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PubMed1992

Host strain, H-2 genotype and immunocompetence do not affect the survival or development of Onchocerca lienalis infective larvae implanted within micropore chambers into mice or rats.

The survival, growth and development of Onchocerca lienalis 3rd-stage (L3) larvae implanted into mice within micropore chambers has been studied with a view to developing a vaccination model for studies of protective immunity in onchocerciasis. The influence of host genetics on worm recoveries and development (growth and moulting rate) was analysed in a panel of inbred mice (CBA, BALB/c, DBA/2, SJL, 129J, C57BL/10 (B10), C3H/He and NIH), together with mice of BALB and B10 backgrounds with different major histocompatibility complex (H-2) genes (BALB/c, BALB.K, BALB.B and B10, B10.D2/n, B10.BR, B10.S). Parasite recoveries and development were similar in all mouse genotypes tested. They were unaffected by procedures designed to block or modulate phagocytic cell function with carbon or carrageenan, or to suppress inflammation by treatment with hydrocortisone acetate. A comparison of chambers sealed with membranes designed to admit (5.0 microns pore size) or exclude (0.2 microns pore size) host cells demonstrated no effect on the percentage recovery of living larvae, although dead larvae were more frequently retrieved when cells were excluded. Recoveries and rates of development of larvae implanted into immunodeficient scid mice and athymic Hooded rats were similar to those recorded in immunocompetent controls. We conclude that host genetic factors and immunocompetence are not significant determinants of survival, growth or development of O. lienalis larvae implanted within micropore chambers into naive mice. Despite its limitations, the use of this system merits further investigation as an approach to the study of protective immunity against developing larvae in onchocerciasis.

Animals↗
PubMed1990

Host specificity of cloned Spironucleus muris in laboratory rodents.

With three clones of Spironucleus muris (S. muris)--established from a mouse, hamster, and rat--homologous and heterologous host species were experimentally infected. Each host was susceptible to the clone originating from the homologous donor. In addition, both mice and hamsters were susceptible to the reciprocal heterologous clones. In contrast, infections of the rat with both heterologous clones were very poor, i.e. quantitatively low and ephemeral. It was not possible to infect hamsters and mice, not even athymic, with S. muris from the rat. This suggests a strain heterogeneity within the genus S. muris. In general, the genetic background of the host influenced the infection, the sex of the host did not.

Animals↗
PubMedDate not supplied

Phenotypic and genotypic variation in the interaction between Arabidopsis thaliana and Albugo candida.

Two biotrophic parasites of the wild crucifer Arabidopsis thaliana (L.) Heynh, are being used to explore the molecular basis and evolution of genotype-spcific recognition and host defense. Genes for recognition of Peronospora parasitica (downy mildew) are numerous in A. thaliana and located on four of the five chromosomes as described previously. Genes for recognition of the closely related parasite Albugo candida (white blister) are described here. In contrast to teh former parasite, less than 15% of the host accessions tested were capable of recognizing either of two isolates of A. candida. The geographic regions represented by these accessions included countries in eastern and western Europe, Asia, North America and Africa. Extensive collections from England and Germany were required to identify examples of incompatible interactions. Phenotypic variation among incompatible interactions included reduced blister formations of complete lack of asexual reproduction by the parasite. Variation in the extent of the host response was also observed. Three host genes for recognition of A. candida (RAC), each associated with different interactions phenotypes, were identified through inheritance studies with three accessions. One of these genes at locus RAC1 appeared to be completely dominant, whereas the other two genes were only partially dominant or recessive under certain conditions, possibly including the effect of genetic background. One of the later two genes defined a second locus RAC2. RAC1 was mapped to the top arm of chromosome 1 in the 1 cM interval between RFLP markers M254 and M253.

Arabidopsis↗
PubMed1985

Patterns of resistance of inbred mice to Trypanosoma cruzi are determined by parasite strain.

Host response and parasite behavior of three different T. cruzi strains (I-Peruvian, II-21SF, III-Colombian) were investigated by evaluating the course of infection in six inbred strains of mice (A/J, AKR, C3H/He, BALB/c, C57BL/10, DBA/1). Resistance was evaluated in terms of the harmonic mean survival time and the infection was monitored by parasitemia, histopathology and immunological parameters (immunoglobulin subclass levels and antibody titers). All six mouse strains showed high susceptibility to the Peruvian strain (Type I). However, they displayed a different spectrum of susceptibility to Types II and III. Each T. cruzi strain maintained its basic features in the different mouse strains. Despite different maximum levels, the parasitemic curves were characteristic for each type of T. cruzi strain. There was a correlation between the degree of resistance of strains DBA and B10 and their high levels of IgG2a and IgG2b, as well as the presence of the H-2d haplotype, indicating that the genetic background of the mice is also important. The inflammatory process varied with each mouse strain and was correlated with the levels of IgG2a, with resistant mice showing predominance of neutrophilic infiltration with a rise in IgG2a. The susceptible strains responded with a mild inflammatory process with predominance of mononuclear cells. These data suggest that the parasite strain is the most important factor determining the resistance of the different mouse strains to infection with T. cruzi.

Animals↗
PubMed1990

Dependence on cell-mediated mechanisms for the appearance of crisis forms during Plasmodium chabaudi AS infection in C57BL/6 mice.

The appearance of crisis forms or degenerate, intraerythrocytic parasites in the peripheral blood of C57BL/6 hosts during the course of Plasmodium chabaudi AS infection was analysed. Following intraperitoneal injection with 10(6) parasitized erythrocytes, C57BL/6 hosts, which are resistant to this species of rodent Plasmodium, eliminate the parasite from the peripheral blood by 4 weeks and recover from acute infection. Elimination of the parasite coincides with the appearance in the peripheral blood of almost all the parasites as crisis forms. A role for cell-mediated immunity in the induction of crisis forms of Plasmodium species has previously been suggested. To define the role of cell-mediated immunity in the appearance of intraerythrocytic crisis forms in the peripheral blood during acute malaria, the outcome of P. chabaudi AS infection, the course of parasitemia and the appearance of crisis forms in mice with either genetically determined or experimentally induced immunodeficiencies on the resistant C57BL-derived background were examined. The mice used were either B-cell deficient (mu-suppressed from birth). T-cell deficient (nu/nu mice), C5 deficient or splenectomized prior to infection. The appearance of intraerythrocytic crisis forms in the peripheral blood during the course of P. chabaudi AS infection is shown to be dependent on cell-mediated mechanisms which require the presence of T cells as well as an intact spleen for the most efficient elimination of this parasite.

Animals↗
PubMed1985

Immunity to leprosy. II. Genetic control of murine T cell proliferative responses to Mycobacterium leprae.

T cell proliferative responses to Mycobacterium leprae were measured after immunization of mice at the base of the tail with antigen and challenging lymphocytes from draining lymph nodes in culture with M. leprae. This T cell response to M. leprae has been compared in 18 inbred strains of mice. C57BL/10J mice were identified as low responder mice. The congenic strains B10.M and B10.Q were found to be high responders, whereas B10.BR and B10.P were low responders. F1 (B10.M X C57BL/10J) and F1 (B10.Q X C57BL/10J) hybrid mice were found to be low responders, similar to the C57BL/10J parent, indicating that the low responsive trait is dominant. Whereas B10.BR mice were shown to be low responders to M. leprae, B10.AKM and B10.A(2R) were clearly high responders, indicating that the H-2D region influences the magnitude of the T cell proliferative response. Gene complementation within the H-2 region was evident. Genes outside the H-2 region were also shown to influence the response to M. leprae. C3H/HeN were shown to be high responder mice, whereas other H-2k strains, BALB.K, CBA/N, and B10.BR, were low responders. Gene loci that influence the T cell proliferation assay have been discussed and were compared to known background genes which may be important for the growth of intracellular parasites. Because mycobacteria are intracellular parasites for antigen-presenting cells, genes that affect bacterial growth in these cells will also influence subsequent immune responses of the host.

Animals↗
PubMed1982

Genetics of murine resistance to Trypanosoma cruzi.

Resistance to the protozoan parasite Trypanosoma cruzi is governed by multiple genetic factors, including at least one coded for by a locus in or near the major histocompatibility complex of the mouse. The influence of the H-2 locus on resistance was evident when H-2 congenic mice on a strain background of intermediate resistance were challenged or when the survival of H-2 typed F2 mice was followed. The H-2k haplotype of the susceptible C3H/An strain was associated with higher mortality when compared with the H-2b haplotype of the resistant C57BL/10 strain. Genetic studies showed that resistance was a dominant trait and increased with genetic heterozygosity. F1 mice derived from crosses between resistant and susceptible strains, or even between two susceptible strains, were much more resistant than either parent. Crosses between two resistant strains, C57BL/6J and DBA/2J, led to resistant progeny in the F1 and F2 generations; but when recombinant inbred strains derived from these parental strains were challenged, susceptible strains were identified, indicating that different genes were responsible for resistance in the two strains.

Animals↗
PubMed1975

Biochemical, immunological and genetic studies in leprosy. II. Profile of immunoglobulins, complement components and C-reactive protein in sera of leprosy patients and healthy controls.

Various classes of immunoglobulins (IgA, IgM, IgG, IgD and IgE), complement components (C3 and C4) and C-reactive protein (CRP) were estimated in sera from normal healthy controls and leprosy (lepromatous and tuberculoid) patients from Ethiopia. Higher levels of IgA, IgM, IgG and IgD were found in lepromatous leprosy compared with normal healthy people while in tuberculoid leprosy only IgM, IgG and IgD levels were increased. Borderline leprosy patients showed increase in IgG level only. Although an increase in IgE was noted in lepromatous leprosy, it was not significant; the variations in IgE levels could be due to different socioeconomic background and exposure to intestinal parasites. C3 component was significantly reduced in leprosy patients compared with healthy controls while no difference in C4 component was observed. The results point towards an involvement of the "alternate pathway". A positive test against C-reactive protein antiserum was given by about 20% of the normal healthy controls while more than 60% lepromatous and tuberculoid leprosy patients were CRP positive. The results are discussed in relation to the status of immunoglobulins and complement components in leprosy and possible factors (environmental and genetic) which might affect them.

C-Reactive Protein↗
PubMed1980

Haemonchus contortus resistance in straightbred and crossbred Barbados Blackbelly sheep.

Resistance to Haemonchus contortus infection was studied in two experiments conducted with 52 lambs of widely different genetic background. Breed groups compared were: Dorset (D), Barbados Blackbelly (B), Dorset x Blackbelly (D x B), Suffolk x Blackbelly (S x B), Suffolk x Dorset x Blackbelly (S x D x B,[1/4 B]) and nonBlackbelly (NB, D and S). In each experiment, lambs were raised on concrete from birth and were essentially parasite free until infective larvae were administered. In Exp. 1, D x B, S x D x B and D wether lambs approximately 3 months old were infected with a standard dose of invective larvae estimated to be 98% H. contortus. D x B lambs had a longer (P < .05) prepatency period and, at necropsy 17-day postinfection, had a higher (P < .05) percentage of female parasites classified as immature than did the other breed groups. These data showed that the development of H. contortus larvae was inhibited in D x B host animals. In Exp. 2, B, D x B, S x B and NB ewe and wether lambs approximately 4 months old were treated with three sensitizing doses of H. contortus larvae. These were followed by a challenge infection. On the basis of fecal egg counts (eggs per gram feces, EPG), there was no evidence that the challenge infection induced a self-cure reaction in any breed group. All lambs with B breeding had significantly higher Hb levels at the end of the experiment than did NB lambs. b and S x B lambs had higher (P < .05) Hb levels than the D x B lambs, and B lambs had the highest (P < .05) mean corpuscular hemoglobin concentrations. Five days after the challenge infection, B, D x B and S x B lambs also had significantly higher white blood cell levels than did NB lambs. Significant sex differences were also observed in Exp. 2. Ewe lambs had lower final EPG levels, higher preinfection and postinfection Hb levels and higher maximum postinfection cosinophil levels. Breed x sex interactions for these parameters were not significant.

Abomasum↗
PubMed1995

T cell and non-T cell compartments can independently determine resistance to Leishmania major.

In experimental murine cutaneous leishmaniasis caused by Leishmania major (Lm), the cellular determinants governing development of protective or exacerbative T cells are not well understood. We, therefore, attempted to determine the influence of T cell and non-T cell compartments on disease outcome. To this end, T cell chimeric mice were constructed using adult thymectomized lethally irradiated, bone marrow-reconstituted (ATXBM) animals of genetically resistant, C57BL/6, or susceptible, BALB/c, backgrounds. These hosts were engrafted with naive T cell populations from H-2-congenic susceptible, BALB.B6-H-2b, or resistant, C57BL/6.C-H-2d, animals, respectively. Chimeric mice were then infected with Lm, and disease outcome was monitored. BALB/c T cell chimeric mice, BALB/c ATXBM hosts given naive C57BL/6.C-H-2d T cells, resolved their infections as indicated by reductions in both lesion size and parasite numbers. Furthermore, the mice developed typical Th1 (interferon[IFN]-gamma hiinterleukin[IL]-4lo) cytokine patterns. In contrast, both sham chimeric, BALB/c ATXBM hosts given naive BALB/c T cells, and control irradiated euthymic mice succumbed to infection, producing Th2 profiles (IFN-gamma loIL-4hiIL-10hi). C57BL/6 T cell chimeras, C57BL/6 ATXBM hosts given naive BALB.B6-H-2b T cells, resolved their infections as did C57BL/6 sham chimeras and euthymic controls. Interestingly, whereas C57BL/6 control animals produced Th1 cytokines, chimeric animals progressed from Th0 (IFN-gamma hiIL-4hiIL-10hi) to Th2 (IFN-gamma loIL-4hiIL-10hi) cytokine profiles as cure ensued. Both reconstitution and chimeric status of all mice were confirmed by flow cytometry. In addition, T cell receptor V beta usage of Lm-specific blasts was determined. In all cases, V beta use was multiclonal, involving primarily V beta 2, 4, 6, 8.1, 8.2, 8.3, 10, and 14, with relative V beta frequencies differing between H-2b and H-2d animals. Most importantly, however, these differences did not segregate between cure and noncure outcomes. These findings indicate that: (a) genetic traits determining cure in Lm infection can direct disease outcome from both T cell and non-T cell compartments; (b) the presence of the curing genotype in only one compartment is sufficient to confer cure; (c) curing genotype T cells autonomously assume a Th1 cytokine profile-mediating cure; (d) noncuring genotype T cells can mediate cure in a curing environment, despite the onset of Th2 cytokine production; and lastly, (e) antigen specificity of responding T cells, as assessed by V beta T cell receptor diversity, is not a critical determinant of disease outcome.

Animals↗
PubMedDate not supplied

[The role of atopic background in the genesis of allergic manifestations in intestinal parasitoses].

The previous literature and personal observations showed the predominant role of the atopic background in the appearance of the allergic manifestation in the parasitic infestation and especially in giardiasis. The lot investigated was made of 52 patients with allergic manifestations, also infested with Giardia intestinalis or with Ascaris lumbricoides. The hereditary collateral and personal allergic antecedents and the clearly deficient histaminopexy (1/20) were present in 1/2 of the patients. Summation of the various parameters of atopic background shows its presence in about 2/3 of the patients investigated. Association of the clinical involvement of trophallergens was present in 1/2 of the patients. The results show that the allergic manifestation in the intestinal parasitoses have a multifactorial determination. The atopic background is predominant in their development. These manifestations are often a result of alimentary allergy due to the absorption of alimentary antigens through the enteral mucous membrane affected by the parasite.

Ascariasis↗
PubMed1989

Biological control of insect pests affecting man and animals in the tropics.

Biological control of pests affecting the health of man and animals is practiced in various forms throughout the tropics. In this paper, the use of parasitic viruses, bacteria, protozoa, predatory arthropods, and fish against pests such as various mosquitoes, tse tse flies, and screwworm flies as published in the literature are reviewed. Mention is also made of the usefulness and applicability of the sterile insect technique, genetic control by chromosomal aberrations, and the exploitation of various incompatabilities. These are reviewed against the background of the present state of technology and limited resources that exist in many tropical countries. Most authors maintain that due to the relative length of time required to get a biological control system working efficiently, and the perennial nature of most tropical pest species, there is often the need to initially reduce the pest population by conventional means. There will thus be a balance between biological and chemical control in most systems. Emphasis is placed on meeting the urgent need for the exchange of research and development information on biological control of pests affecting man and his animals in the tropics.

Animals↗
PubMed2025

Naturally occurring variation in a cytochrome P450 modifies thiabendazole responses independently of beta-tubulin.

Widespread anthelmintic resistance has complicated the management of parasitic nematodes. Resistance to the benzimidazole (BZ) drug class is nearly ubiquitous in many species and is associated with mutations in beta-tubulin genes. However, mutations in beta-tubulin alone do not fully explain all BZ resistance. We performed a genome-wide association study using a genetically diverse panel of Caenorhabditis elegans strains to identify loci that contribute to resistance to the BZ drug thiabendazole (TBZ). We identified a quantitative trait locus (QTL) on chromosome V independent of all beta-tubulin genes and overlapping with two promising candidate genes, the cytochrome P450 gene cyp-35D1 and the nuclear hormone receptor nhr-176. Both genes were previously demonstrated to play a role in TBZ metabolism. NHR-176 binds TBZ and induces the expression of CYP-35D1, which metabolizes TBZ. We generated single gene deletions of cyp-35D1 and nhr-176 and found that both genes play a role in TBZ response. A predicted high-impact lysine-to-glutamate substitution at position 267 (K267E) in CYP-35D1 was identified in a sensitive strain, and reciprocal allele replacement strains in different genetic backgrounds were used to show that the lysine allele conferred increased TBZ resistance. Using competitive fitness assays, we found that neither allele was deleterious, but the lysine allele was selected in the presence of TBZ. Additionally, we found that the lysine allele significantly increased the rate of TBZ metabolism compared to the glutamate allele. Moreover, yeast expression assays showed that the lysine version of CYP-35D1 had twice the enzymatic activity of the glutamate allele. To connect our results to parasitic nematodes, we analyzed four Haemonchus contortus cytochrome P450 orthologs but did not find variation at the 267 position in fenbendazole-resistant populations. Overall, we confirmed that variation in this cytochrome P450 gene is the first locus independent of beta-tubulin to play a role in BZ resistance.

Animals↗
PubMed2026

Disentangling host genetic variation for avoidance and resistance to pathogens.

BACKGROUND: Hosts can use avoidance (e.g., behavior) to reduce their contact rates with pathogens; after contact, they can use resistance (e.g., immunity) to reduce the establishment and proliferation of an infection. Because both defenses preserve host fitness and reduce pathogen fitness, we expect that their epidemiological and evolutionary effects will be interdependent. This study used a two-locus model to understand the evolution of allelic associations (i.e., linkage disequilibrium or LD) between genes determining levels of avoidance and resistance in the presence of an infectious disease or a parasite. RESULTS: We found that polymorphism in both avoidance and resistance was possible, but only for a limited range of parameter values. At equilibrium within these polymorphic populations, avoidance and resistance alleles were negatively associated (i.e., in negative LD). However, most commonly, polymorphism was only stably maintained at one defense locus, and the other locus became fixed for one allele. CONCLUSIONS: The model shows that avoidance and resistance are likely to influence each other's evolution because of their joint effects on infection and their costs; however, predictions about their relationship are not necessarily straightforward or intuitive. For example, avoidance and resistance may be more likely to covary across than within populations.

Animals↗
PubMed1989

MHC restriction of the antibody repertoire to secretory antigens, and a major allergen, of the nematode parasite Ascaris.

Humans vary considerably in the antigen specificity of their immune responses to parasitic nematodes, and in the infection loads of individuals living in the same environment. The possibility that the former has a genetic basis operating through repertoire control of the immune system was investigated using infection of mice with the nematode Ascaris. The specificity of the antibody response was examined using excretory/secretory (ES) materials of the parasite as target Ag. No strain of mouse was found to recognize all of the potentially antigenic components of ES, and the Ag recognition patterns varied considerably from strain to strain. Using H-2 congenic mice on both the BALB and B10 backgrounds, it was established that the antigen recognition patterns were MHC-determined. Focusing on one particular component of ES, of Mr 14,000, only H-2s strains responded in IgG. This MHC restriction of the repertoire was confined to infection, and broke down under adjuvant-assisted immunization with the purified protein. The Mr 14,000 molecule was also found to be a potent allergen in a passive cutaneous anaphylaxis assay, and the IgE response to it was also restricted to H-2s. This haplotype was, however, a low IgE responder on the SJL background. There is, therefore, MHC control of the specificity of the immune response to this molecule, but non-MHC control of the amplitude of the IgE antibody response to it. Hybrids between responder and nonresponder strains (BALB/c x SJL)F1, responded to the Mr 14,000, but their responses to other ES components could not be predicted from the response patterns of parental strains. For example, the BALB/c parent responded to a 118-kDa component, but the SJL parent and the F1 progeny did not. Moreover, the response to a 41-kDa Ag was substantially down-regulated in the F1, whereas both parental strains responded vigorously. This new model system, therefore, has implications for MHC control of responses to the allergens of pathogens, and for the complex immunoregulation in heterozygotes in the context of infection.

Allergens↗
PubMed2025

Helminth infections affect host immune responses to viral infections and vaccines.

Helminths are highly prevalent in many regions of the world. Due to the chronic nature of most helminth infections, these parasites are proficient immunomodulators of their hosts. This modulation often leads to skewed or even impaired immune responses against unrelated antigens, such as viruses and vaccines, which can be both beneficial and detrimental for the host. The extent of these effects and the impact on the outcomes of viral infection depends on a variety of factors including timing and tropism of both infections, pathological mechanisms, genetic background, and environmental factors. In this review, we dissect these complex interactions between virus and helminths in the context of coinfection and the impact of helminth infection on antiviral vaccine efficacy. We characterize the key contributing mechanisms that have been defined in preclinical models and human trials and describe the immune actors involved in the modulation of the antiviral and vaccine immune response by helminths. Finally, we address the limitations of our current understanding of helminth-virus interactions.

Helminthiasis↗
PubMed1993

Candidate vaccine antigens identified by antibodies from mice vaccinated with 15- or 50-kilorad-irradiated cercariae of Schistosoma mansoni.

In murine schistosomiasis, the highest levels of resistance to cercarial challenge are obtained by vaccination with radiation-attenuated cercariae. To identify candidate vaccine antigens relevant to the vaccine model, we examined parasite antigens recognized by antibodies from mice vaccinated with irradiated cercariae of Schistosoma mansoni. To optimize recognition of a wide spectrum of antigens, several factors that influence the level of protection in this model were varied; specifically, we examined the effect of (i) single versus multiple vaccinations with irradiated cercariae, (ii) the dose of irradiation (15 or 50 kilorads) administered to the cercariae, and (iii) the genetic background of mouse strains, high-responder (C57BL/6J) versus moderate-responder (CBA/J) mice. We found that the number of vaccinations did not alter antibody specificity but modified the relative antibody titers against particular antigens. The dose of irradiation used to attenuate the immunizing cercariae had a similar effect on antibody titers but in addition influenced antibody specificity. Only mice that had been vaccinated with moderately irradiated cercariae recognized cathepsin B (Sm31) and Sm32. Interestingly, when vaccinated mice of the two strains, C57BL/6J and CBA/J, were compared, differences in antibody responses to particular antigens were observed. Both strains recognized the integral membrane protein Sm23, glutathione S-transferase, and cathepsin B, whereas Sm32 and paramyosin were recognized only by CBA/J mice, and heat shock protein 70 was recognized exclusively by C57BL/6J mice. In this study, we conclusively identified six distinct antigens that are specifically recognized by the humoral immune response of vaccinated mice.

Animals↗
PubMed1984

The impact of new technologies on vaccine development.

The ability to move genetic determinants between species using in vitro gene-manipulation techniques has opened up new approaches to vaccine development. This has rapidly grown into an exciting area of research in both academic and industrial laboratories. There are numerous scientific challenges which require multidisciplinary teams to solve problems in creating new immunogens. This has challenged our existing knowledge about protein structure and conformation, microbial pathogenicity and the immune system. Recombinant-DNA techniques are invaluable as tools of analysis and antigen production. The surface of micro-organisms can also be minutely explored with the use of synthetic peptides and monoclonal antibodies. Nevertheless, these new technologies do not allow us to circumvent the need for detailed understanding of pathogens and the disease process. What is apparent from the work carried out so far is that there are few easy answers to vaccine development and it is not realistic to expect rapid solutions to these problems. As there are many potential targets for constructing novel vaccines for both human and animal diseases, it is helpful to establish some priorities. There is a tendency to look at the existing effective vaccines and simply direct research at producing them more economically or with enhanced safety and stability. The advantage of this approach is that considerable background work will have already been carried out establishing the basis for the application of recombinant DNA techniques. However, this can also lead to conflicts (often within the same institute or company) between the new and old technologies. This could be to the detriment of the new technologies which are still only partly developed and may not be good enough yet to compete with existing vaccines in cost or efficacy. The more ambitious, and eventually more rewarding, approach is to attempt to develop new vaccines where none had existed before. There is a vast untapped market, especially in the parasitic diseases, but the scientific problems may be considerable and much more background work is likely to be necessary. Indeed, most of the work in this area is more accurately referred to as basic research rather than vaccine development as totally new, effective vaccines are still some way off. Having directed research towards a specific organism or disease there are still many options available as to the scientific strategy to adopt. As discussed in this review it may be possible to consider subunits, synthetic antigens and live (attenuated or heterologous) organisms as possible vaccines.(ABSTRACT TRUNCATED AT 400 WORDS)

Adjuvants, Immunologic↗