Apoptosis in virus infection dynamics models

Fan, Ruili; Dong, Yueping; Huang, Gang; Takeuchi, Yasuhiro

doi:10.1080/17513758.2014.895433

Cited by 7 publications

(3 citation statements)

References 58 publications

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“…Our finding that disease outcome in experimental FIP infection is associated with the degree of lymphopenia is in agreement with a conclusion made by de Groot-Mijnes et al (2005), who studied experimental disease caused by the highly virulent type II FIPV-70-1146 -''Our combined observations suggest a model for FIP pathogenesis in which virus-induced T-cell depletion and the antiviral T-cell response are opposing forces and in which the efficacy of early T-cell responses critically determines the outcome of the infection.'' This conclusion has been mirrored by Fan et al (2014), who postulated that ''depending on intensity of the apoptosis of healthy cells, the apoptosis can either promote or comfort the long-term evolution of HIV infection.' ' We did not determine the lymphocyte subclasses that were most affected although the severity of the lymphocyte depletion suggested that both T and B subsets were involved.…”

Section: Discussionmentioning

confidence: 91%

Levels of feline infectious peritonitis virus in blood, effusions, and various tissues and the role of lymphopenia in disease outcome following experimental infection

Pedersen

Eckstrand

Liu

et al. 2015

Veterinary Microbiology

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Twenty specific pathogen free cats were experimentally infected with a virulent cat-passaged type I field strain of FIPV. Eighteen cats succumbed within 2-4 weeks to effusive abdominal FIP, one survived for 6 weeks, and one seroconverted without outward signs of disease. A profound drop in the absolute count of blood lymphocytes occurred around 2 weeks post-infection (p.i.) in cats with rapid disease, while the decrease was delayed in the one cat that survived for 6 weeks. The absolute lymphocyte count of the surviving cat remained within normal range. Serum antibodies as measured by indirect immunofluorescence appeared after 2 weeks p.i. and correlated with the onset of disease signs. Viral genomic RNA was either not detectable by reverse transcription quantitative real-time PCR (RT-qPCR) or detectable only at very low levels in terminal tissues not involved directly in the infection, including hepatic and renal parenchyma, cardiac muscle, lung or popliteal lymph node. High tissue virus loads were measured in severely affected tissues such as the omentum, mesenteric lymph nodes and spleen. High levels of viral genomic RNA were also detected in whole ascitic fluid, with the cellular fraction containing 10-1000 times more viral RNA than the supernatant. Replicating virus was strongly associated with macrophages by immunohistochemistry. Virus was usually detected at relatively low levels in feces and there was no evidence of enterocyte infection. Viral genomic RNA was not detected at the level of test sensitivity in whole blood, plasma, or the white cell fraction in terminal samples from the 19 cats that succumbed or in the single survivor. These studies reconfirmed the effect of lymphopenia on disease outcome. FIPV genomic RNA was also found to be highly macrophage associated within diseased tissues and effusions as determined by RT-qPCR and immunohistochemistry but was not present in blood.

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Section: Discussionmentioning

confidence: 91%

Levels of feline infectious peritonitis virus in blood, effusions, and various tissues and the role of lymphopenia in disease outcome following experimental infection

Pedersen

Eckstrand

Liu

et al. 2015

Veterinary Microbiology

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“…Guo and Ma [12] introduced a model based on Bystander apoptosis and studied its global behaviour. Fan et al [8] proposed a mathematical model which included the activation-induced apoptosis phenomenon and examined the effect of apoptosis on viral infection dynamics, with special emphasis on HIV.…”

Section: Introductionmentioning

confidence: 99%

A delayed HIV infection model with apoptosis and viral loss

Sahani

Yashi

2018

Journal of Biological Dynamics

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In this paper, a delayed human immunodeficiency virus (HIV) model with apoptosis of cells has been studied. Both immunological and intracellular delay have been incorporated to make the model more relevant. Firstly, the model has been investigated using local stability analysis. Next, the global stability analysis of steady states has been performed. The stability switch criteria taking the delay as the bifurcating parameter, leading to Hopf bifurcation has been studied. The transition of the system from order to chaos has been explored, and the analytical results have been verified by numerical simulations. The results thus can be used to describe the extensive dynamics exhibited by the model introduced in this article. The effects of apoptosis on viral load has been studied in the model numerically.

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“…HIV infects vital cells such as helper T cells, specifically CD4 + T cells, dendritic cells and macrophages in the human immune system [3]. The infection of HIV which can self-replicate leads to low levels of CD4 + T cells through a number of mechanisms, including apoptosis of uninfected bystander cells (see, e.g., [17,18,45]). The cellmediated immunity is easily inactivated, and the body becomes gradually very susceptible to opportunistic infections if CD4 + T cells fall below a critical level.…”

mentioning

confidence: 99%

Global behavior of delay differential equations model of HIV infection with apoptosis

Guo¹,

Ma²

2015

DCDS-B

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In this paper, a class of delay differential equations model of HIV infection dynamics with nonlinear transmissions and apoptosis induced by infected cells is proposed, and then the global properties of the model are considered. It shows that the infection-free equilibrium of the model is globally asymptotically stable if the basic reproduction number R 0 < 1, and globally attractive if R 0 = 1. The positive equilibrium of the model is locally asymptotically stable if R 0 > 1. Furthermore, it also shows that the model is permanent, and some explicit expressions for the eventual lower bounds of positive solutions of the model are given.

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Apoptosis in virus infection dynamics models

Cited by 7 publications

References 58 publications

Levels of feline infectious peritonitis virus in blood, effusions, and various tissues and the role of lymphopenia in disease outcome following experimental infection

Levels of feline infectious peritonitis virus in blood, effusions, and various tissues and the role of lymphopenia in disease outcome following experimental infection

A delayed HIV infection model with apoptosis and viral loss

Global behavior of delay differential equations model of HIV infection with apoptosis

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