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Human interleukin‐6 induces human herpesvirus‐8 replication in a body cavity‐based lymphoma cell line
Author(s) -
Song Jian,
Ohkura Takako,
Sugimoto Masamichi,
Mori Yasuko,
Inagi Reiko,
Yamanishi Koichi,
Yoshizaki Kazuyuki,
Nishimoto Norihiro
Publication year - 2002
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.10218
Subject(s) - virology , lytic cycle , biology , transcription (linguistics) , capsid , viral replication , reverse transcriptase , virus , antibody , jurkat cells , gene , cell culture , microbiology and biotechnology , t cell , immunology , polymerase chain reaction , genetics , immune system , philosophy , linguistics
Human herpesvirus‐8 (HHV‐8) is etiologically associated with Kaposi's sarcoma (KS), body cavity‐based lymphoma (BCBL), and multicentric Castleman's disease (MCD). These HHV‐8‐associated diseases arise predominantly in acquired immunodeficiency syndrome (AIDS) patients. Human interleukin‐6 (huIL‐6) elevated in the serum of AIDS patients is suggested to stimulate the growth of KS and BCBL and to augment the symptoms of MCD. To determine whether huIL‐6 stimulates HHV‐8 replication directly, expression of the HHV‐8 ORF‐50 immediate‐early gene (transcription activator) and ORF‐26 late lytic gene (a capsid protein) was assessed in a BCBL‐1 cell line stimulated by huIL‐6 by means of real‐time reverse transcription‐polymerase chain reaction. huIL‐6 induced both ORF‐50 and ORF‐26 expression, and the maximal ORF‐50 expression appeared earlier than that of ORF‐26. The data indicate that huIL‐6 reactivates HHV‐8 in BCBL‐1 cells through inducing ORF‐50. We also confirmed the previously reported activities of HHV‐8‐encoded huIL‐6 homologue (viral interleukin‐6 [vIL‐6]) on human immunodeficiency virus (HIV) replication in U1 cell line and huIL‐6 production by MT‐4 T cells, and utilizing monoclonal antibodies to the huIL‐6 receptor components, we elucidated that gp130 is the signaling molecule necessary for these vIL‐6 activities. These data suggest the possible existence of interaction between HIV and HHV‐8 via IL‐6, and that the blockade of IL‐6 signal by anti‐IL‐6R antibody or anti‐gp130 antibody can constitute a strategy to treat HIV/HHV‐8 dually infected patients. J. Med. Virol. 68:404–411, 2002. © 2002 Wiley‐Liss, Inc.