The relationship between enteroviruses, especially type B Coxsackieviruses (CV-B) and T1D, in genetically predisposed individuals has been highlighted largely through epidemiological studies [7–11]. Several mechanisms see more not mutually exclusive have been suggested to elucidate the viral pathogenesis of T1D [11,12]. One of the possible mechanisms is the disturbance of central tolerance

as a result of the infection of thymus with viruses. Clinical evidence and experimental findings show that viral infections are responsible for thymus abnormalities and dysfunctions, although in some cases the organ has not been reached BIBW2992 molecular weight by the infectious agent. HIV, belonging to the Retroviridae family, is the virus that has been associated most frequently with thymus disorders in the literature. HIV has been detected in thymuses of infected individuals [13–16]. In addition, human intrathymic T cell precursors and their progeny, representing many stages of T cell ontogeny, have been demonstrated to be susceptible to HIV-1 infection in vitro[17]. The chimeric severe combined immunodeficiency–human (SCID-hu) xenograft mouse model (bearing human T cells derived from transplantation of human thymic fragments

and liver tissue under the renal capsule) showed that human thymocytes are also susceptible to HIV

infection in vivo[18,19]. Moreover, it is likely that HIV infects the thymic microenvironment, as marked disruptions and significant viral loads have been observed in the thymic compartment in HIV-infected SCID-hu mice [19], a finding that was confirmed later by the demonstration of infected thymic dendritic cells [20]. Whether or not the thymic epithelium is also infected by this virus is an issue that deserves further investigation. Indeed, thymic epithelial cells (TEC) were shown previously to contain HIV RNA in human autopsy samples and also in the SCID-hu mouse model, Tenofovir cell line although productive infection of these cells could not be demonstrated definitively [14,19]. Furthermore, the same SCID-hu mouse model showed degenerating TEC even without detection of HIV in these cells [19]. The relevance of TEC infection lies in the fact that these cells play a critical role in the differentiation of T cell precursors, providing a microenvironment with a unique capacity to generate functional and self-tolerant T cells [21,22]. HIV infection is generally accompanied by several cytological and histological abnormalities in the thymus network.