Epstein-Barr virus (EBV), a ubiquitous human herpesvirus and an aetiological agent of infectious mononucleosis, has a unique tropism for B lymphocytes. Clinical and laboratory features of chronic active EBV infections are chronic or persistent infectious mononucleosis-like symptoms and high antibody titre against early antigens (EA). Kawasaki disease (KD), aetiology unknown, is thought to be self-limited immunologically mediated vasculitis. Clinical features of KD are fever, rash, mucositis, lymphadenopathy and coronary artery damage. We report here a child with chronic active EBV infection accompanied by dilatation of coronary arteries. All the EBV-determined nuclear antigen (EBNA)-positive lymphocytes had exclusively CD4 antigen, as revealed by dual staining immunofluorescence analysis. Southern blot hybridization showed that the purified CD4+ cells harboured EBV genome.

Lymphoproliferative disease of granular lymphocytes (LDGL) is a heterogeneous disorder and the pathogenesis is likely to be complex. Some patients with chronic active EBV (CAEBV) infection also have LDGL. To investigate the relationship between EBY infection and the pathogenesis of LDGL, we conducted a survey for EBV DNA sequences by Southern blot analysis of DNA obtained from the peripheral blood of seven patients with LDGL including one with CAEBV infection.

Epstein-Barr virus (EBV) nuclear antigen leader protein (EBNA-LP

SUMMARYHybridomas were formed between mouse myeloma ceils and spleen cells from mice immunized with Marek's disease virus (MDV) or with herpesvirus of turkeys (HVT). Three monoclonal antibodies were obtained, two (M26 and M34) from MDV clones and one (H9) from an HVT clone, all of which were specific for cross-reactive membrane antigen (MA) expressed on the surface of cells infected with MDV or HVT. All three antibodies also reacted with MDV-and HVT-specific glycoproteins in the molecular weight (mol. wt.) ranges 54K to 70K (MDV-gp54/70) and 50K to 64K (HVTgp50/64), respectively. These glycoproteins constitute the putative 'A' antigens which are found in the medium of cultures infected with MDV or HVT. These results suggest that the cross-reactive MA may correspond to 'A' antigen. Pulse-chase experiments using monoclonal antibodies revealed the presence in virus-infected cells of precursor and processed forms of MDV-gp54/70 and HVT-gp50/64 which differ in size. Moreover, by two-dimensional gel electrophoresis we found that MDV and HVT glycoproteins were separated to heterogeneous spots by electric charge as well as mol. wt. The several spots with higher mol. wt. and with more acidic isoelectric points among them were lost by treatment with neuraminidase, suggesting that the processing was, at least in part, due to the addition of sialic acid to the precursor forms. Tunicamycin blocked the surface expression of cross-reactive HVT-MA on HVTinfected cells. Phosphonoacetic acid inhibited both the appearance of HVT-MA on the cell surface and synthesis of HVT-gp50/64, indicating that the MA and secreted glycoprotein were late gene products of the HVT genome.

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