INTRODUCTION

In the general context of genetic dissection of complex traits, genetics of human infectious diseases present the following several advantages and specificities: (1) there is a known causative agent which is absolutely required to become infected and to get the disease, but generally not sufficient stressing the importance of the host background; (2) environmental factors influencing the risk of infection are generally known and can be taken into account in the analysis when they are accurately measured; (3) there is a strong orientation in the choice of candidate genes based on the function of the gene and its known role in the response to the studied pathogen and/or on mouse–human chromosome homology exploiting the identification of murine resistance loci; and (4) the identification of major genes involved in the response to a given infectious pathogen takes advantage of the opportunity to study several complementary traits related to this pathogen. Among these traits are clinical phenotypes which are usually binary (affected/unaffected) but can take into account time to onset of the disease (e.g., time of progression to AIDS for HIV-infected patients), biological phenotypes measuring infection which can be either quantitative (e.g., infection intensities measured by fecal egg counts in schistosomiasis) or binary (HIV seropositive/seronegative), and immunological phenotypes measuring the immune response (antibody or cytokine levels, skin test response, etc.) more or less specific to a given antigen.