Altered HIV expression and EBV-induced transformation in coinfected PBLs and PBL subpopulations.
Human immunodeficiency virus (HIV) IIIB expression and Epstein-Barr virus (EBV) B95.8-induced transformation were studied during coinfection. Coinfection of peripheral blood lymphocyte (PBL) cultures with HIV and EBV resulted in down-regulation of HIV expression. EBV-induced and spontaneous transformation were markedly reduced in PBL cultures exposed to HIV before EBV. On the other hand, transformation was enhanced when PBL cultures were infected with HIV either simultaneous to or after EBV. Reconstitution of EBV-infected B cell cultures with autochthonous T cells demonstrated that HIV-infected T cells had a reduced ability to inhibit EBV-induced transformation. PHA stimulation of HIV-infected T cells eliminated their ability to inhibit EBV-induced transformation. Lymphoblastoid cell lines (LCLs) established from coinfected PBLs expressed B cell markers and were EBV positive, while a large proportion of the LCLs expressed HIV antigens, released reverse transcriptase activity into the supernatant, and produced syncytia when cocultivated with indicator cell line SupT1. HIV provirus could be detected in LCLs established from coinfected cultures by PCR amplification using specific sets of amplimers for gag and env genes of HIV. To more closely examine the role of various cell types in lymphocyte transformation and HIV replication during coinfection, experiments were carried out using subpopulations enriched for either B or T cells. Simultaneous coinfection of purified B cells with EBV and HIV resulted in a marked reduction of HIV expression, whereas EBV-induced transformation was enhanced. In contrast, spontaneous B cell transformation was inhibited by HIV. A proportion of LCLs established from purified B cells coinfected with EBV and HIV expressed HIV antigens, released reverse transcriptase activity, and produced syncytia on SupT1 cells. These results demonstrate that the IIIB strain of HIV and B95.8 strain of EBV can interact during coinfection of B cells to alter the course of virus expression.
Henderson
E E
EE
Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.
Yang
J Y
JY
Zhang
R D
RD
Bealer
M
M
D001402:B-Lymphocytes / Q000382:microbiology; D001483:Base Sequence; D002459:Cell Fusion; D002460:Cell Line; D002472:Cell Transformation, Viral; D005434:Flow Cytometry; D015967:Gene Expression Regulation, Viral; D015752:Genes, env; D015750:Genes, gag; D006678:HIV / Q000201:enzymology / Q000235:genetics*; D015699:HIV Envelope Protein gp120 / Q000235:genetics; D004854:Herpesvirus 4, Human / Q000235:genetics*; D006801:Humans; D066298:In Vitro Techniques; D008214:Lymphocytes / Q000382:microbiology*; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction; D012367:RNA, Viral / Q000235:genetics; D012194:RNA-Directed DNA Polymerase / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology / Q000382:microbiology; D013997:Time Factors; D014779:Virus Replication
D015699:HIV Envelope Protein gp120; D012367:RNA, Viral; D012194:RNA-Directed DNA Polymerase