18 results
Search Results
2. Stability of a general CTL-mediated immunity HIV infection model with silent infected cell-to-cell spread.
- Author
-
Elaiw, A. M. and AlShamrani, N. H.
- Subjects
BASIC reproduction number ,HIV infections ,CYTOTOXIC T cells ,GLOBAL asymptotic stability ,HIV - Abstract
This paper proposes and analyzes a CTL-mediated HIV infection model. The model describes the interaction between healthy CD4
+ T cells, silent infected cells, active infected cells, free HIV particles, and cytotoxic T lymphocytes (CTLs). The healthy CD4+ T cells can be infected when contacted by one of the following: (i) free HIV particles, (ii) silent infected cells, and (iii) active infected cells. The incidence rates of the healthy CD4+ T cells with free HIV particles, silent infected cells, and active infected cells are given by general functions. Moreover, the production/proliferation and removal/death rates of all compartments are represented by general functions. The model is an improvement of the existing HIV infection models which have neglected the incidence between the silent infected cells and healthy CD4+ T cells. We first show that the model is well posed. The proposed model has three equilibria and their existence is governed by derived two threshold parameters: the basic HIV reproduction number ℜ 0 and the HIV-specific CTL-mediated immunity reproduction number ℜ 1 . Under a set of conditions on the general functions and the parameters ℜ 0 and ℜ 1 , we have proven the global asymptotic stability of all equilibria by using Lyapunov method. We have illustrated the theoretical results via numerical simulations. We have studied the effect of cell-to-cell (CTC) transmission on the dynamical behavior of the system. We have shown that inclusion of CTC transmission decreases the concentration of healthy CD4+ T cells and increases the concentrations of infected cells and free HIV particles. [ABSTRACT FROM AUTHOR]- Published
- 2020
- Full Text
- View/download PDF
3. LRRK2 kinase inhibition reverses G2019S mutation-dependent effects on tau pathology progression
- Author
-
Lubben, Noah, Brynildsen, Julia K., Webb, Connor M., Li, Howard L., Leyns, Cheryl E. G., Changolkar, Lakshmi, Zhang, Bin, Meymand, Emily S., O’Reilly, Mia, Madaj, Zach, DeWeerd, Daniella, Fell, Matthew J., Lee, Virginia M. Y., Bassett, Dani S., and Henderson, Michael X.
- Published
- 2024
- Full Text
- View/download PDF
4. Analysis of a stochastic HIV-1 infection model with degenerate diffusion.
- Author
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Feng, Tao, Qiu, Zhipeng, Meng, Xinzhu, and Rong, Libin
- Subjects
- *
HIV infections , *STOCHASTIC models , *STOCHASTIC convergence , *PARAMETERS (Statistics) , *PROBABILITY theory - Abstract
Abstract This paper studies a stochastic HIV-1 infection model with degenerate diffusion. The asymptotic dynamics of the stochastic model are shown to be governed by a threshold parameter. When the parameter is negative, the infection is predicted to go extinct exponentially while the level of healthy cells converges weakly to a unique invariant measure. When the threshold parameter is positive, the solution of the stochastic model converges polynomially to a unique invariant probability measure, indicating that the system admits a unique ergodic stationary distribution. Numerical simulations are conducted to show the analytical results. These results highlight the role of environmental noise in the spread of HIV-1. The method can also be applied to the non-degenerate systems. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
5. Duck plague virus tegument protein vp22 plays a key role in the secondary envelopment and cell-to-cell spread
- Author
-
Wu, Liping, Wang, Mingshu, Cheng, Anchun, Tian, Bin, Huang, Juan, Wu, Ying, Yang, Qiao, Ou, Xumin, Sun, Di, Zhang, Shaqiu, Zhao, Xinxin, Gao, Qun, He, Yu, Zhu, Dekang, Chen, Shun, Liu, Mafeng, and Jia, Renyong
- Published
- 2023
- Full Text
- View/download PDF
6. Optimal control of an HIV infection model with logistic growth, celluar and homural immune response, cure rate and cell-to-cell spread
- Author
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Najmeh Akbari and Rasoul Asheghi
- Subjects
Logistic growth ,Cure rate ,Cellular immune response ,Humoral immune response ,Cell-to-Cell spread ,Article ,Analysis ,QA299.6-433 - Abstract
Abstract In this paper, we propose an optimal control problem for an HIV infection model with cellular and humoral immune responses, logistic growth of uninfected cells, cell-to-cell spread, saturated infection, and cure rate. The model describes the interaction between uninfected cells, infected cells, free viruses, and cellular and humoral immune responses. We use two control functions in our model to show the effectiveness of drug therapy on inhibiting virus production and preventing new infections. We apply Pontryagin maximum principle to study these two control functions. Next, we simulate the role of optimal therapy in the control of the infection by numerical simulations and AMPL software.
- Published
- 2022
- Full Text
- View/download PDF
7. Modelling the interaction of T-Cells, antigen presenting cells, and HIV-1 in vivo
- Author
-
Lou, Jie and Shao, Yiming
- Subjects
- *
T cells , *LYMPHOCYTES , *ANTIGENS , *IMMUNITY , *BIOLOGY - Abstract
Abstract: We develop and analyze a model for the interactions of T-cells, antigen presenting cells (APCs), and HIV-1. Our model consists of five components: APCs, resting helper T-cells, activated uninfected helper T-cells, activated and infected helper T-cells, and the free virus. We emphasize the impact of APCs during HIV infection and the cell-to-cell contact manner in the transference of HIV-1 in vivo. The existence and stability of the uninfected steady state and those of the infected steady states are discussed. The uniform persistence of the system is also obtained. As a novel approach, multiple exposures of HIV-1 are illustrated and discussed in the paper. Through numerical stimulations, we check the sensitivity of APCs and helper T-cells in impacting the infection outcome and obtain some relevant results. We also give the lowest infectioe dose for certain individuals. [Copyright &y& Elsevier]
- Published
- 2004
- Full Text
- View/download PDF
8. The LORF5 Gene Is Non-essential for Replication but Important for Duck Plague Virus Cell-to-Cell Spread Efficiently in Host Cells.
- Author
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Shen, Bingjie, Li, Yunjiao, Cheng, Anchun, Wang, Mingshu, Wu, Ying, Yang, Qiao, Jia, Renyong, Tian, Bin, Ou, Xumin, Mao, Sai, Sun, Di, Zhang, Shaqiu, Zhu, Dekang, Chen, Shun, Liu, Mafeng, Zhao, Xin-Xin, Huang, Juan, Gao, Qun, Liu, Yunya, and Yu, Yanling
- Subjects
BACTERIAL artificial chromosomes ,VIRAL transmission ,PLAGUE ,GENETIC recombination ,BACTERIAL genomes ,GENES ,DUCK plague - Abstract
Duck plague virus (DPV) can cause high morbidity and mortality in many waterfowl species within the order Anseriformes. The DPV genome contains 78 open reading frames (ORFs), among which the LORF2, LORF3, LORF4, LORF5, and SORF3 genes are unique genes of avian herpesvirus. In this study, to investigate the role of this unique LORF5 gene in DPV proliferation, we generated a recombinant virus that lacks the LORF5 gene by a two-step red recombination system, which cloned the DPV Chinese virulent strain (DPV CHv) genome into a bacterial artificial chromosome (DPV CHv-BAC); the proliferation law of LORF5-deleted mutant virus on DEF cells and the effect of LORF5 gene on the life cycle stages of DPV compared with the parent strain were tested. Our data revealed that the LORF5 gene contributes to the cell-to-cell transmission of DPV but is not relevant to virus invasion, replication, assembly, and release formation. Taken together, this study sheds light on the role of the avian herpesvirus-specific gene LORF5 in the DPV proliferation life cycle. These findings lay the foundation for in-depth functional studies of the LORF5 gene in DPV or other avian herpesviruses. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
9. Stability of an adaptive immunity delayed HIV infection model with active and silent cell-to-cell spread
- Author
-
A. M. Elaiw, N. H. AlShamrani, and A. D. Hobiny
- Subjects
hiv infection ,cell-to-cell spread ,intracellular delay ,global stability ,silent infected cells ,adaptive immune response ,lyapunov function ,Biotechnology ,TP248.13-248.65 ,Mathematics ,QA1-939 - Abstract
This paper investigates an adaptive immunity HIV infection model with three types of distributed time delays. The model describes the interaction between healthy CD4+T cells, silent infected cells, active infected cells, free HIV particles, Cytotoxic T lymphocytes (CTLs) and antibodies. The healthy CD4+T cells can be infected when they contacted by free HIV particles or silent infected cells or active infected cells. The incidence rates of the healthy CD4+T cells with free HIV particles, silent infected cells, and active infected cells are given by general functions. Moreover, the production/proliferation and removal/death rates of the virus and cells are represented by general functions. The model is an improvement of the existing HIV infection models which have neglected the infection due to the incidence between the silent infected cells and healthy CD4+T cells. We show that the model is well posed and it has five equilibria and their existence are governed by five threshold parameters. Under a set of conditions on the general functions and the threshold parameters, we have proven the global asymptotic stability of all equilibria by using Lyapunov method. We have illustrated the theoretical results via numerical simulations. We have studied the effect of cell-to-cell (CTC) transmission and time delays on the dynamical behavior of the system. We have shown that the inclusion of time delay can significantly increase the concentration of the healthy CD4+ T cells and reduce the concentrations of the infected cells and free HIV particles. While the inclusion of CTC transmission decreases the concentration of the healthy CD4+ T cells and increases the concentrations of the infected cells and free HIV particles.
- Published
- 2020
- Full Text
- View/download PDF
10. Stability of a general CTL-mediated immunity HIV infection model with silent infected cell-to-cell spread
- Author
-
A. M. Elaiw and N. H. AlShamrani
- Subjects
HIV infection ,Cell-to-cell spread ,Global stability ,Silent infected cells ,CTL-mediated immune response ,Lyapunov function ,Mathematics ,QA1-939 - Abstract
Abstract This paper proposes and analyzes a CTL-mediated HIV infection model. The model describes the interaction between healthy CD4+T cells, silent infected cells, active infected cells, free HIV particles, and cytotoxic T lymphocytes (CTLs). The healthy CD4+T cells can be infected when contacted by one of the following: (i) free HIV particles, (ii) silent infected cells, and (iii) active infected cells. The incidence rates of the healthy CD4+T cells with free HIV particles, silent infected cells, and active infected cells are given by general functions. Moreover, the production/proliferation and removal/death rates of all compartments are represented by general functions. The model is an improvement of the existing HIV infection models which have neglected the incidence between the silent infected cells and healthy CD4+T cells. We first show that the model is well posed. The proposed model has three equilibria and their existence is governed by derived two threshold parameters: the basic HIV reproduction number ℜ 0 $\Re _{0}$ and the HIV-specific CTL-mediated immunity reproduction number ℜ 1 $\Re _{1}$ . Under a set of conditions on the general functions and the parameters ℜ 0 $\Re _{0}$ and ℜ 1 $\Re _{1}$ , we have proven the global asymptotic stability of all equilibria by using Lyapunov method. We have illustrated the theoretical results via numerical simulations. We have studied the effect of cell-to-cell (CTC) transmission on the dynamical behavior of the system. We have shown that inclusion of CTC transmission decreases the concentration of healthy CD4+T cells and increases the concentrations of infected cells and free HIV particles.
- Published
- 2020
- Full Text
- View/download PDF
11. Stability of a general adaptive immunity HIV infection model with silent infected cell-to-cell spread.
- Author
-
AlShamrani, N.H.
- Subjects
- *
CYTOTOXIC T cells , *HIV infections , *GLOBAL asymptotic stability , *T cells , *HIV infection transmission , *IMMUNITY , *DYNAMICAL systems - Abstract
This paper proposes and analyzes an adaptive immunity HIV infection model. The model describes the interaction between healthy CD 4 + T cells, silent (latent) infected cells, active infected cells, free HIV particles, Cytotoxic T lymphocytes (CTLs) and antibodies. The healthy CD 4 + T cells can be infected when they are contacted by one of the following: (i) free HIV particles, and this is known as virus-to-cell (VTC) transmission (ii) silent infected cells, and we call this mode of infection as silent HIV-infected cell-to-cell (CTC) transmission, and (iii) active infected cells, and we call this mechanism active HIV-infected CTC transmission. The incidence rates of the healthy CD 4 + T cells with free HIV particles, silent infected cells, and active infected cells are given by general functions. Moreover, the production/proliferation and removal/death rates of all compartments are represented by general functions. The model is an improvement of the existing HIV infection models which have neglected the incidence between the silent infected cells and healthy CD 4 + T cells. We first show that the model is well-posed. Then, we show that the model has five equilibria and their existence are governed by five threshold parameters. Under a set of conditions on the general functions and the threshold parameters, we have proven the global asymptotic stability of all equilibria by using Lyapunov's method. We have illustrated the theoretical results via numerical simulations. We have studied the effect of CTC transmission on the dynamical behavior of the system. We have shown that inclusion of CTC transmission decreases the concentration of the healthy CD4 + T cells and increases the concentrations of the infected cells and free HIV particles. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
12. HCMV trimer- and pentamer-specific antibodies synergize for virus neutralization but do not correlate with congenital transmission.
- Author
-
Vanarsdall, Adam L., Chin, Andrea L., Jing Liu, Jardetzky, Theodore S., Mudd, James O., Orloff, Susan L., Streblow, Daniel, Mussi-Pinhata, Marisa M., Yamamoto, Aparecida Y., Duarte, Geraldo, Britt, William J., and Johnson, David C.
- Subjects
HUMAN cytomegalovirus ,IMMUNE response ,IMMUNOGLOBULINS ,BLOOD proteins ,IMMUNOLOGY ,EPITHELIAL cells ,CYTOMEGALOVIRUS diseases - Abstract
Human cytomegalovirus (HCMV) causes substantial disease in transplant patients and harms the development of the nervous system in babies infected in utero. Thus, there is a major focus on developing safe and effective HCMV vaccines. Evidence has been presented that a major target of neutralizing antibodies (NAbs) is the HCMV pentamer glycoprotein gH/gL/UL128-131. In some studies, most of the NAbs in animal or human sera were found to recognize the pentamer, which mediates HCMV entry into endothelial and epithelial cells. It was also reported that pentamer-specific antibodies correlate with protection against transmission from mothers to babies. One problem with the studies on pentamer-specific NAbs to date has been that the studies did not compare the pentamer to the other major form of gH/gL, the gH/gL/gO trimer, which is essential for entry into all cell types. Here, we demonstrate that both trimer and pentamer NAbs are frequently found in human transplant patients' and pregnant mothers' sera. Depletion of human sera with trimer caused reductions in NAbs similar to that observed following depletion with the pentamer. The trimer- and pentamer-specific antibodies acted in a synergistic fashion to neutralize HCMV and also to prevent virus cell-to-cell spread. Importantly, there was no correlation between the titers of trimer- and pentamer-specific NAbs and transmission of HCMV from mothers to babies. Therefore, both the trimer and pentamer are important targets of NAbs. Nevertheless, these antibodies do not protect against transmission of HCMV from mothers to babies. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
13. Hepatitis B virus: virology, molecular biology, life cycle and intrahepatic spread
- Author
-
Karayiannis, P.
- Published
- 2017
- Full Text
- View/download PDF
14. Stability of a general CTL-mediated immunity HIV infection model with silent infected cell-to-cell spread
- Author
-
Ahmed M. Elaiw and N. H. AlShamrani
- Subjects
Silent infected cells ,Cell ,Human immunodeficiency virus (HIV) ,Global stability ,medicine.disease_cause ,01 natural sciences ,Immunity ,Infected cell ,medicine ,Cytotoxic T cell ,0101 mathematics ,Mathematics ,Cell-to-cell spread ,Lyapunov function ,Algebra and Number Theory ,CTL-mediated immune response ,Functional analysis ,Applied Mathematics ,lcsh:Mathematics ,010102 general mathematics ,HIV infection ,lcsh:QA1-939 ,Virology ,010101 applied mathematics ,CTL ,medicine.anatomical_structure ,Analysis - Abstract
This paper proposes and analyzes a CTL-mediated HIV infection model. The model describes the interaction between healthy CD4+T cells, silent infected cells, active infected cells, free HIV particles, and cytotoxic T lymphocytes (CTLs). The healthy CD4+T cells can be infected when contacted by one of the following: (i) free HIV particles, (ii) silent infected cells, and (iii) active infected cells. The incidence rates of the healthy CD4+T cells with free HIV particles, silent infected cells, and active infected cells are given by general functions. Moreover, the production/proliferation and removal/death rates of all compartments are represented by general functions. The model is an improvement of the existing HIV infection models which have neglected the incidence between the silent infected cells and healthy CD4+T cells. We first show that the model is well posed. The proposed model has three equilibria and their existence is governed by derived two threshold parameters: the basic HIV reproduction number $\Re _{0}$ ℜ 0 and the HIV-specific CTL-mediated immunity reproduction number $\Re _{1}$ ℜ 1 . Under a set of conditions on the general functions and the parameters $\Re _{0}$ ℜ 0 and $\Re _{1}$ ℜ 1 , we have proven the global asymptotic stability of all equilibria by using Lyapunov method. We have illustrated the theoretical results via numerical simulations. We have studied the effect of cell-to-cell (CTC) transmission on the dynamical behavior of the system. We have shown that inclusion of CTC transmission decreases the concentration of healthy CD4+T cells and increases the concentrations of infected cells and free HIV particles.
- Published
- 2020
15. Cell entry mechanisms of HSV: what we have learned in recent years.
- Author
-
Agelidis, Alex M and Shukla, Deepak
- Abstract
HSV type-1 and -2 are widespread pathogens producing lifelong infection with multiple sequelae, including oral, ocular and genital disease. The process of herpesvirus entry is a highly complex process involving numerous viral and cellular factors. Entry begins with attachment of virus to the cell surface followed by interactions between viral glycoproteins and cellular receptors to facilitate capsid penetration. The nucleocapsid is then transported along microtubules to the nuclear membrane, where viral DNA is released for replication in the nucleus. The work reviewed here comprises the most recent advancements in our understanding of the mechanism involved in the herpesvirus entry process. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
16. Pathological consequences of systemic measles virus infection.
- Author
-
Ludlow, Martin, McQuaid, Stephen, Milner, Dan, de Swart, Rik L, and Duprex, W Paul
- Abstract
The identification of poliovirus receptor-like 4 ( PVRL4) as the second natural receptor for measles virus ( MV) has closed a major gap in our understanding of measles pathogenesis, and explains how this predominantly lymphotropic virus breaks through epithelial barriers to transmit to a susceptible host. Advances in the development of wild-type, recombinant MVs which express fluorescent proteins making infected cells readily detectable in living tissues and animals, has also increased our understanding of this important and highly transmissible human disease. Thus, it is timely to review how these advances have provided new insights into MV infection of immune, epithelial and neural cells. This demands access to primate samples that help us understand the early and acute stages of the disease, which are challenging to dissect due to the mild/self-limiting nature of the infection. It also requires well-characterized and rather rare human tissue samples from patients who succumb to neurological sequelae to help study the consequences of the long-term persistence of this RNA virus in vivo. Collectively, these studies have provided unique insights into how the use of two cellular receptors, CD150 and PVRL4, governs the in vivo tissue-specific temporal patterns of virus spread and resulting pathological lesions. Analysis of tissue samples has also demonstrated the importance of differing mechanisms of virus cell-to-cell spread within lymphoid, epithelial and neural tissues in the dissemination of MV during acute and long-term persistent infections. Given the incentive to eradicate MV globally, and the inevitable question as to whether or not vaccination should cease in light of the existence of closely related morbilliviruses, a thorough understanding of measles pathological lesions is essential. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
17. Cell-to-cell movement of viruses via plasmodesmata
- Author
-
Kumar, Dhinesh, Kumar, Ritesh, Hyun, Tae Kyung, and Kim, Jae-Yean
- Published
- 2015
- Full Text
- View/download PDF
18. Modelling the interaction of T-Cells, antigen presenting cells, and HIV-1 in vivo
- Author
-
Zhien Ma, Litao Han, Jie Lou, and Yiming Shao
- Subjects
Cell-to-cell spread ,Human immunodeficiency virus (HIV) ,uniform persistence ,medicine.disease_cause ,Virus ,Computational Mathematics ,Computational Theory and Mathematics ,In vivo ,Modelling and Simulation ,Modeling and Simulation ,Immunology ,medicine ,HIV-1 ,APCs ,Antigen-presenting cell ,Mathematics - Abstract
We develop and analyze a model for the interactions of T-cells, antigen presenting cells (APCs), and HIV-1. Our model consists of five components: APCs, resting helper T-cells, activated uninfected helper T-cells, activated and infected helper T-cells, and the free virus. We emphasize the impact of APCs during HIV infection and the cell-to-cell contact manner in the transference of HIV-1 in vivo. The existence and stability of the uninfected steady state and those of the infected steady states are discussed. The uniform persistence of the system is also obtained. As a novel approach, multiple exposures of HIV-1 are illustrated and discussed in the paper. Through numerical stimulations, we check the sensitivity of APCs and helper T-cells in impacting the infection outcome and obtain some relevant results. We also give the lowest infectioe dose for certain individuals.
- Full Text
- View/download PDF
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