Trans-dominant inactivation of HTLV-1 and HIV-1 gene expression by mutation of the HTLV-1 Rex transactivator

Article Abstract:

The authors used genetic engineering techniques to begin developing new anti-viral agents. Various proteins are needed for the human T-cell leukemia virus (HTLV-1) to reproduce. Reproduction, or replication, of the virus spreads the disease within the body and scientists would like to develop ways to block this process. One of the key proteins needed for HTLV-1 replication has been given the name Rex protein. The investigators sought to understand how the structure of the Rex protein could be altered to make it biologically inactive. The Rex protein was actually disrupted by way of its gene, the rex gene. Genes direct the body's manufacture of proteins by coding for their exact structure. The investigators caused mutations (abnormal changes) at 18 different sites on the rex gene. Abnormal versions of the Rex protein resulted from the gene mutations. Biological inactivity was achieved by disrupting either of two sections of the Rex protein; these sections are known as functional domains. The genetically-engineered genes for biologically ineffective Rex proteins are dominant mutants, meaning that they will override the effect of a normal gene. They could be used as medications to block viral replication, if safe and effective means of administration are developed. Other dominant mutants meant to disrupt other viruses have been engineered as well. Some dominant mutant proteins might be able to fight more than one virus, for example, the HTLV-1 Rex dominant mutants also inhibit HIV-1, a human immunodeficiency virus.

Methods, Usage, Drug therapy, Genetic aspects, Genetic engineering, Viral research, Viruses, Mutation (Biology), Mutation, Virus research, Immunogenetics, HTLV (Viruses), HTLV viruses

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Cellular APOBEC3G restricts HIV-I infection in resting CD4(super+) T cells

Article Abstract:

Activated CD4+ T cells, resting human CD4(super +)T cells circulating in blood are highly resistant to infection with human immunodeficiency virus (HIV). It is also stated that mitogen activation induces the recruitment of LMM (low molecular mass) APOBEC3G into the hmm (high molecular mass) complex and this correlates with a sharp increase in permisssivity for HIV infection in stimulated cells.

United States, Science & research, Risk factors, CD4 lymphocytes

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HIV-1 Nef inhibits ASK1-dependent death signalling providing a potential mechanism for protecting the infected host cell

Article Abstract:

Research is presented concerning the role of the human immunodeficiency virus type 1 in the infection of tissues of the lymphatic system. The resulting enhancement to apoptosis in infected and bystander cells is discussed.

Infection, Causes of, Physiological aspects, Cell death, T cells, Letter to the Editor, Lymphatic diseases

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