependent antibody production by B cells. Injection of anti–4-1BB mAbs into mice being immunized with cellular or soluble protein antigens induced long-term anergy of antigen-specific T cells. The immune response to the type II T cell–independent antigen trinintrophenol-conjugated Ficoll, however, was not suppressed. Inhibition of humoral immunity occurred only when anti–4-1BB mAb was given within 1 wk after immunization. Anti–4-1BB inhibition was observed in mice lacking functional CD8+ T cells, indicating that CD8+ T cells were not required for the induction of anergy. Analysis of the requirements for the anti–4-1BB–mediated inhibition of humoral immunity revealed that suppression could not be adoptively transferred with T cells from anti–4-1BB–treated mice. Transfer of BALB/c splenic T cells from sheep red blood cell (SRBC)-immunized and anti–4-1BB–treated mice together with normal BALB/c B cells into C.B-17 severe combined immunodeficient mice failed to generate an anti-SRBC response. However, B cells from the SRBC-immunized, anti–4-1BB–treated BALB/c mice, together with normal naive T cells, exhibited a normal humoral immune response against SRBC after transfer, demonstrating that SRBC-specific B cells were left unaffected by anti–4-1BB mAbs.

Global Dynamics of a Parasite-Host Model with Nonlinear Incidence Rate

2015 ◽  
Vol 25 (08) ◽  
pp. 1550102 ◽  
Author(s):  
Yilei Tang
Keyword(s):  
Incidence Rate ◽  
Global Attractor ◽  
Exponential Function ◽  
Limit Cycles ◽  
Hopf Bifurcations ◽  
Global Dynamics ◽  
Nonlinear Incidence Rate ◽  
Nonlinear Incidence ◽  
Dynamical Behaviors ◽  
Fractional Function

The paper is concerned with the effect of a nonlinear incidence rate Sp Iq on dynamical behaviors of a parasite-host model. It is shown that the global attractor of the parasite-host model is an equilibrium if q = 1, which is similar to that of the parasite-host model with a nonlinear incidence rate of the fractional function [Formula: see text]. However, when q is greater than one, more positive equilibria appear and limit cycles arise from Hopf bifurcations at the positive equilibria for the model with the incidence rate Sp Iq. It reveals that the nonlinear incidence rate of the exponential function Sp Iq for generic p and q can lead to more complicated and richer dynamics than the bilinear incidence rate or the fractional incidence rate for this model.

Efficacy of two adjuvant systems to promote humoral immunity to the pre-proghrelin peptide obestatin in pigs: consequences for the growth of piglets to weaning

2020 ◽  
Vol 60 (3) ◽  
pp. 356
Author(s):  
P. F. Geale ◽  
P. A. Sheehy ◽  
C. Giles ◽  
P. C. Thomson ◽  
P. C. Wynn
Keyword(s):  
Humoral Immunity ◽  
Feeding Behaviour ◽  
Plasma Concentrations ◽  
Significant Negative Correlation ◽  
Lactation Period ◽  
Large White ◽  
Peptide Antigens ◽  
Humoral Immune ◽  
Plasma Antibody ◽  
Antibody Titres

The poor antigenicity of peptide antigens demands the selection of effective adjuvants to induce humoral immunity. The peptides obestatin and ghrelin from the pro-hormone pre-proghrelin were initially identified as antagonistic in regulating feeding behaviour, with obestatin being suppressive. The efficacy of two adjuvant systems, DEAE with the oil polysorbate emulsion of BP85:Span80 and the surfactant-oil system Montanide (ISA 50v) were therefore assessed with an obestatin-ovalbumin conjugate injected into late pregnant sows. This enabled the supply of antibodies directed against obestatin to newborn piglets through colostrum with the objective of promoting ghrelin secretion and therefore increasing feeding behaviour. Pregnant Landrace × Large White sows (n = 28) were immunised with 0.5 mg obestatin-ovalbumin in 2 mL DEAE:BP85:Span80 (DEAE; n = 14) or with 2 mL Montanide (ISA 50v: n = 14) as adjuvants at days 91 and 105 of gestation. After farrowing, piglets remained with their mothers during the lactation period and were weighed after weaning at Day 28. Antibody titres (unitless) in colostrum were assessed by ELISA as 5543 ± 2388 and 3139 ± 1151 for the DEAE and Montanide adjuvants respectively. These were associated with total IgG of 67.7 ± 3 and 82.3 ± 4.8 mg/mL respectively (P = 0.018). Piglet plasma titres were 5100 ± 1576 and 5762 ± 1688 for DEAE and Montanide respectively at Day 5 postpartum. These titres were still detectable through to Day 28 (titres of 1213 ± 389 and 665 ± 203 respectively (P = 0.176). However, sow colostral antibody titres were not related to piglet antibody concentrations on D5 (r = –0.225, P = 0.341). Sow plasma antibody titres were not related to titres at Day 28 in piglets across treatments (r = 0.198, P = 0.402). The concentration of ghrelin in colostrum was 672 ± 78 and 666 ± 39 pg/mL for the DEAE and Montanide groups, respectively, leading to piglet plasma concentrations on Day 5 of 1105 ± 164 and 530 ± 84 pg/mL (P = 0.002). Animals grew from birthweights of 1.7 ± 0.1 and 1.8 ± 0.1 (P = 0.993) to 7.7 ± 1.2 and 7.8 ± 1.0 kg (P = 0.295) at weaning, representing growth rates of 200.5 ± 52.9 and 225.5 ± 53.4 g/day (P = 0.181). There was a significant negative correlation between piglet D28 antibody titre and growth rate to weaning with the Montanide adjuvant (r = 0.116, P = 0.035) but not for the DEAE (r = –0.118, P = 0.411). Although both adjuvants were capable of generating high antibody titres, the DEAE dextran was likely to be the most effective adjuvant to induce a humoral immune response to develop further with a commercial vaccine.

scholarly journals Stability and Hopf Bifurcation in a Computer Virus Model with Multistate Antivirus

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Tao Dong ◽  
Xiaofeng Liao ◽  
Huaqing Li
Keyword(s):  
Hopf Bifurcation ◽  
Time Delay ◽  
Computer Virus ◽  
Normal Form Theory ◽  
Center Manifold Theorem ◽  
Local Hopf Bifurcation ◽  
Dynamical Behaviors ◽  
Form Theory ◽  
Virus Model ◽  
Theoretical Results

By considering that people may immunize their computers with countermeasures in susceptible state, exposed state and using anti-virus software may take a period of time, a computer virus model with time delay based on an SEIR model is proposed. We regard time delay as bifurcating parameter to study the dynamical behaviors which include local asymptotical stability and local Hopf bifurcation. By analyzing the associated characteristic equation, Hopf bifurcation occurs when time delay passes through a sequence of critical value. The linerized model and stability of the bifurcating periodic solutions are also derived by applying the normal form theory and the center manifold theorem. Finally, an illustrative example is also given to support the theoretical results.

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