VACCINE DEVELOPMENT: There have been attempts to systematically fund research for vaccine development against certain parasitics infections with schistosomiasis perhaps receiving most attention. This program has led to the development of several defined vaccines against Schistosomes that have been tested in animals and at least one of which is now in human trials; (Bergquist et al., 2000). While this represents a significant step forward, it is important to note that there is no certainty that any of these vaccines will reach the market and moreover, that during development these vaccines have been shown to be only partially effective. The hope is that, in conjunction with a greater appreciation of immune response induction mechanisms, our understanding of basic parasitic biology will improve sufficiently in the coming years and allow the rational development of more efficacious vaccines; basic research on model vaccines continues and the reader is directed to an excellent recent article on this subject; (Yadanbakhsh et al., 1999).
Intriguingly, the application of anti-parasitic vaccines is more advanced in veterinary medicine than in human medicine, with a history of the use of attenuated vaccines against certain nematode parasites and more recently the development of recombinant protein and DNA vaccines against the sheep tape treatment (Rolfe et al., 2000). This probably reflects a combination of factors including the greater commercial potential of veterinary vaccines that can be sold in the developed world and the less stringent safety requirements for products intended for veterinary versus human use.
IMMUNE RESPONSE EVASION IN PARASITIC INFECTIONS AND vaccine
The long-term survival of parasitic infection within mammalian host indicates that they have developed sophisticated mechanisms to evade the cytotoxic effects of the immune response; (Sher et al., 1987).
Early work provided some clues as to how this could occur for example, antibiotics in the sera of schistosome-infected hosts fail to bind to the surface of the living parasites are able to modulate their surface structure in a way that prevents recognition.
Recent studies have begun to provide mechanistic explanations for evasion; (Carvalho et al., 2000). For example serpins made by the microfiariae of B malayi are able to inhibit neutrophil serine proteases and a cystatin homologque from the same parasite can inhibit class II major histocompatibility complex-restricted Ag processing; (Watts et al., 2001),
Deeper understanding of the basis requirements of metazoan life have revealed areas in which interactions between helminths and their hosts that could influence immune effector functions are likely to occur. Prominent among these is the Expression of transforming growth factor β receptor family members by parasites and in the case of nematodes at least, a homologue of transforming growth factor β itself; (Maizels et al., 1998).