The study investigated the genetic make-up of different ecotypes of indigenous chickens (ICs) in Kenya based on major histocompatibility complex (MHC)-linked and non-MHC microsatellite markers. Blood samples were collected from eight regions (48 birds per region) of Kenya: Kakamega (KK), Siaya (BN), West Pokot (WP), Turkana (TK), Bomet (BM), Narok (NR), Lamu (LM) and Taita-Taveta (TT) and genotyped using two MHC-linked and ten non-MHC markers. All MHC-linked and non-MHC markers were polymorphic with a total of 140 alleles, of which 56 were identified in MHC-linked markers. Mean number of alleles (Na and Ne), private alleles, heterozygosity and genetic distances were higher for MHC-linked markers compared with non-MHC markers. The ad hoc statistic ΔK detected the true numbers of clusters to be three for MHC-linked markers and two in non-MHC markers. In conclusion, Kenyan ICs belong into two to three genetically distinct groups. Different markers systems have different clustering system. MHC-linked markers divided ICs into three mixed clusters, composing of individuals from the different ecotypes whereas non-MHC markers grouped ICs into two groups. These IC ecotypes host many and highly diverse MHC-linked alleles. Higher allelic diversity indicated a huge amount of genetic variation in the MHC region of ICs and supported their reputation of being hardy and resistant to diseases.

We develop the hypothesis that parasites do not invade extreme environments, i.e. hostile hosts, but rather ‘create’ them. We argue that parasites may have driven the evolution of the constitutive and adaptive immune system. This leads to several implications. First, parasites respond to ‘genes to kill’ by ‘genes to survive’ and this triggers an indefinite selection of measures and counter-measures. Second, these revolutionary arms races may lead to local adaptation, in which parasite populations perform better on local hosts. Third, the evolution of the immune system, whose responses are predictable, may allow parasites to specialize, to evade and even to manipulate. Finally we show that the correlations between the increase in the antibody repertoire, the expansion of MHC loci and parasite pressures support our hypothesis that both host complexity and parasite pressures can be invoked to explain the diversity of antibodies, T-receptors and MHC molecules.

The course of primary infection was studied in BALB and B10 H-2 congenic mouse strains. The duration of infection, as assessed with regular faecal egg counts and worm burdens, was shorter in mice carrying the H-2s, H-2d or H-2q haplotypes when compared to mice with H-2b. Strains with H-2k were intermediate. An experiment was carried out to test the hypothesis proposed by Wassom, Krco & David (1987) predicting that the progeny of I–E+ve mouse strains crossed with I–E-ve strains, would show susceptibility rather than resistance to infection. This hypothesis was not substantiated by our data and we conclude that it does not apply to primary infections with Heligmosomoides polygyrus. It is proposed that the gene products of at least two loci within the H-2 (associated with the H-2b and H-2k haplotypes) are crucial in determining the response phenotype of mice to primary infection with H. polygyrus. One allele, (associated with the H-2b haplotype) may be preferentially affected by parasite-mediated immunosuppression.

Multiple sclerosis (MS) is an autoimmune disease with an important genetic component. The strongest genetic association is with the major histocompatibility complex (MHC) region. Several MHC alleles predispose to the disease, the most prominent of which are certain alleles in the HLA-DR2 haplotype. Functional and structural studies have helped to explain the molecular basis of these associations. Although there is currently no curative treatment for MS, an increased understanding of the disease has aided the design of immunotherapies that act on the immune system more specifically than the longstanding drugs. Many of these therapies work at the antigen-specific level, disrupting the interaction between T-cell receptors and MHC molecules that leads to disease.

The major histocompatibility complex (MHC) harbours genes whose primary function in regulating immune responsiveness to infection is to present foreign antigens to cytotoxic T lymphocytes (CTLs) and T helper cells. In the case of infection by human immunodeficiency virus (HIV), defining the optimal HIV epitopes that are recognised by CTLs is important for vaccine design, and this in turn will depend on the characteristics of the predominant infecting virus. Moreover, the particular MHC human leukocyte antigens (HLAs) expressed by a geographical population is important since these are likely to determine which HIV epitopes are immunodominant in the anti-HIV immune response. Consideration of these aspects has lead to the dawn of a new era of MHC-based vaccine design, in which the CTL epitopes are selected on the basis of the frequency of restricting MHC alleles. This article reviews data on the distribution patterns of molecular subtypes of HLA class I and class II extended haplotypes, discussing distribution among Asian Indians but with reference to global distributions. These data provide a genetic basis for the possible predisposition and fast progression of HIV infections in the Indian population. Since there is selective predominance of different HLA alleles and haplotypes in different populations, a dedicated screening effort is required at the global level to develop MHC-based vaccines against infectious diseases. It is hoped that this might lead to the development of multivalent, poly-epitope, subtype-specific HIV vaccines that are specific for the target geographical location.

The human leukocyte antigen class I allele HLA-B27 is a major histocompatibility complex (MHC) antigen that is strongly associated with the spondyloarthritic group of human rheumatic diseases, the most commmon of which is ankylosing spondylitis. Although the mechanism underlying this disease association remains unknown, numerous theories have been proposed. Much more is known of the natural role of HLA-B27 in binding and presenting antigenic peptides to T cells. The ‘arthritogenic peptide hypothesis’ suggests that the role of HLA-B27 in disease relates to its specificity for binding certain peptides. Recently, it has also been shown that HLA-B27 has an unusual cell biology and can adopt a novel homodimeric structure. In this review, a molecular model of the HLA-B27 homodimer is presented and the possible pathogenic significance of such a structure is discussed.

Parasitic exploitation occurs within and between a wide variety of taxa in a plethora of diverse contexts. Theoretical and empirical analyses indicate that parasitic exploitation can generate substantial genetic and phenotypic polymorphism within species. Under some circumstances, parasitic exploitation may also be an important factor causing reproductive isolation and promoting speciation. Here we review research relevant to the relationship between parasitic exploitation, within species-polymorphism, and speciation in some of the major arenas in which such exploitation has been studied. This includes research on the vertebrate major histocompatibility loci, plant–pathogen interactions, the evolution of sexual reproduction, intragenomic conflict, sexual conflict, kin mimicry and social parasitism, tropical forest diversity and the evolution of language. We conclude by discussing some of the issues raised by comparing the effect of parasitic exploitation on polymorphism and speciation in different contexts.

The results from experimental studies about genetic factors (‘major genes’) involved in disease resistance and their effects in different genetic backgrounds are reviewed and discussed. The major genes considered are (1) Tv-A and Tv-B, gene loci controlling resistance to infection from avian leukosis virus (ALV), (2) B blood groups which represent the major histocompatibility complex (MHC) of the domestic fowl and are indicators of genetic differences in resistance to Marek's disease (MD) and, only tentatively, (3) endogenous viral (ev) genes which can influence reactions to leukosis infection. For these experiments purebred and crossbred progeny from three genetically different experimental White Leghorn lines have been used extensively. The results concerned with leukosis are based on a comparison between groups of chickens which were homozygous resistant or susceptible to ALV infection. The variability in the amount of damage from leukosis points to interactions between the genotype of resistance to ALV infection and genetic characteristics of the line or lines involved. In this respect the negative influence of ev 6 on the immune response to ALV infection could play a role. To study the association of B blood groups and resistance to MD, an experimental line which still segregated at the B locus (B2, B13, B14 and B21) was crossed with two other lines which were homozygous, respectively, for B2 and B15. Mortality caused by MD in birds carrying the same segregating B blood groups showed a completely different pattern in the two crosses. Rather unexpectedly, the difference in MD mortality was largest between the two types of crossbred layers carrying B21, which points to an interaction between line and B blood group type. Further studies suggested that this interaction depends on genes within the MHC for which the lines crossed might differ. The availability of information from different genetic groups allowed an evaluation of the importance of each ‘major gene’ in relation to the comparative effects of other factors influencing the trait under consideration. Apart from becoming aware of possible interactions resulting from genetic differences between lines, simultaneous results from genetically different experimental lines also provide a safeguard against overestimating or underestimating the potential of such ‘major genes’ for practical utilization in poultry breeding.