Coinfection of Hepatic Cell Lines with Human Immunodeficiency Virus and Hepatitis B Virus Leads to an Increase in Intracellular Hepatitis B Surface Antigen

被引:42
|
作者
Iser, David M. [1 ,2 ]
Warner, Nadia [3 ]
Revill, Peter A. [3 ]
Solomon, Ajantha [4 ]
Wightman, Fiona [4 ]
Saleh, Suha [4 ]
Crane, Megan [4 ]
Cameron, Paul U. [1 ,4 ]
Bowden, Scott [3 ]
Nguyen, Tin [3 ]
Pereira, Candida F. [4 ,5 ,6 ]
Desmond, Paul V. [2 ]
Locarnini, Stephen A. [3 ]
Lewin, Sharon R. [1 ,4 ,5 ]
机构
[1] Alfred Hosp, Infect Dis Unit, Melbourne, Vic 3004, Australia
[2] Univ Melbourne, Dept Med, St Vincents Hosp, Melbourne, Vic, Australia
[3] Victorian Infect Dis Reference Lab, Dept Res & Mol Dev, Melbourne, Vic, Australia
[4] Monash Univ, Dept Med, Melbourne, Vic 3004, Australia
[5] Burnet Inst, Ctr Virol, Melbourne, Vic, Australia
[6] Monash Univ, Monash Micro Imaging, Clayton, Vic 3800, Australia
基金
英国医学研究理事会;
关键词
GROUND GLASS HEPATOCYTES; LONG TERMINAL REPEAT; PRE-S MUTANTS; ENVELOPE PROTEINS; X-PROTEIN; IN-VITRO; HIV-1; INFECTION; REPLICATION; LIVER;
D O I
10.1128/JVI.02594-09
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Liver-related mortality is increased in the setting of HIV-hepatitis B virus (HBV) coinfection. However, interactions between HIV and HBV to explain this observation have not been described. We hypothesized that HIV infection of hepatocytes directly affects the life cycle of HBV. We infected human hepatic cell lines expressing HBV (Hep3B and AD38 cells) or not expressing HBV (Huh7, HepG2, and AD43 cells) with laboratory strains of HIV (NL4-3 and AD8), as well as a vesicular stomatitis virus (VSV)-pseudotyped HIV expressing enhanced green fluorescent protein (EGFP). Following HIV infection with NL4-3 or AD8 in hepatic cell lines, we observed a significant increase in HIV reverse transcriptase activity which was infectious. Despite no detection of surface CD4, CCR5, and CXCR4 by flow cytometry, AD8 infection of AD38 cells was inhibited by maraviroc and NL4-3 was inhibited by AMD3100, demonstrating that HIV enters AD38 hepatic cell lines via CCR5 or CXCR4. High-level infection of AD38 cells (50%) was achieved using VSV-pseudotyped HIV. Co-infection of the AD38 cell line with HIV did not alter the HBV DNA amount or species as determined by Southern blotting or nucleic acid signal amplification. However, coinfection with HIV was associated with a significant increase in intracellular HBsAg when measured by Western blotting, quantitative HBsAg, and fluorescence microscopy. We conclude that HIV infection of HBV-infected hepatic cell lines significantly increased intracellular HBsAg but not HBV DNA synthesis and that increased intrahepatic HBsAg secondary to direct infection by HIV may contribute to accelerated liver disease in HIV-HBV-coinfected individuals.
引用
收藏
页码:5860 / 5867
页数:8
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