The implications for childhood leukemia of infection with adenovirus.
Adenoviruses have mechanisms that allow persistence in lymphoid cells and immunoevasion. They downregulate major histocompatibility complex (MHC) class I antigen expression and may trigger an autoimmune reaction against MHC class II antigens through mimicry. Adenoviral persistence could be facilitated by human leukocyte antigens A2 and DR53, thereby allowing a preleukemic clone to escape immune surveillance and progress to leukemia.
Dorak
M T
MT
Department of Haematology, University of Wales College of Medicine, Cardiff, UK.
D000256:Adenoviridae / Q000737:chemistry / Q000276:immunology; D000257:Adenoviridae Infections / Q000276:immunology*; D000293:Adolescent; D000956:Antigens, Viral / Q000276:immunology; D015551:Autoimmunity; D002648:Child; D002675:Child, Preschool; D015789:HLA-A2 Antigen / Q000276:immunology; D006684:HLA-DR Antigens / Q000276:immunology; D059845:HLA-DRB4 Chains; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance; D007157:Immunologic Surveillance; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000821:virology*; D017735:Virus Latency
D000956:Antigens, Viral; D015789:HLA-A2 Antigen; D006684:HLA-DR Antigens; C050610:HLA-DR53; D059845:HLA-DRB4 Chains; D015395:Histocompatibility Antigens Class I; D000949:Histocompatibility Antigens Class II