• 제목/요약/키워드: HIV pathogenesis model

검색결과 2건 처리시간 0.016초

STABILITY ANALYSIS OF AN HIV PATHOGENESIS MODEL WITH SATURATING INFECTION RATE AND TIME DELAY

  • Liao, Maoxin;Zhao, Sa;Liu, Manting
    • Journal of applied mathematics & informatics
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    • 제32권3_4호
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    • pp.475-489
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    • 2014
  • In this paper, a mathematical model for HIV infection with saturating infection rate and time delay is established. By some analytical skills, we study the global asymptotical stability of the viral free equilibrium of the model, and obtain the sufficient conditions for the local asymptotical stability of the other two infection equilibria. Finally, some related numerical simulations are also presented to verify our results.

Interaction of HIV-1 Core p24 Antigen with Human Monocytic Cell Line THP1 Results in TNF-${\alpha}$ Dependent Secretion of Matrix Metalloproteinase-9

  • Sung, Ji-Hye;Yoo, Seung-Hee;Park, Hae-Kyung;Chong, Young-Hae
    • 대한미생물학회지
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    • 제35권1호
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    • pp.9-18
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    • 2000
  • Immunological mechanisms involving the release of inflammatory factors by HIV-1 infected microglia in the brain have been implicated in the pathogenesis of HIV dementia (HIVD). Since the regulation of matrix metalloproteinases (MMPs) activity can be influenced by variety of inflammatory mediators, this study was undertaken to look for a correlation between the MMP-9 release and the production of TNF-${\alpha}$ in response to HIV-1 p24 in the human monocyte cell line THP-1 as a model for microglia. First, it was shown that HIV-l core p24 antigen induced THP-1 to secrete MMP-9 in a dose response manner while it elicited a little effect on MMP-2 release in human astroglial cell line T98G. Next, it was found that p24 induced THP-1 to secrete TNF-${\alpha}$ without prior differentiation into macrophages by phorbol myristate acetate (PMA) treatment. Furthermore, anti-TNF-${\alpha}$ neutralizing antibodies significantly blocked p24-induced MMP-9 release in a dose dependent manner. Our data indicate that p24 antigen induces monocytic MMP-9 release by triggering up-regulation of TNF-${\alpha}$ secretion.

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