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pubmed-article:7881191pubmed:abstractTextThe administration of a genetically engineered defective interfering virus (DIV) that interferes with HIV-1 replication has been proposed as a therapy for HIV-1 infection and AIDS. The proposed interfering virus, which is designed to superinfect HIV-1 infected cells, carries ribozymes that cleave conserved regions in HIV-1 RNA that code for the viral envelope protein. Thus DIV infection of HIV-1 infected cells should reduce or eliminate viral production by these cells. The success of this therapeutic strategy will depend both on the intercellular interaction of DIV and HIV-1, and on the overall dynamics of virus and T cells in the body. To study these dynamical issues, we have constructed a mathematical model of the interaction of HIV-1, DIV, and CD4+ cells in vivo. The results of both mathematical analysis and numerical simulation indicate that survival of the engineered DIV purely on a peripheral blood HIV-1 infection is unlikely. However, analytical results indicate that DIV might well survive on HIV-1 infected CD4+ cells in lymphoid organs such as lymph nodes and spleen, or on other HIV-1 infected cells in these organs.lld:pubmed
pubmed-article:7881191pubmed:languageenglld:pubmed
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pubmed-article:7881191pubmed:authorpubmed-author:PerelsonA SASlld:pubmed
pubmed-article:7881191pubmed:authorpubmed-author:NelsonG WGWlld:pubmed
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pubmed-article:7881191pubmed:volume125lld:pubmed
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pubmed-article:7881191pubmed:pagination127-53lld:pubmed
pubmed-article:7881191pubmed:dateRevised2009-11-11lld:pubmed
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pubmed-article:7881191pubmed:year1995lld:pubmed
pubmed-article:7881191pubmed:articleTitleModeling defective interfering virus therapy for AIDS: conditions for DIV survival.lld:pubmed
pubmed-article:7881191pubmed:affiliationLos Alamos National Laboratory, New Mexico 87545.lld:pubmed
pubmed-article:7881191pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:7881191pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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