Global dynamics of humoral and cellular immune responses to virus infection
We study the global stability of a model of virus dynamics with consideration of humoral and cellular immune responses. We use a Lyapunov direct method to obtain sufficient conditions for the global s tability of virus-free and viruspresence equilibriums. First, we analyze the model without an imm...
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Formato: | article |
Lenguaje: | EN ES |
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Pontificia Universidad Javeriana
2019
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Acceso en línea: | https://doaj.org/article/bfb64f36eb974980a297591624bd079f |
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Sumario: | We study the global stability of a model of virus dynamics with consideration
of humoral and cellular immune responses. We use a Lyapunov direct method
to obtain sufficient conditions for the global s tability of virus-free and viruspresence equilibriums. First, we analyze the model without an immune response
and found that if the reproductive number of the virus is less than or equal to
one, the virus-free equilibrium is globally asymptotically stable. However, for
the virus-presence equilibrium, global stability is obtained if the virus entrance
rate into the target cells is less than one. We analyze the model with humoral and
cellular immune responses and found similar results. The difference is that in the
reproductive number of the virus and in the virus entrance rate into the target
cells appear parameters of humoral and cellular immune responses, which means
that the adaptive immune response will cease or control the rise of the infectionWe study the global stability of a model of virus dynamics with consideration
of humoral and cellular immune responses. We use a Lyapunov direct method
to obtain sufficient conditions for the global s tability of virus-free and viruspresence equilibriums. First, we analyze the model without an immune response
and found that if the reproductive number of the virus is less than or equal to
one, the virus-free equilibrium is globally asymptotically stable. However, for
the virus-presence equilibrium, global stability is obtained if the virus entrance
rate into the target cells is less than one. We analyze the model with humoral and
cellular immune responses and found similar results. The difference is that in the
reproductive number of the virus and in the virus entrance rate into the target
cells appear parameters of humoral and cellular immune responses, which means
that the adaptive immune response will cease or control the rise of the infection. |
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