La dépression est un phénomène très fréquent dans le monde occidental. Deux types de théories évolutionnistes peuvent être distinguées : 1 : les théories utilitaristes psychologiques pour lesquelles la dépression est une adaptation psycho-sociale qui ne remplit plus son rôle dans notre monde moderne ; 2 : les théories utilitaristes biologiques pour lesquelles la dépression accompagne notre lutte contre des agents pathogènes en vue de concentrer nos efforts sur cette lutte.

1. Théories utilitaristes psychologiques [1,2] : la dépression pourrait être un signal utile pour amener l’individu atteint à réorienter ses buts de vie, afin d’économiser de l’énergie et des ressources allouées à des objectifs inatteignables. Elle pourrait aussi servir de signalisation sociale, soit en vue de diminuer une agression dans le cadre d’une compétition hiérarchique, en donnant une information d’absence de menace, soit en appuyant une demande d’aide par l’entourage. Les conditions de vie moderne pourraient expliquer pourquoi un mécanisme utile s’est transformé en pathologie chronique : impossibilité de réorienter ses investissements faute d’opportunité alternative, difficulté à quitter des milieux dans lesquels on occupe une place hiérarchique défavorable et rétrécissement des cercles sociaux qui font que l’appel à l’aide résonne dans le vide.

2. Théories utilitaristes biologiques [3,4] : la dépression pourrait être utile pour réorienter les ressources de l’individu en vue de combattre une infection. Cependant, le stress psycho-social, l’obésité, le changement de diète, la diminution du temps de sommeil et l’isolement social pourraient avoir contribué à modifier l’équilibre de notre flore intestinale. La diminution de la coopération issue d’une co-évolution avec certains micro-organismes intestinaux (« les vieux amis ») serait responsable d’une activité inflammatoire chronique, indépendamment de toute lutte contre un agent infectieux pathogène, ce qui favoriserait les allergies, les maladies auto-immunitaires, la dépression et la fatigue chronique.

The chicken major histocompatibility complex B (MHC-B) – a cluster of genes associated with natural disease resistance or susceptibility – has been investigated in experimental and inbred lines by serological typing. However, that method showed some weaknesses for its use on out breeds. This study aims to explore the genetic diversity of the MHC-B of Cameroon indigenous chicken through molecular typing with LEI0258 and MCW0371 microsatellite markers. MHC-B haplotypes of 290 chickens from four agro-ecological zones were identified and compared with published haplotypes. Alleles were analysed for genetic diversity and relationship among Cameroon chicken populations. Hypothetically new LEI0258 alleles and haplotypes were detected. Overall, polymorphism parameters were relatively high in the Cameroon western highlands. The analysis of molecular variance revealed great variability (80.00 percent) between individuals than among and within ecotypes. The inbreeding coefficients of overall populations (FIT), among population (FST) and within population (FIS) were 0.26, 0.04 and 0.22, respectively, and all were highly significant (P < 0.001). A UPGMA tree based on Nei's DA genetic distances showed a clear distinction between Cameroon and out-groups and a structuring of within-country populations into three clusters. There is a great genetic diversity of the MHC-B in Cameroon native chicken and also a need of sequencing of the identified alleles for an accurate identification prior to their assessment for natural disease resistance and responsiveness to vaccination.

Cellular and humoral immune responses against arthropod vector antigens in invertebrate hosts affect vector physiology and significantly modulate the transmission of pathogens. This phenomenon may be the basis for novel methods of disease control based on immunization against arthropod antigens. Current research in this field is briefly reviewed.

Different modes of immune reactions of insect vectors of human and animal diseases to nematode and protozoan parasites, fungi, bacteria, viruses and to other biological materials e.g. xenografts are discussed in this paper. Since most of the insect vectors of diseases are adult dipterans with low numbers of circulating haemocytes, their mode of defence against metazoan parasites and fungal pathogens is primarily by means of humoral encapsulation, with little haemocyte participation. Although earlier workers reported that humoral capsules in dipterans were formed without direct participation by haemocytes, this paper reveals increasing evidence of cellular involvement in the formation of humoral capsules, both at the initial and terminal stages of the encapsulation process. The role of phenoloxidase system in non-self recognition and in the process of melanization of haemolymph and capsules formed around parasites and fungal pathogens is also discussed. Immune defence of insect vectors against bacterial invasion by means of haemocytic reactions e.g. phagocytosis and nodule formation and by synthesis and release of humoral antibacterial factors e.g. lysozyme, attacins and cecropins is described and compared with similar reactions reported to occur in other insects. The role of lectins in defence of insect vectors against the parasites they transmit e.g. sandflies against Leishmania, blackflies against Onchocerca and tsetse against Trypanosomes is discussed and the possible mechanisms by which some parasites evade recognition and attack by the vector immune systems are also briefly discussed.