Frozen Evolution. Or, that’s not the way it is, Mr. Darwin. A Farewell to Selfish Gene.

The most common physiological changes induced by parasites include interventions in the functioning of the immune system (Chandra 1982; Binaghi 1993). In some cases, the parasite acts only as a passive agent here – its presence in the organism causes a specific immunity directed against this kind of parasite.In other cases, the influence of the parasite is active.Through specific or nonspecific immunosuppression, some kinds of parasites are capable of eliminating a certain part of the immune system of the host from functioning (Landolfo, Martinetto, & Cavallo 1978).For example, it has been found that, in the acute phase of infection, the protozoa Toxoplasma gondii is capable of inducing apoptosis (programmed cell suicide) of the T-lymphocytes in infected mice, drastically reducing the immunity of the infected animals (Khan, Matsuura, & Kasper 1996).Very frequent and often very conspicuous manifestations of manipulation of the immune system of the host can be observed for parasitic helminths (Wilson 1993).Helminths are typically accompanied by a shift in the equilibrium between T-lymphocytes of the Th₁and Th₂subgroups towards the Th₂-helper cells (these are lymphocytes that increase the production of antibodies and, to the contrary, reduce the intensity of most cell immune reactions).This change also leads to substantial shifts in the concentrations of the individual lymphokins and subsequently also a shift to a certain type of effector reactions (humoral, rather than cellular) (Dimier, Woodman, & Bout 1992).s

In textbooks, it is generally stated that these shifts, for example towards elevated production of class IgE immunoglobulin, are adaptive from the viewpoint of host resistance and that they assist in eliminating the helminths.From the beginning of this century, an increasing number of works have appeared indicating that these shifts in the lymphokin level and the level of the individual classes of immunoglobulins tend rather to be a product of targeted manipulation of the immune system by the parasite with a tendency towards its protection (Allen & Maizels 1996).There is, in fact, an interesting (and well-founded) hypothesis that assumes that the current increase in allergic diseases in civilized countries is caused by the absence of intestinal helminths in modern humans and thus absence of the mentioned shift in the levels of the individual lymphokins (Bell 1996).The author of this hypothesis, R.G. Bell points out that improved hygiene, which allows people to avoid infection by helminths, is a phenomenon that has occurred only in the past century.Until that time, similar to developing countries at the present time, it was normal to suffer from permanent infection by some kinds of intestinal helminths (and thus to express the relevant shift in lymphokin levels).From the viewpoint of the long-term history of development of our species, the abnormal lymphokin levels or the very absence of the relevant antigens in modern humans could be the primary cause of allergic diseases.

The ability of parasites to cause specific or generalized immunity or immunosuppression constitutes an adaptive trait that is or was, in the past, an object of natural selection.For parasites, it is important from the standpoint of their life cycle whether they allow immunity to be formed against them in the host organism or whether they prevent this through specific mechanisms.If it is probable that a certain individualwillparasitize repeatedly on the same host (some kinds of ectoparasites, for example fleas) or if its offspring will parasitize on this host (for example lice), then it is advantageous from the standpoint of the inclusive fitness of the parasite if it prevents the formation of immunity.To the contrary, if it is probable that the host will be repeatedly infected, by mutually unrelated individuals, then it is advantageous if the parasite immunizes its host against the invasive stage of the parasite and simultaneously changes its own surface antigens (most endoparasites) or passes on to another host before the immune reaction commences (ticks) and thus burdens the initial position and thus the fitness of any competitors (see spiteful behavior, XVI.4.2).Analogous phenomena, but in the opposite direction, are understandably also active in the case of parasite-induced immunosuppression.If there is no danger of infection by unrelated parasites during the infection, i.e. by either members of the same species or of some other species, it is frequently advantageous for the parasite if it can inactivate the host’s immune system.If it is in the interests of the parasite that the host survive for as long as possible, this is not a very expedient tactic and the parasite must develop more specific mechanisms of defense, frequently including elimination of only part of the host’s defense system and, to the contrary, strengthening some other defense functions.These processes were studied in detail on some models of parasites of invertebrate hosts (Loker 1994).

For example, certain taxa of parasitic and parasitoid wasps have created a very interesting means of eliminating a certain part of the defense system of their insect hosts.They live in permanent symbiosis with viruses of the polydnavirus group where, in many cases, the relevant provirus is directly incorporated into the nuclear DNA of the parasitoid (Fleming & Summers 1991).When they lay eggs in their host, they simultaneously infect the host with these viruses.The viruses multiply in the host (in some cases, this is not necessary, and virus capsids not containing DNA work just as well (Schmidt & Schuchmann-Feddersen 1989)) and simultaneously they drastically reduce the defense system of the plasmatocytes , i.e. important effector cells of the insect immune system (Davies & Vinson 1988).Simultaneously, the suppressor effect is highly species-specific and frequently inhibits the function of the defense system only in one specific kind of host (Loker 1994).Thus, it is possible that the specificity of this defense system is responsible for the extremely large species diversity of this group of parasitoids.A similar system is employed by some species of nematods, for example of the Steinernema and Heterorhabditis genera.These nematods contain bacteria of the Xenorhabdus genus in their digestive systems (Forst et al. 1997).After penetration into the host organism, e.g. into the butterfly Galleria mellonella, these bacteria are released into the hemolymph of the host, where they multiply massively.For some species of helminths, these bacteria subsequently act as the main source of nutrition for the parasite.However, in other cases, the bacteria preferentially eliminate (inactivate) the hemocytes of the host and thus effectively prevent encapsulation and destruction of the helminth (Dunphy 1994).Simultaneously, the bacteria also produce a number of substances with strong bactericidal and fungicidal action, preventing destruction of the host by other species of parasitic (and in later phases, saprophytic) organisms (Li, Chen, & Webster 1997).

 Larvae of helminth of the genus Moniliformis (Acanthocephala), parasites in the tissues of cockroaches of the Periplaneta genus, are capable of specifically inhibiting some elements of the defense system of the insect host.The inhibition is again quite targeted (specific) and does not affect defense against pathogenic bacteria (Loker 1994).Similarly, the ability of the larvae of fluke worms to survive and reproduce in the host organism is frequently dependent on their ability to inactivate a certain defense system of the host.For example, the Echinostoma paraensei fluke worm is capable of very effectively inactivating the hemocytes of its intermediate host, the snail Biomphalaria glabrata (DeGaffe & Loker 1998).However, this example is in no way exceptional.It is known that a number of species of fluke worms (Trematoda) are capable of infecting a certain host only when its defense system is inactivated by previous infection by a different kind of parasite.This phenomenon is called acquired sensitivity (Lie, Lim, & Ow-Yang 1973b).Simultaneously, a number of cases of acquired resistance are known, where a previous infection by a certain type of fluke worm prevents subsequent infection by some other (even unrelated) species (Lie, Lim, & Ow-Yang 1973b; Lie, Lim, & Ow-Yang 1973a).It is possible that the high frequency of this phenomenon in fluke worms parasitizing on molluscs is connected with the fact that fluke worms reproduce asexually in these intermediate hosts, so that they form a genetically identical clone there.This means that, from the viewpoint of the inclusive fitness of the parasite, it is very advantageous when the individual is capable, in the host, of protecting not only itself against the defense system of the host (for example by masking employing the host proteins on its surface) but also its relatives by inactivating the defense system.