Serialin VivoPassage of HIV-1 Infection inMacaca nemestrina
Autor: | Greg Schaefer, Ann Schmidt, Michael B. Agy, Michael G. Katze, William R. Morton, Marnix L. Bosch, Lawrence Corey, Mary Jo Florey, Bryan J Kennedy |
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Rok vydání: | 1997 |
Předmět: |
Viremia
HIV Infections Biology HIV Envelope Protein gp120 Virus Replication Virus Immune system Serial passage Virology medicine Animals Humans Seroconversion Serial Passage Cells Cultured Viral culture Macaca nemestrina virus diseases Sequence Analysis DNA medicine.disease Adaptation Physiological Coculture Techniques Disease Models Animal Viral replication Immunology HIV-1 Leukocytes Mononuclear |
Zdroj: | Virology. 238(2):336-343 |
ISSN: | 0042-6822 |
DOI: | 10.1006/viro.1997.8832 |
Popis: | In an earlier study we found that pigtailed macaques (Macaca nemestrina) that were experimentally infected with human immunodeficiency virus type 1 (HIV-1) initially became viremic and seroconverted, but HIV-1 replication diminished markedly over time. In an attempt to develop a longer term pathogenic model, blood from HIV-1-infected macaques was serially transfused into three groups of naive macaques. Transfer was successful through two transfusions as shown by repeated virus isolations and confirmed by the development of cell-free plasma viremia and by seroconversion. Three to five weeks after transfusion, plasma levels of HIV-1 RNA from several macaques in the first two groups exceeded those of the initially inoculated macaques. However, animals in the third group had diminished RNA levels, were virus culture negative, and did not seroconvert. Sequence analyses of env-region clones from infected animals revealed only minimal changes over the course of the passages. These results confirm HIV-1 replication inM. nemestrinaduring the acute phase of infection. However, adaptation of HIV-1 to a macaque-pathogenic variant did not occur during serial passage, possibly because the animals were able to restrict HIV-1 replication below a level required for a pathogenic variant to emerge. Whether such containment is a function of the host's immune response or a virus cell incompatibility remains to be determined. |
Databáze: | OpenAIRE |
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