YOU ARE NOW CONNECTED TO THE TOXLINE (1981 FORWARD, NON-ROYALTY) FILE. ==ADENO VIRUS AND LEUKEMIA== 6 AUTHOR Rio B AUTHOR Louvet C AUTHOR Gessain A AUTHOR Dormont D AUTHOR Gisselbrecht C AUTHOR Martoia R AUTHOR Auzanneau G AUTHOR Miclea JM AUTHOR Baumelou E AUTHOR Dombret H AUTHOR et al TITLE [Adult T-cell leukemia and non-malignant adenopathies associated with HTLV I virus. Apropos of 17 patients born in the Caribbean region and Africa] SOURCE Presse Med; VOL 19, ISS 16, 1990, P746-51 (REF: 26) ABSTRACT Adult T-cell leukaemia is the first blood disease caused by a retrovirus: HTLV-1. The authors report the first French series of 15 patients, of whom 9 came from the classical endemic areas--the Antilles and outer Caribbean Islands--and 6 from Africa where the serological prevalence of HTLV-1 is high but few cases of adult T-cell leukaemia have been reported. Emphasis is laid on the importance of immunodeficiency (refractory strongyloidiasis, Pneumocystis carinii pneumonia, polyclonal B lymphoproliferative syndrome) and of other pathologies associated with the retrovirus (polyarthritis, lymphocytic interstitial pneumonia). The authors also describe the presence of adenopathy in healthy carriers: either adenitis suggestive of retroviral infection, or Castelman's disease adenopathy. These clinical presentations are similar to those described in lymphadenopathy syndromes due to the human immunodeficiency viruses. Aggressive lymphomas require chemotherapy, but sooner or later resistance develops, and the prognosis is very poor. The indications for allogeneic bone marrow transplantation are still to be determined. The diagnosis of adult T-cell leukaemia must be considered in all patients with blood disease coming from the endemic areas. 43 AUTHOR Yakinoglu AO AUTHOR Heilbronn R AUTHOR Burkle A AUTHOR Schlehofer JR AUTHOR zur Hausen H TITLE DNA amplification of adeno-associated virus as a response to cellular genotoxic stress. SOURCE Cancer Res; VOL 48, ISS 11, 1988, P3123-9 ABSTRACT We studied DNA amplification of helper virus-dependent parvoviruses [adeno-associated virus (AAV)] following genotoxic treatment of a number of mammalian cell lines from different species including primary, immortalized, and tumorigenic cells. All cell lines, either infected with AAV or transfected with parvoviral DNA, readily amplified AAV DNA in the absence of helper virus following treatment of cells with a wide variety of genotoxic agents like chemical carcinogens, UV, heat shock, and metabolic inhibitors of DNA replication or protein synthesis. In addition, we show that in the SV40-transformed Chinese hamster cell lines CO60 and CO631 carcinogen-induced AAV DNA amplification may result in a complete AAV replication cycle giving rise to infectious AAV progeny. Our results demonstrate that AAV DNA amplification induced by genotoxic agents is completely independent of the presence of viral helper functions. Because its induction is not restricted to a specific cell type or to a malignant phenotype, AAV DNA amplification may represent a marker for cellular genotoxic stress response. 46 AUTHOR Yates VJ AUTHOR Dawson GJ AUTHOR Pronovost AD TITLE Serologic evidence of avian adeno-associated virus infection in an unselected human population and among poultry workers. SOURCE Am J Epidemiol; VOL 113, ISS 5, 1981, P542-5 ABSTRACT Six (6.0%) of 100 serum samples from an unselected adult population were positive for antibody to avian adeno-associated virus (A-AV) by agar gel precipitation (AGP), and 10 (15.6%) of 64 were positive by virus neutralization (VN). Three (14.3%) of 21 samples from poultry workers (industry or research) were positive for avian A-AV antibody by AGP and 14 (66.7%) of 21 were positive by VN. All sera positive by AGP were also positive by VN. Twenty-two of 244 sera positive for antibody to avian A-AV by VN were positive for human adenovirus antibody. None of the sera were positive for avian adenoviral antibody by AGP. No cross reaction was noted by AGP when antiserum to avian A-AV was reacted against primate antigens of serotypes 1-4 or when antiserum to A-AV serotypes 1-14 were reacted against avian A-AV antigen. Antiserum prepared against primate A-AV serotypes 1-4 did not neutralize the avian A-AV. These results suggest that avian A-AV infections are not restricted to avian species but are found in the human adult population.