title: Morphological and phenotypical changes in EBV positive lymphoblastoid cells infected by HIV-1.
abstract: Human Immunodeficiency Virus type 1 (HIV-1) infects CD4+ T lymphocytes and various other cell types, including B cells. Since HIV-1 seropositive individuals have high numbers of B cells carrying Epstein-Barr Virus (EBV), and are at high risk for development of EBV-associated lymphoproliferative diseases, we studied the mode of HIV-1 infection in four EBV-positive lymphoblastoid B-cell lines (LCLs) as well as some molecular and biological features of the B cells infected by both viruses. We found that LCL cells were successfully infected in vitro by HIV-1, despite the lack of CD4 antigen expression on the cell membrane. LCL cells displayed a persistent, productive, and non-cytopathic infection. Moreover, HIV-1 infection induced reactivation of EBV latent genomes in one cell line. Following HIV-1 infection, LCL cells showed a decrease in B-cell activation markers CD23 and CD39, and an increase in CD10 immature B-cell antigen. Not all cells in each LCL expressed HIV-1 antigens, but all CD10+ cells also co-expressed the HIV-1 envelope protein gp 120. Furthermore, HIV-1 infected LCL cells grew as disperse suspensions, and formed more agar colonies than control, non-HIV-1-infected LCLs. These findings raise the possibility that HIV-1 might play a role in EBV reactivation, and in B-cell lymphoma pathogenesis in AIDS patients.
authors.affiliation: Institute of Oncology, University of Padova, Italy.
authors.forename: A
authors.initials: A
authors.lastname: De Rossi
authors.forename: M L
authors.initials: ML
authors.lastname: Calabro
authors.forename: E
authors.initials: E
authors.lastname: D'Andrea
authors.forename: M
authors.initials: M
authors.lastname: Panozzo
authors.forename: D
authors.initials: D
authors.lastname: Saggiori
authors.forename: F
authors.initials: F
authors.lastname: Mammano
authors.forename: S
authors.initials: S
authors.lastname: Roncella
authors.forename: M
authors.initials: M
authors.lastname: Ferrarini
authors.forename: L
authors.initials: L
authors.lastname: Chieco-Bianchi
mesh_terms: D000251:Adenosine Triphosphatases; D015703:Antigens, CD / Q000032:analysis; D000944:Antigens, Differentiation, B-Lymphocyte / Q000032:analysis; D001081:Apyrase; D001402:B-Lymphocytes / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D002478:Cells, Cultured; D004279:DNA, Viral / Q000032:analysis; D015658:HIV Infections / Q000382:microbiology* / Q000473:pathology; D015497:HIV-1; D004854:Herpesvirus 4, Human / Q000235:genetics / Q000254:growth & development; D006801:Humans; D010641:Phenotype; D011961:Receptors, Fc / Q000032:analysis; D017455:Receptors, IgE; D014412:Tumor Virus Infections / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D014775:Virus Activation
chemical_list: D015703:Antigens, CD; D000944:Antigens, Differentiation, B-Lymphocyte; D004279:DNA, Viral; D011961:Receptors, Fc; D017455:Receptors, IgE; D000251:Adenosine Triphosphatases; D001081:Apyrase; C067869:CD39 antigen