Fighting a virus with a virus: a dynamic model for HIV-1 therapy

Revilla, Tomás A.; Garcı́a-Ramos, Gisela

doi:10.1016/s0025-5564(03)00091-9

Cited by 37 publications

(66 citation statements)

References 23 publications

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“…For a first glance at the idea of the ''police virus'', we have chosen a simple deterministic approach ignoring any spatial effects (Steinmeyer and Wilke 2009). In addition, the concept of engineering viruses to infect and kill HIV infected cells has already been explored both experimentally (Schnell et al 1997) and in mathematical models (Revilla and García-Ramos 2003). Defective interfering virus particles have also been considered (Dropulić et al 1996;Nelson and Perelson 1995;Berencsi et al 1989).…”

Section: Discussionmentioning

confidence: 99%

A mathematical model of HIV dynamics in the presence of a rescuing virus with replication deficiency

Ζιντζαράς

Kowald

2011

Theory Biosci.

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Recently, an enzyme (Cre recombinase) has been developed by directed evolution that successfully removes the HIV genome from the nuclear DNA of infected cells. To explore this idea further, we hypothesized that a replication deficient virus (called ''police virus''), added externally, can deliver such a recombinase which excises the integrated HIV DNA from the genome of infected cells. Such a ''police virus'' could attack and remove the integrated provirus which is not possible using contemporary strategies. The hypothesis was tested by developing a mathematical model that describes the dynamics of virus-host cell interaction and the consequences of introducing the ''police virus''. The simulations show that such a therapeutic vector may eradicate all HIV viruses from the system in the long term. All components of the HIV infection (free virus, latently, and actively infected cells) can be cleared and the system ends up only with susceptible CD4? cells. The proposed model may provide new insights in the dynamical behavior and future alternative treatments of HIV.

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Section: Discussionmentioning

confidence: 99%

A mathematical model of HIV dynamics in the presence of a rescuing virus with replication deficiency

Ζιντζαράς

Kowald

2011

Theory Biosci.

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“…So delays are not considered for z or w in this model. To the best of our knowledge, only the case f (x, v) = βxv has been considered in the literature, such as [26,27]. In [26,27], the corresponding ordinary differential system of (1.2) was studied.…”

Section: X(t) Y(t) V(t) Is the Density Of Virus-free Host Cells (Momentioning

confidence: 99%

“…To the best of our knowledge, only the case f (x, v) = βxv has been considered in the literature, such as [26,27]. In [26,27], the corresponding ordinary differential system of (1.2) was studied. Only the structure of the equilibria was analysed in [27], and some numerical simulations were presented.…”

Section: X(t) Y(t) V(t) Is the Density Of Virus-free Host Cells (Momentioning

confidence: 99%

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Effect of time delays in an HIV virotherapy model with nonlinear incidence

Tian

Yuan

2016

Proc. R. Soc. A.

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In this paper, we propose a mathematical model for HIV infection with delays in cell infection and virus production. The model examines a viral therapy for controlling infections through recombining HIV with a genetically modified virus. For this model, we derive two biologically insightful quantities (reproduction numbers) R 0 and R z , and their threshold properties are discussed. When R 0 < 1, the infection-free equilibrium E 0 is globally asymptotically stable. If R 0 > 1 and R z < 1, the single-infection equilibrium E s is globally asymptotically stable. When R z > 1, there occurs the double-infection equilibrium E d , and there exists a constant R b such that E d is asymptotically stable if 1 < R z < R b . Some simulations are performed to support and complement the theoretical results.

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“…The authors showed that the introduction of this engineered virus can achieve HIV load reduction of 92% and recovery of host cells to 17% of their normal levels (see also the mathematical model in Ref. [40]). …”

Section: Article In Pressmentioning

confidence: 99%

Modeling viral coevolution: HIV multi-clonal persistence and competition dynamics

Bagnoli

Lió

Sguanci

2006

Physica A: Statistical Mechanics and its Applications

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The coexistence of different viral strains (quasispecies) within the same host are nowadays observed for a growing number of viruses, most notably HIV, Marburg and Ebola, but the conditions for the formation and survival of new strains have not yet been understood. We present a model of HIV quasispecies competition, which describes the conditions of viral quasispecies coexistence under different immune system conditions. Our model incorporates both T and B cells responses, and we show that the role of B cells is important and additive to that of T cells. Simulations of coinfection (simultaneous infection) and superinfection (delayed secondary infection) scenarios in the early stages (days) and in the late stages of the infection (years) are in agreement with emerging molecular biology findings. The immune response induces a competition among similar phenotypes, leading to differentiation (quasispeciation), escape dynamics and complex oscillations of viral strain abundance. We found that the quasispecies dynamics after superinfection or coinfection has time scales of several months and becomes even slower when the immune system response is weak. Our model represents a general framework to study the speed and distribution of HIV quasispecies during disease progression, vaccination and therapy. r

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Fighting a virus with a virus: a dynamic model for HIV-1 therapy

Cited by 37 publications

References 23 publications

A mathematical model of HIV dynamics in the presence of a rescuing virus with replication deficiency

A mathematical model of HIV dynamics in the presence of a rescuing virus with replication deficiency

Effect of time delays in an HIV virotherapy model with nonlinear incidence

Modeling viral coevolution: HIV multi-clonal persistence and competition dynamics

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