scholarly journals Semen Protects CD4+ Target Cells from HIV Infection but Promotes the Preferential Transmission of R5 Tropic HIV

2010 ◽  
Vol 185 (12) ◽  
pp. 7596-7604 ◽  
Author(s):  
Emmanuel Balandya ◽  
Siddharth Sheth ◽  
Katherine Sanders ◽  
Wendy Wieland-Alter ◽  
Timothy Lahey
Keyword(s):  
Hiv Infection ◽  
Target Cells ◽  
Preferential Transmission

scholarly journals Viral Dynamics of Acute HIV-1 Infection

1999 ◽  
Vol 190 (6) ◽  
pp. 841-850 ◽  
Author(s):  
Susan J. Little ◽  
Angela R. McLean ◽  
Celsa A. Spina ◽  
Douglas D. Richman ◽  
Diane V. Havlir
Keyword(s):  
Antiretroviral Therapy ◽  
Hiv Infection ◽  
Doubling Time ◽  
Basic Reproductive Number ◽  
Reproductive Number ◽  
Target Cells ◽  
Viral Dynamics ◽  
Acute Hiv Infection ◽  
Acute Hiv ◽  
The Mean

Viral dynamics were intensively investigated in eight patients with acute HIV infection to define the earliest rates of change in plasma HIV RNA before and after the start of antiretroviral therapy. We report the first estimates of the basic reproductive number (R0), the number of cells infected by the progeny of an infected cell during its lifetime when target cells are not depleted. The mean initial viral doubling time was 10 h, and the peak of viremia occurred 21 d after reported HIV exposure. The spontaneous rate of decline (α) was highly variable among individuals. The phase 1 viral decay rate (δI = 0.3/day) in subjects initiating potent antiretroviral therapy during acute HIV infection was similar to estimates from treated subjects with chronic HIV infection. The doubling time in two subjects who discontinued antiretroviral therapy was almost five times slower than during acute infection. The mean basic reproductive number (R0) of 19.3 during the logarithmic growth phase of primary HIV infection suggested that a vaccine or postexposure prophylaxis of at least 95% efficacy would be needed to extinguish productive viral infection in the absence of drug resistance or viral latency. These measurements provide a basis for comparison of vaccine and other strategies and support the validity of the simian immunodeficiency virus macaque model of acute HIV infection.

Asymptotic Analysis of an Age-Structured HIV Infection Model with Logistic Target-Cell Growth and Two Infecting Routes

2020 ◽  
Vol 30 (04) ◽  
pp. 2050059
Author(s):  
Dongxue Yan ◽  
Xianlong Fu
Keyword(s):  
Steady State ◽  
Hiv Infection ◽  
Logistic Growth ◽  
Infection Model ◽  
Target Cells ◽  
Cell Infection ◽  
Numerical Examples ◽  
Distribution Of Eigenvalues ◽  
Age Structured ◽  
Hiv Infection Model

This paper deals with an age-structured HIV infection model with logistic growth for target cells and both virus-to-cell and cell-to-cell infection routes. Based on the existence of the infection-free and infection equilibria and some rigorous analyses for the considered model, we study the asymptotic stability of these equilibria via determining the distribution of eigenvalues. We also address the persistence of the solution semi-flow by proving the existence of a global attractor. Furthermore, Hopf bifurcation occurring at the positive steady state is exploited. At last, some numerical examples are provided to illustrate the obtained results.

scholarly journals Global Dynamics of an HIV Infection Model with Two Classes of Target Cells and Distributed Delays

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
A. M. Elaiw
Keyword(s):  
T Cells ◽  
Steady State ◽  
Hiv Infection ◽  
Infection Model ◽  
Target Cells ◽  
Global Dynamics ◽  
Asymptotically Stable ◽  
Globally Asymptotically Stable ◽  
Hiv Infection Model ◽  
Nonlinear Delay

We investigate the global dynamics of an HIV infection model with two classes of target cells and multiple distributed intracellular delays. The model is a 5-dimensional nonlinear delay ODEs that describes the interaction of the HIV with two classes of target cells, CD4+T cells and macrophages. The incidence rate of infection is given by saturation functional response. The model has two types of distributed time delays describing time needed for infection of target cell and virus replication. This model can be seen as a generalization of several models given in the literature describing the interaction of the HIV with one class of target cells, CD4+T cells. Lyapunov functionals are constructed to establish the global asymptotic stability of the uninfected and infected steady states of the model. We have proven that if the basic reproduction numberR0is less than unity then the uninfected steady state is globally asymptotically stable, and ifR0>1then the infected steady state exists and it is globally asymptotically stable.

Global properties of a cell mediated immunity in HIV infection model with two classes of target cells and distributed delays

2014 ◽  
Vol 07 (05) ◽  
pp. 1450055 ◽  
Author(s):  
A. M. Elaiw ◽  
R. M. Abukwaik ◽  
E. O. Alzahrani
Keyword(s):  
Immune Response ◽  
Steady State ◽  
Hiv Infection ◽  
Infection Model ◽  
Target Cells ◽  
Cell Mediated Immunity ◽  
Globally Asymptotically Stable ◽  
Global Properties ◽  
Hiv Infection Model ◽  
Ctl Immune Response

In this paper, we study the global properties of a human immunodeficiency virus (HIV) infection model with cytotoxic T lymphocytes (CTL) immune response. The model is a six-dimensional that describes the interaction of the HIV with two classes of target cells, CD4+ T cells and macrophages. The infection rate is given by saturation functional response. Two types of distributed time delays are incorporated into the model to describe the time needed for infection of target cell and virus replication. Using the method of Lyapunov functional, we have established that the global stability of the model is determined by two threshold numbers, the basic infection reproduction number R0 and the immune response activation number [Formula: see text]. We have proven that if R0 ≤ 1, then the uninfected steady state is globally asymptotically stable (GAS), if [Formula: see text], then the infected steady state without CTL immune response is GAS, and if [Formula: see text], then the infected steady state with CTL immune response is GAS.

Enhancing antibodies in HIV infection

Parasitology ◽  
1997 ◽  
Vol 115 (7) ◽  
pp. 127-140 ◽  
Author(s):  
G. FÜST
Keyword(s):  
Hiv Infection ◽  
Clinical Significance ◽  
Target Cells ◽  
Complement Receptor ◽  
Hiv Disease ◽  
Cross Sectional ◽  
Antibody Dependent Enhancement ◽  
Hiv 1

The author has summarized the history of discovery, the mechanism and the clinical significance of antibody-dependent enhancement (ADE) of HIV infection. ADE has two major forms: (a) complement-mediated antibody-dependent enhancement (C-ADE) and (b) complement-independent Fc receptor-dependent ADE (FcR-ADE). The most important epitope responsible for the development of C-ADE-mediating antibodies is present in the immunodominant region of gp41 while antibodies mediating FcR-ADE react mainly with V3 loop of gp120. There are at least three fundamentally different hypotheses for the explanation of ADE in vitro: (a) increased adhesion of HIV-antibody-(complement) complexes to FcR or complement receptor carrying cells; (b) facilitation of HIV-target cell fusion by complement fragment deposited on the HIV-virions and (c) complement activation products may have a non-specific stimulatory effect on target cells resulting in enhanced virus production. FcR-ADE and C-ADE have been measured in vitro mostly by using FcR-carrying and complement receptor-carrying cell lines, respectively; no efforts have been made to standardize these methods. Several data support the possible clinical significance of FcR-ADE and C-ADE: (a) Cross-sectional and longitudinal studies indicate a correlation between the amounts of FcR-ADE and C-ADE-mediating antibodies and clinical, immunological and virological progression of the HIV-disease; (b) ADE may facilitate maternal–infant HIV-1 transmission; (c) According to experiments in animal models, ADE are present and may modify the course of SIV (simian immunodeficiency) infection as well. The author raises a new hypothesis on the mechanism of the in vivo effect of C-ADE. According to the hypothesis, C-ADE-mediating antibodies exert their effect through enhancement of HIV propagation and consequent facilitation of the progression of HIV disease. Finally, according to observations from animal experiments and human clinical trials it cannot be excluded that ADE-mediating antibodies may develop, diminish the beneficial effect or may be harmful in volunteers vaccinated with HIV-1 candidate vaccines.

scholarly journals The Cationic Properties of SEVI Underlie Its Ability To Enhance Human Immunodeficiency Virus Infection

2008 ◽  
Vol 83 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Nadia R. Roan ◽  
Jan Münch ◽  
Nathalie Arhel ◽  
Walther Mothes ◽  
Jason Neidleman ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Viral Infection ◽  
Amyloid Fibrils ◽  
Underlying Mechanism ◽  
Target Cells ◽  
Mutant Form ◽  
Immunodeficiency Virus ◽  
Microbicide Development ◽  
Future Direction

ABSTRACT Human semen contains peptides capable of forming amyloid fibrils termed semen-derived enhancer of viral infection (SEVI) that can greatly increase human immunodeficiency virus (HIV) infection. While SEVI appears to enhance virion attachment to target cells, its underlying mechanism of action is unknown. We now demonstrate that the intrinsic positive charges of SEVI (pI = 10.21) facilitate virion attachment to and fusion with target cells. A mutant form of SEVI in which lysines and arginines are replaced with alanines retains the ability to form amyloid fibrils but is defective in binding virions and enhancing infection. In addition, the interaction of wild-type SEVI with virions and the ability of these fibrils to increase infection are abrogated in the presence of various polyanionic compounds. These anionic polymers also decrease the enhancement of HIV infection mediated by semen. These findings suggest that SEVI enhances viral infection by serving as a polycationic bridge that neutralizes the negative charge repulsion that exists between HIV virions and target cells. Combinations of agents that neutrale SEVI action and produce HIV virucidal effects are an attractive future direction for microbicide development.

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