Bakiri et al they could suppress pathologic symptoms due to inhibition of the innate immunity, later they might anticipate the pro- viding of specific humoral immunity abandoning the host due to induction of the respiratory symptoms [71]. Thus, the soluble G glycoprotein acts as bacterial cytokine with inhibiting expression of ICAM-1, IL-8 and NF-κB during incubatory period of respiratory syncytial virus (RSV) [71- 74]. The experimental infection of BALB/c mice with a RSV mutant lacking the glycoprotein G gene increases NK and neutrophil trafficking to the lungs compared to control mice infected with a strain of RSV that has glycoprotein G [71, 73]. Although the secreted form of glycoprotein G accounts for no more than 20% of the total glycoprotein synthesized in cell culture through the course of infection, secreted gly- coprotein represents about 80% of the protein released into the medium early in infection, during the first 24 h [73, 74]. This scenario first could assure a maximal multiplication for the infectious agents; then the host abandonment on time to catch a next one assures maximal successive reproduction [71]. Taken together, these data demonstrate that parasites and other infective agents can be efficient host manipulators using them for their reproductive success, independently to the fact if they induce or inhibit the host pathology [16, 50, 71]. Conclusions Based on the current knowledge, it could be concluded that parasites try to manipulate the host behavior for its own ben- efit in different ways, altering its (epi)genetic, biochemical, immunologic or physiologic functions as well as altering its behavior and activity [13-16, 62, 65, 75, 76]. Current data in- dicate that skin allergy may be associated with certain stages of the parasites’ life cycle, but not necessarily with pres- ence of the parasitosis in the host organism. As compared to Th1 response, the Th2 one (including the IgE production), the eosinophilic infiltration and the complement inhibition might assure better conditions for the development of some parasites (Fig. 1). The ambiguity of the host immune re- sponse during parasitic infection remains a puzzle, but much evidence stresses the fact that the sum effect of the deviated host reactivity may create an environment, which is also favorable for the parasite survival [33]. Taken together, the combination of suggested hypotheses could be a plausible explanation for the epidemiological association’s paradox between skin allergy (including urticaria), IgE response and parasitoses [10]. Nevertheless, further studies focused on the stages of parasites’ development may lead to the providing of better-based conclusions and invention of novel therapeu- tic strategies [16, 70]. 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