The morphogenesis of a Chinese strain of HIV-1 forming inclusion bodies in Jurkat-tat III cells

Article Abstract:

A new rapidly replicating HIV-1 (BC9101) was found in a 52-year-old Chinese physician who had worked in Zaire, Africa for two years. He had returned to China, where he soon developed symptoms. His HIV infection advanced to AIDS in less than three years, although the usual incubation period is between six and nine years. The strain was cultured in Jurkat-tat III T-cell cells and a genetic analysis was performed. Electron microscopy showed significant changes in cell cytoplasm. Vacuoles containing viral particles formed in the culture cells. Rapidly replicating HIV sometimes accumulated as inclusion bodies which contained as many as 30,000 virons. Inclusion bodies were discharged during disintegration of infected cells, a late stage in replication. The genetic structure of the BC9101 seemed unusual because one gene lacked a start codon, which may be a reason the virus reproduces quickly.

Development and progression, HIV infection, HIV infections, HIV (Viruses), HIV, Virus replication

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Development of zidovudine (AZT) resistance in Jurkat T cells is associated with decreased expression of the thymidine kinase (TK) gene and hypermethylation of the 5' end of human TK gene

Article Abstract:

Changes in the expression of an enzyme that processes the drug zidovudine (AZT) may explain how HIV becomes resistant to the drug. An enzyme in T cells called thymidine kinase (TK) normally adds phosphate groups to zidovudine, which results in the active form of the drug. Researchers studied TK in zidovudine-resistant T cell cultures. The concentration of TK mRNA in these cultures was significantly less than the concentration in T cell cultures that were not resistant to zidovudine. DNA analysis of the TK gene revealed that the promoter region was heavily methylated compared to the promoter region of the normal gene. This methylation may cause the gene to stop producing mRNA, which eventually produces the enzyme. A reduction in enzyme levels would prevent zidovudine from becoming activated, which would make the drug ineffective against HIV.

Drug resistance in microorganisms, Microbial drug resistance, Zidovudine

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Comparison of HTLV-I basal transcription and expression of CREB/ATF-1/CREM family members in peripheral blood mononuclear cells and Jurkat T cells

Article Abstract:

The persistence of HTLV-I in blood cells called mononuclear cells may result from the fact that transcription factors are always in the activated state. HTLV-I is a virus related to HIV that causes adult T-cell leukemia. The virus usually infects mononuclear cells. Researchers stimulated mononuclear cells and a cell line resembling T cells called the Jurkat T cell line to produce transcription factors. These are proteins that turn on genes. The transcription factors can be inactive or active. In the mononuclear cells, the transcription factors remained active, whereas in the Jurkat cells, they were inactivated.

Genetic transcription, Transcription (Genetics), HTLV-I infections

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