dorsal/arxiv
View SchemaOpportunistic infection as a cause of transient viremia in chronically infected HIV patients under treatment with HAART
| Authors | Laura E. Jones, Alan S. Perelson |
|---|---|
| Categories | |
| ArXiv ID | q-bio/0411040 |
| URL | https://arxiv.org/abs/q-bio/0411040 |
| DOI | 10.1016/j.bulm.2005.01.006 |
| Journal | Bulletin of Mathematical Biology (67) 1227-1251 (2005) |
Abstract
When highly active antiretroviral therapy is administered for long periods of time to HIV-1 infected patients, most patients achieve viral loads that are ``undetectable'' by standard assay (i.e., HIV-1 RNA $ < 50$ copies/ml). Yet despite exhibiting sustained viral loads below the level of detection, a number of these patients experience unexplained episodes of transient viremia or viral "blips". We propose here that transient activation of the immune system by opportunistic infection may explain these episodes of viremia. Indeed, immune activation by opportunistic infection may spur HIV replication, replenish viral reservoirs and contribute to accelerated disease progression. In order to investigate the effects of concurrent infection on chronically infected HIV patients under treatment with highly active antiretroviral therapy (HAART), we extend a simple dynamic model of the effects of vaccination on HIV infection [Jones and Perelson, JAIDS 31:369-377, 2002] to include growing pathogens. We then propose a more realistic model for immune cell expansion in the presence of pathogen, and include this in a set of competing models that allow low baseline viral loads in the presence of drug treatment. Programmed expansion of immune cells upon exposure to antigen is a feature not previously included in HIV models, and one that is especially important to consider when simulating an immune response to opportunistic infection. Using these models we show that viral blips with realistic duration and amplitude can be generated by concurrent infections in HAART treated patients.
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"abstract": "When highly active antiretroviral therapy is administered for long periods of\ntime to HIV-1 infected patients, most patients achieve viral loads that are\n``undetectable\u0027\u0027 by standard assay (i.e., HIV-1 RNA $ \u003c 50$ copies/ml). Yet\ndespite exhibiting sustained viral loads below the level of detection, a number\nof these patients experience unexplained episodes of transient viremia or viral\n\"blips\". We propose here that transient activation of the immune system by\nopportunistic infection may explain these episodes of viremia. Indeed, immune\nactivation by opportunistic infection may spur HIV replication, replenish viral\nreservoirs and contribute to accelerated disease progression. In order to\ninvestigate the effects of concurrent infection on chronically infected HIV\npatients under treatment with highly active antiretroviral therapy (HAART), we\nextend a simple dynamic model of the effects of vaccination on HIV infection\n[Jones and Perelson, JAIDS 31:369-377, 2002] to include growing pathogens. We\nthen propose a more realistic model for immune cell expansion in the presence\nof pathogen, and include this in a set of competing models that allow low\nbaseline viral loads in the presence of drug treatment. Programmed expansion of\nimmune cells upon exposure to antigen is a feature not previously included in\nHIV models, and one that is especially important to consider when simulating an\nimmune response to opportunistic infection. Using these models we show that\nviral blips with realistic duration and amplitude can be generated by\nconcurrent infections in HAART treated patients.",
"arxiv_id": "q-bio/0411040",
"authors": [
"Laura E. Jones",
"Alan S. Perelson"
],
"categories": [
"q-bio.PE",
"q-bio.QM"
],
"doi": "10.1016/j.bulm.2005.01.006",
"journal_ref": "Bulletin of Mathematical Biology (67) 1227-1251 (2005)",
"title": "Opportunistic infection as a cause of transient viremia in chronically infected HIV patients under treatment with HAART",
"url": "https://arxiv.org/abs/q-bio/0411040"
},
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