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Venereal Vaccines

Posted by on Tuesday, October 27, 2009, 16:03
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The two hundred year history of vaccination has generated only one success story against a sexually transmitted pathogen, the hepatitis B vaccine. This program was put in action during the early 1990s. It looked good at the outset but is already showing signs of trouble. Hepatitis B, like HIV, can generate variation quickly through mutation

Why have vaccines not been as successfully applied against sexually transmitted pathogens as against other kinds of pathogens? Each sexually transmitted pathogen has its own history, but there are some general reasons that the standard approach to vaccination is not particularly effective against venereal diseases.

The immunological problem isĀ  a problem. Sexually transmitted pathogens have to be able to avoid destruction by the immune system, and vaccines rely on the immune system, to destroy sexually transmitted pathogens. This is the problem that seems to be making the hepatitis B vaccine program show hairline cracks. Hepatitis B stays ahead of the immune system by mutating its form. If the vaccine primes the immune system to combat one form of virus, the door is left open to another form.

Vaccines against cancer have generated much hope but little success in the way of disease control. If most cancers turn out to be caused by viruses, all of this might change. Consider cervical cancer. Once cervical cancer became recognized as an infectious disease, new opportunity arose. The papillomavirus that causes this cancer offers several distinct antigens that would not have been availbale as immunological targets if the cancer has been caused solely by mutations.

AIDS vaccines present a different set of problems and opportunities. On the positive side, the infected cells are not cloistered inside tumors. On the negative side, the virus is so mutation prone that a vaccine that would protect against all variants id probably unattainable.

Still, the virulence antigen strategy may provide substantial protection if it is used early in the infection as a therapeutic vaccine. This kind of usage requires that the most damaging forms of HIV proteins be identified and used in the vaccine. When these forms then arise by mutation, they may be quickly knocked out before they have a chance to gain a foothold.

The protein HIV uses to attach to and enter cells, for example, typically changes during the course of infection, allowing HIV increasingly to enter and damage the helper T cells. This change is critical because these T cells tend to be far more important to the orchestration of the immune response than are the other cells HIV infects when it does not have this altered form. If the latered form of this protein was used in a vaccine early during infection, the more damaging virusesĀ  might be controlled longer because the immune system would be ready for them when they arose.

In this case the normal immunity generated by the less damaging HIV in the body is supplemented by a vaccine induced immunity that specifically suppresses the more damaging form. The more of the harmful forms that could be included in such a therapeutic virulence antigen vaccine, the longer the delay in the breakdown of the immune system.

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