Endemic diseases are caused by environmental and genetic factors. While in this special issue several chapters deal with environmental factors, including infections, the present focus is on genetic causes of disease clustering due to inbreeding and recessive disease mechanisms. Consanguinity is implying sharing of genetic heritage because of marriage between close relatives originating from a common ancestor. With limited natural selection, recessive genes may become more frequent in an inbred compared with an outbred population. Consanguinity is common in North Africa (NA), and the estimates range from 40 to 49% of all marriages in Tunisia and 29-33% in Morocco. As a consequence, recessive disorders are common in the NA region, and we give some examples. Thalassaemia and sickle cell disease/anaemia constitute the most common inherited recessive disorders globally and they are common in NA, but with immigration they have spread to Europe and to other parts of the world. Another example is familial Mediterranean fever, which is common in the Eastern Mediterranean area. With immigrantion from that area to Sweden, it has become the most common hereditary autoinflammatory disease in that country, and there is no evidence that any native Swede would have been diagnosed with this disease. The examples discussed in this chapter show that the historic movement of populations and current immigration are influencing the concept of 'endemic' disease.

The epidemiological transition has reduced infectious diseases mortality in most European countries, yet increased migrant influx risks importing diseases. All reported prevalence rates must be considered on a case-by-case basis depending on the disease in question, respective European Union (EU) country and migratory patterns at work. Tuberculosis has seen a re-emergence in Europe and is concentrated among migrants. Migrants arriving from North Africa (NA) and sub-Saharan Africa (SSA) carry higher rates of hepatitis C and B than the local EU population. The human immunodeficiency virus (HIV) impact of NA migrants to Europe is very low but a hallmark of the HIV epidemic is the penetration and circulation of non-B strains, recombinant forms and HIV-drug-resistant profiles through SSA migrants using NA as a transit point into Europe. Leishmaniasis is a re-emerging zoonotic disease prevalent to Southern Europe although not specifically isolated in migrant groups. Although not endemic in NA countries, malaria represent S: a risk in terms of re-emergence in Europe through transitory migrants arriving from SSA with the destination to Europe. Schistosomiasis has been largely eliminated from NA. High migrant flux into European countries has resulted in changing patterns of communicable disease and collectively requires a continuous surveillance. World Health Organization guidelines recommend targeted screening and preventative vaccination, followed by integration of migrants into the local health-care systems allowing for long-term treatment and follow-up. Finally, effective public health campaigns as a form of prevention are essential for the mitigation of disease dissemination in the migrant pool and for second-generation children of migrants.

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Cell surface-associated viral glycoproteins are thought to play a major role as target antigens in cellular cytotoxicity and antiviral immunosurveillance. One such glycoprotein is the Epstein-Barr virus (EBV)-encoded glycoprotein 350 (gp350), which is expressed on both virion envelope and EBV producer cells and carries the virus attachment protein moiety. Although it is known that some antibodies to gp350 can neutralize the virus, the role of this glycoprotein in EBV-specific cellular cytotoxicity is not yet clear. We describe here a study in which we successfully used a new approach to demonstrate that gp350 is a target antigen for EBV-specific antibody-dependent cellular cytotoxicity (ADCC). Transfection of gp350-negative cells resistant to natural killer (NK) cell activity (i.e., Raji) with a recombinant vector (pZIP-MA) containing the gene encoding the EBV-gp350 and the neomycin resistance gene enabled us to isolate cell clones with a stable and strong expression of gp350 on their surface membranes. ADCC determined by using two clones clearly demonstrated that gp350 is the target of the EBV ADCC. Interestingly, this ADCC was comparable to that obtained against the EBV-superinfected (coated) Raji cells expressing the same percentage of gp350 positivity as the two clones. No cytotoxic activity was detected against either nontransfected (gp350-negative) Raji cells or cells transfected with the vector [pZIP-neo-SV(X)1] lacking the gp350 gene. In addition to demonstrating that gp350 is a target molecule for EBV-specific ADCC, our approach in using NK-resistant transfectants provides a lead for probing the role of cell surface-associated viral antigens in specific cellular killing and immunosurveillance.