Ultrastructure of Kaposi's sarcoma-associated herpesvirus (KSHV)/human herpesvirus-8 (HHV-8) in a primary effusion lymphoma cell line treated with tetradecanoyl phorbol acetate (TPA)

1999 ◽  
Vol 32 (2) ◽  
pp. 94-99 ◽  
Author(s):  
Yuji Ohtsuki ◽  
Jun Iwata ◽  
Mutsuo Furihata ◽  
Tamotsu Takeuchi ◽  
Hiroshi Sonobe ◽  
...  
2002 ◽  
Vol 76 (20) ◽  
pp. 10530-10532 ◽  
Author(s):  
Gábor Gáspár ◽  
Erik De Clercq ◽  
Johan Neyts

ABSTRACT We demonstrate that human herpesvirus 8, obtained from the lymphoma cell line BC-3 as well as from Kaposi's sarcoma lesions, carries a gene that encodes a functional thymidylate synthase (TS). The particular characteristics of this enzyme are studied and compared to the characteristics of TSs encoded by other organisms.


2002 ◽  
Vol 68 (3) ◽  
pp. 404-411 ◽  
Author(s):  
Jian Song ◽  
Takako Ohkura ◽  
Masamichi Sugimoto ◽  
Yasuko Mori ◽  
Reiko Inagi ◽  
...  

2002 ◽  
Vol 76 (5) ◽  
pp. 2551-2556 ◽  
Author(s):  
Isabelle Widmer ◽  
Marion Wernli ◽  
Felix Bachmann ◽  
Fred Gudat ◽  
Gieri Cathomas ◽  
...  

ABSTRACT Expression of human herpesvirus 8 viral Bcl-2 protein was demonstrated in spindle cells of late-stage Kaposi's sarcoma lesions but not in primary effusion lymphoma cell lines. In contrast, strong expression of human Bcl-2 was found in stimulated primary effusion lymphoma cells, whereas in Kaposi's sarcoma lesions preferential mononuclear cells, and to a lesser extent spindle cells, stained positive.


1999 ◽  
Vol 73 (12) ◽  
pp. 10329-10338 ◽  
Author(s):  
Vasundhara Varthakavi ◽  
Philip J. Browning ◽  
Paul Spearman

ABSTRACT Human immunodeficiency virus (HIV) and Kaposi’s sarcoma-associated herpesvirus (KSHV) coinfect many individuals in North America and in parts of Africa. Infection with HIV is a leading risk factor for the development of Kaposi’s sarcoma (KS). In this study, we tested the hypothesis that HIV infection of common or adjacent cells would stimulate replication and spread of KSHV. Infection of a primary effusion lymphoma cell line by vesicular stomatitis virus type G-pseudotyped HIV type 1 led to a rapid induction of lytic-phase KSHV replication. Induction of lytic KSHV replication by HIV required active replication of HIV. The addition of the nucleoside reverse transcriptase inhibitor azidothymidine or the protease inhibitor indinavir to the culture prevented HIV spread and inhibited the associated induction of KSHV lytic replication. Lytic replication occurred in both HIV-infected and HIV-uninfected cells within the culture, and could be induced in uninfected cells via a soluble factor released from the HIV-infected cells. Transmission of infectious KSHV to an uninfected target cell was enhanced by HIV replication and was inhibited by antiretroviral drugs. These results may have implications for the pathogenesis and treatment of KS in individuals coinfected with KSHV and HIV.


2002 ◽  
Vol 76 (2) ◽  
pp. 165-172 ◽  
Author(s):  
Jun-ichi Miyagi ◽  
Masato Masuda ◽  
Nobuyuki Takasu ◽  
Akitoshi Nagasaki ◽  
Tetsuharu Shinjyo ◽  
...  

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