Defective viruses and AIDS

Article Abstract:

It has been suggested that defective viruses, those that can not replicate, may play a role in the development of acquired immunodeficiency syndrome (AIDS). A defective virus can combine with other viruses that can replicate to produce a recombinant virus, which has characteristics derived from both parent viruses. There is evidence from studies in mice and cats that recombinant viruses are involved in diseases, some of which are similar to AIDS. However, there is evidence that this does not occur in humans. Because defective viruses can not replicate, large amounts of two parent viruses (the defective virus and a virus which can replicate) would have to be present and transmitted to other individuals in order to cause disease. Large amounts of viruses are not seen in AIDS patients. If large amounts of the virus that causes AIDS were present, the body could develop immunity against the virus during the long latency period of AIDS, which is approximately seven years. Such an immunity is not seen. Therefore, it does not seem likely that defective viruses are involved in AIDS.

Disease transmission, AIDS (Disease), AIDS research

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When its better to lie low

Article Abstract:

The envelope protein of the flavivirus is found to be lying down with the features of its two-fold axis coinciding with those of the symmetrical internal nucleocapsid observed in alphaviruses. Soluble envelope fragment monomers have three different domains, namely, the central domain, the dimerization domain and the carboxy terminal domain. The structure of a flavivirus' major envelope protein gives rise to several new questions and shows how viruses can become resourceful when attacking cells.

Glycoproteins

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Quantification of latent tissue reservoirs and total body viral load in HIV-1 infection

Article Abstract:

The human immunodeficiency virus (HIV-1) is found in a latent form at stages throughout the progress of infection. Measurements of virus load in activated CD4+ T white blood cells indicate that less than ten(super(7)) CD4+ T cells are infected with the replication-competent integrated provirus. Much of the HIV-1 deoxyribonucleic acid is full-length, linear, and unintegrated. The virus's capacity to cause infection appears to be unaffected by its presence in small numbers.

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