THE NEW GERM THEORY OF DISEASE: VENEREAL VACCINES
Posted: April 24th, 2011 | Author: admin | Filed under: HIV | Comments OffThe 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. Recent data indicate that a massive hepatitis B vaccination program in Taiwan is causing the virus to evolve around the vaccine.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 story, but there are some general reasons that the standard approach to vaccination is not particularly effective against venereal diseases.Sexually transmitted pathogens are the beneficiaries of several psychological idiosyncrasies. First there is morality. People have little control over whether they will inhale air laden with viruses, whether a mosquito will get lucky, or whether some of their food has been contaminated because of neglected hand washing. But people are supposed to have some control over whether they engage in sex. Treating syphilis with an antibiotic is remedying a past moral lapse, but vaccinating people against syphilis can be seen as encouraging immoral behavior. Allocating money for the development of venereal vaccines can be politically risky for the same reason.There is also the immunological 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 the 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 opportunities arose. The papillomavirus that causes this cancer offers several distinct antigens that would not have been available as immunological targets if the cancer had been caused solely by mutations. Even with vi-rally caused cancer there is the problem of getting the immune system to knock out a lump of the body’s own cells, but at least there is a chance that the cells are hanging the virus’s body parts as a kill me sign for the immune system. Cells infected with the most deadly forms of papillomavirus do seem to post such signs using parts of the E6 and E7 proteins; and cells that were engineered to express these proteins were destroyed by the cytotoxic T cells that would need to be mustered to take care of these cells in the body. There is still the problem of killing a big lump of cells from the outside. Once the lump gets too big, no amount of immunological activity may be sufficient. But the immunological action triggered by an E6 or E7 vaccine may work much earlier in the course of infection, long before a distinct lump is seen.If such a vaccine does act against infected cells, it could have a much greater long-term punch than its developers suspect. The E6 and E7 proteins are the ones that sabotage the cell’s ability to control its division. A vaccine derived from them would therefore be a virulence antigen vaccine that might provide an extra evolutionary punch by tipping the competitive balance in favor of the papillomaviruses without the damaging form of these proteins. These mild strains of papillomavirus would then be left to generate additional protection against the harmful strains by triggering immunity to antigens that the mild arid harmful strains share.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 is 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’s 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 altered form of this protein was used in a vaccine early during infection, the more damaging viruses 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.*63\225\2*
