Humoral Immunity

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Fucheng Liao - One of the best experts on this subject based on the ideXlab platform.

  • stability and hopf bifurcation for a virus infection model with delayed Humoral Immunity response
    Journal of Mathematical Analysis and Applications, 2014
    Co-Authors: Tianlei Wang, Zhixing Hu, Fucheng Liao
    Abstract:

    Abstract In this paper, we investigate the dynamical behavior of a virus infection model with delayed Humoral Immunity. By using suitable Lyapunov functional and the LaSalleʼs invariance principle, we establish the global stabilities of the two boundary equilibria. If R 0 1 , the uninfected equilibrium E 0 is globally asymptotically stable; if R 1 1 R 0 , the infected equilibrium without Immunity E 1 is globally asymptotically stable. When R 1 > 1 , we obtain the sufficient conditions to the local stability of the infected equilibrium with Immunity E 2 . The time delay can change the stability of E 2 and lead to the existence of Hopf bifurcations. The stabilities of bifurcating periodic solutions is also studied. We check our theorems with numerical simulations in the end.

  • global stability analysis for delayed virus infection model with general incidence rate and Humoral Immunity
    Mathematics and Computers in Simulation, 2013
    Co-Authors: Tianlei Wang, Zhixing Hu, Fucheng Liao
    Abstract:

    In this paper, we investigate the dynamical behavior of a virus infection model with general incidence rate and Humoral Immunity. By using suitable Lyapunov functional and the LaSalle's invariance principle, we establish the global stability of the three equilibria. The uninfected equilibrium E0 is globally asymptotically stable if R0≤1, the infected equilibrium without Immunity E1 is globally asymptotically stable if R1≤1 and R0>1, the infected equilibrium with Humoral Immunity E2 is globally asymptotically stable if R1>1. We check our theorems with numerical simulation in the end.

John Chan - One of the best experts on this subject based on the ideXlab platform.

  • the role of b cells and Humoral Immunity in mycobacterium tuberculosis infection
    Seminars in Immunology, 2014
    Co-Authors: John Chan, Arturo Casadevall, Simren Mehta, Sushma Bharrhan, Yong Chen, Jacqueline M Achkar, Joanne L Flynn
    Abstract:

    Mycobacterium tuberculosis remains a major public health burden. It is generally thought that while B cell- and antibody-mediated Immunity plays an important role in host defense against extracellular pathogens, the primary control of intracellular microbes derives from cellular immune mechanisms. Studies on the immune regulatory mechanisms during infection with M. tuberculosis, a facultative intracellular organism, has established the importance of cell-mediated Immunity in host defense during tuberculous infection. Emerging evidence suggest a role for B cell and Humoral Immunity in the control of intracellular pathogens, including obligatory species, through interactions with the cell-mediated immune compartment. Recent studies have shown that B cells and antibodies can significantly impact on the development of immune responses to the tubercle bacillus. In this review, we present experimental evidence supporting the notion that the importance of Humoral and cellular Immunity in host defense may not be entirely determined by the niche of the pathogen. A comprehensive approach that examines both Humoral and cellular Immunity could lead to better understanding of the immune response to M. tuberculosis.

  • the role of b cells and Humoral Immunity in mycobacterium tuberculosis infection
    Advances in Experimental Medicine and Biology, 2013
    Co-Authors: Lee Kozakiewicz, Jiayao Phuah, Joanne L Flynn, John Chan
    Abstract:

    Tuberculosis (TB) remains a serious threat to public health, causing 2 million deaths annually world-wide. The control of TB has been hindered by the requirement of long duration of treatment involving multiple chemotherapeutic agents, the increased susceptibility to Mycobacterium tuberculosis infection in the HIV-infected population, and the development of multi-drug resistant and extensively resistant strains of tubercle bacilli. An efficacious and cost-efficient way to control TB is the development of effective anti-TB vaccines. This measure requires thorough understanding of the immune response to M. tuberculosis. While the role of cell-mediated Immunity in the development of protective immune response to the tubercle bacillus has been well established, the role of B cells in this process is not clearly understood. Emerging evidence suggests that B cells and Humoral Immunity can modulate the immune response to various intracellular pathogens, including M. tuberculosis. These lymphocytes form conspicuous aggregates in the lungs of tuberculous humans, non-human primates, and mice, which display features of germinal center B cells. In murine TB, it has been shown that B cells can regulate the level of granulomatous reaction, cytokine production, and the T cell response. This chapter discusses the potential mechanisms by which specific functions of B cells and Humoral Immunity can shape the immune response to intracellular pathogens in general, and to M. tuberculosis in particular. Knowledge of the B cell-mediated immune response to M. tuberculosis may lead to the design of novel strategies, including the development of effective vaccines, to better control TB.

Hanneke Schuitemaker - One of the best experts on this subject based on the ideXlab platform.

  • cross reactive neutralizing Humoral Immunity does not protect from hiv type 1 disease progression
    The Journal of Infectious Diseases, 2010
    Co-Authors: Zelda Euler, Marit J. Van Gils, Evelien M. Bunnik, Becky Schweighardt, Terri Wrin, Pham Phung, Hanneke Schuitemaker
    Abstract:

    : Broadly reactive neutralizing antibodies are the focus of human immunodeficiency virus (HIV) type 1 vaccine design. However, only little is known about their role in acquired immunodeficiency syndrome (AIDS) pathogenesis and the factors associated with their development. Here we used a multisubtype panel of 23 HIV-1 variants to determine the prevalence of cross-reactive neutralizing activity in serum samples obtained approximately 35 months after seroconversion from 82 HIV-1 subtype B-infected participants from the Amsterdam Cohort Studies on HIV Infection and AIDS. Of these patients, 33%, 48%, and 20%, respectively, had strong, moderate, or absent cross-reactive neutralizing activity in serum. Viral RNA load at set point and AIDS-free survival were similar for the 3 patient groups. However, higher cross-reactive neutralizing activity was significantly associated with lower CD4(+) T cell counts before and soon after infection. Our findings underscore the importance of vaccine-elicited Immunity in protecting from infection. The association between CD4(+) T cell counts and neutralizing Humoral Immunity may provide new clues as to how to achieve this goal.

  • Rapid Escape from Preserved Cross-Reactive Neutralizing Humoral Immunity without Loss of Viral Fitness in HIV-1-Infected Progressors and Long-Term Nonprogressors
    Journal of Virology, 2010
    Co-Authors: Marit J. Van Gils, Evelien M. Bunnik, Judith A. Burger, Yodit Jacob, Becky Schweighardt, Terri Wrin, Hanneke Schuitemaker
    Abstract:

    A substantial proportion of human immunodeficiency virus type 1 (HIV-1)-infected individuals has cross-reactive neutralizing activity in serum, with a similar prevalence in progressors and long-term nonprogressors (LTNP). We studied whether disease progression in the face of cross-reactive neutralizing serum activity is due to fading neutralizing Humoral Immunity over time or to viral escape. In three LTNP and three progressors, high-titer cross-reactive HIV-1-specific neutralizing activity in serum against a multiclade pseudovirus panel was preserved during the entire clinical course of infection, even after AIDS diagnosis in progressors. However, while early HIV-1 variants from all six individuals could be neutralized by autologous serum, the autologous neutralizing activity declined during chronic infection. This could be attributed to viral escape and the apparent inability of the host to elicit neutralizing antibodies to the newly emerging viral escape variants. Escape from autologous neutralizing activity was not associated with a reduction in the viral replication rate in vitro. Escape from autologous serum with cross-reactive neutralizing activity coincided with an increase in the length of the variable loops and in the number of potential N-linked glycosylation sites in the viral envelope. Positive selection pressure was observed in the variable regions in envelope, suggesting that, at least in these individuals, these regions are targeted by Humoral Immunity with cross-reactive potential. Our results may imply that the ability of HIV-1 to rapidly escape cross-reactive autologous neutralizing antibody responses without the loss of viral fitness is the underlying explanation for the absent effect of potent cross-reactive neutralizing Humoral Immunity on the clinical course of infection.

  • autologous neutralizing Humoral Immunity and evolution of the viral envelope in the course of subtype b human immunodeficiency virus type 1 infection
    Journal of Virology, 2008
    Co-Authors: Evelien M. Bunnik, Linaida Pisas, Ad C Van Nuenen, Hanneke Schuitemaker
    Abstract:

    Most human immunodeficiency virus type 1 (HIV-1)-infected individuals develop an HIV-specific neutralizing antibody (NAb) response that selects for escape variants of the virus. Here, we studied autologous NAb responses in five typical CCR5-using progressors in relation to viral NAb escape and molecular changes in the viral envelope (Env) in the period from seroconversion until after AIDS diagnosis. In sera from three patients, high-titer neutralizing activity was observed against the earliest autologous virus variants, followed by declining Humoral immune responses against subsequent viral escape variants. Autologous neutralizing activity was undetectable in sera from two patients. Patients with high-titer neutralizing activity in serum showed the strongest positive selection pressure on Env early in infection. In the initial phase of infection, gp160 length and the number of potential N-linked glycosylation sites (PNGS) increased in viruses from all patients. Over the course of infection, positive selection pressure declined as the NAb response subsided, coinciding with reversions of changes in gp160 length and the number of PNGS. A number of identical amino acid changes were observed over the course of infection in the viral quasispecies of different patients. Our results indicate that although neutralizing autologous Humoral Immunity may have a limited effect on the disease course, it is an important selection pressure in virus evolution early in infection, while declining HIV-specific Humoral Immunity in later stages may coincide with reversion of NAb-driven changes in Env.

Joanne L Flynn - One of the best experts on this subject based on the ideXlab platform.

  • the role of b cells and Humoral Immunity in mycobacterium tuberculosis infection
    Seminars in Immunology, 2014
    Co-Authors: John Chan, Arturo Casadevall, Simren Mehta, Sushma Bharrhan, Yong Chen, Jacqueline M Achkar, Joanne L Flynn
    Abstract:

    Mycobacterium tuberculosis remains a major public health burden. It is generally thought that while B cell- and antibody-mediated Immunity plays an important role in host defense against extracellular pathogens, the primary control of intracellular microbes derives from cellular immune mechanisms. Studies on the immune regulatory mechanisms during infection with M. tuberculosis, a facultative intracellular organism, has established the importance of cell-mediated Immunity in host defense during tuberculous infection. Emerging evidence suggest a role for B cell and Humoral Immunity in the control of intracellular pathogens, including obligatory species, through interactions with the cell-mediated immune compartment. Recent studies have shown that B cells and antibodies can significantly impact on the development of immune responses to the tubercle bacillus. In this review, we present experimental evidence supporting the notion that the importance of Humoral and cellular Immunity in host defense may not be entirely determined by the niche of the pathogen. A comprehensive approach that examines both Humoral and cellular Immunity could lead to better understanding of the immune response to M. tuberculosis.

  • the role of b cells and Humoral Immunity in mycobacterium tuberculosis infection
    Advances in Experimental Medicine and Biology, 2013
    Co-Authors: Lee Kozakiewicz, Jiayao Phuah, Joanne L Flynn, John Chan
    Abstract:

    Tuberculosis (TB) remains a serious threat to public health, causing 2 million deaths annually world-wide. The control of TB has been hindered by the requirement of long duration of treatment involving multiple chemotherapeutic agents, the increased susceptibility to Mycobacterium tuberculosis infection in the HIV-infected population, and the development of multi-drug resistant and extensively resistant strains of tubercle bacilli. An efficacious and cost-efficient way to control TB is the development of effective anti-TB vaccines. This measure requires thorough understanding of the immune response to M. tuberculosis. While the role of cell-mediated Immunity in the development of protective immune response to the tubercle bacillus has been well established, the role of B cells in this process is not clearly understood. Emerging evidence suggests that B cells and Humoral Immunity can modulate the immune response to various intracellular pathogens, including M. tuberculosis. These lymphocytes form conspicuous aggregates in the lungs of tuberculous humans, non-human primates, and mice, which display features of germinal center B cells. In murine TB, it has been shown that B cells can regulate the level of granulomatous reaction, cytokine production, and the T cell response. This chapter discusses the potential mechanisms by which specific functions of B cells and Humoral Immunity can shape the immune response to intracellular pathogens in general, and to M. tuberculosis in particular. Knowledge of the B cell-mediated immune response to M. tuberculosis may lead to the design of novel strategies, including the development of effective vaccines, to better control TB.

Tianlei Wang - One of the best experts on this subject based on the ideXlab platform.

  • stability and hopf bifurcation for a virus infection model with delayed Humoral Immunity response
    Journal of Mathematical Analysis and Applications, 2014
    Co-Authors: Tianlei Wang, Zhixing Hu, Fucheng Liao
    Abstract:

    Abstract In this paper, we investigate the dynamical behavior of a virus infection model with delayed Humoral Immunity. By using suitable Lyapunov functional and the LaSalleʼs invariance principle, we establish the global stabilities of the two boundary equilibria. If R 0 1 , the uninfected equilibrium E 0 is globally asymptotically stable; if R 1 1 R 0 , the infected equilibrium without Immunity E 1 is globally asymptotically stable. When R 1 > 1 , we obtain the sufficient conditions to the local stability of the infected equilibrium with Immunity E 2 . The time delay can change the stability of E 2 and lead to the existence of Hopf bifurcations. The stabilities of bifurcating periodic solutions is also studied. We check our theorems with numerical simulations in the end.

  • global stability analysis for delayed virus infection model with general incidence rate and Humoral Immunity
    Mathematics and Computers in Simulation, 2013
    Co-Authors: Tianlei Wang, Zhixing Hu, Fucheng Liao
    Abstract:

    In this paper, we investigate the dynamical behavior of a virus infection model with general incidence rate and Humoral Immunity. By using suitable Lyapunov functional and the LaSalle's invariance principle, we establish the global stability of the three equilibria. The uninfected equilibrium E0 is globally asymptotically stable if R0≤1, the infected equilibrium without Immunity E1 is globally asymptotically stable if R1≤1 and R0>1, the infected equilibrium with Humoral Immunity E2 is globally asymptotically stable if R1>1. We check our theorems with numerical simulation in the end.