Protection of chimpanzees from infection by HIV-1 after vaccination with recombinant glycoprotein gp120 but not gp160

Article Abstract:

Virtually all the major advances against viral disease have come in the form of preventive immunization rather than a cure. Although research continues for effective treatments for AIDS, the greatest long-term hope lies in prevention. Unfortunately, the AIDS virus has not proved as amenable to vaccine development as have viruses like smallpox and polio. However, researchers have now demonstrated that an experimental vaccine can protect chimpanzees against infection with the AIDS virus. Two experimental vaccines were evaluated, one based upon the viral envelope protein gp120, and the other on the gp160 protein. The proteins were prepared by recombinant DNA technology, and therefore the vaccines contained no trace of actual viruses. The adjuvant, which is an additional material designed to stimulate the immune response to a vaccine, was aluminum hydroxide. This is significant, since aluminum hydroxide is already approved for use in humans. The investigators found that immunization with gp120 protected the chimpanzees against infection when they were later injected with the AIDS virus. The immunization with gp160 was ineffective, and when these animals were injected with HIV-1, they developed infections within seven weeks. However, it is uncertain that humans will have the same protective antibody response as the chimpanzees. Furthermore, for a vaccine to be practical in humans, the immunity must be long-lasting. In addition, there are numerous varieties of the AIDS virus in the human population, and it is uncertain that a single vaccine can provide protection against them all. Nevertheless, it is significant that protective immunity can be achieved using only protein molecules produced by molecular biology. This may eliminate the problems of using live attenuated virus as a vaccine, and should speed up the development and approval process for an AIDS vaccine. (Consumer Summary produced by Reliance Medical Information, Inc.)

Prevention

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Fast-acting slow viruses

Article Abstract:

The AIDS crisis has stimulated an explosion of data about the lentiviruses, which is the group of viruses that includes HIV. The techniques of molecular biology have been brought to bear on the problems of AIDS virus research, and have resulted in impressive gains. Two research groups have now reported the molecular cloning of SIV, which is considered the simian, or ape, version of the AIDS virus. Kestler et al., reporting in a recent issue of the journal Science, and Dewhurst et al., discussing their findings in the June 14, 1990 issue of Nature, have provided a means for quickly learning a great deal about this virus. They obtained DNA clones that contain all the necessary information for the production of new virus particles. This permits the development of viruses that are tailored to specific criterion, allowing investigators to carefully evaluate the contribution of each individual viral gene to the overall disease process. One particularly striking aspect of the viral clones is their ability to produce acute disease. Unlike natural AIDS, in which the low-level viral infection slowly undermines the immune system until the patient dies of an infection, some strains of SIV produce a rapidly fatal infection in which the experimental animals die directly from the effects of the virus itself. The fact that this rapid infection can be produced from a molecularly cloned virus is positive proof that the infection cannot be attributed to some viral contaminant, but is a direct effect of SIV. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Development and progression, Simian immunodeficiency virus, editorial

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A viral inhibitor of peptide transporters for antigen presentation

Article Abstract:

A study was conducted to determine how the herpes simplex virus (HSV) evades detection by the body's immune system. The results show that HSV expresses the cytoplasmic protein ICP47, which binds to the peptide transporter (TAP) to inhibit the transport of antigenic peptides into the endoplasmic reticulum. This leads to the retention of class I major histocompatibility complex molecules in the endoplasmic reticulum and prevents them from presenting peptide antigens to T-cells.

Herpes simplex virus

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