【转移帖】HIV and HBV co-infection: HIV increases intracellular HBsAg in
原帖由yaoming发表于 2010-4-14 14:19HBV 和HIV的共感染有很多报道，并且临床上的资料显示，HIV可以促进HBV DNA水平。由于HIV可以破坏机体免疫系统，因此HIV对HBV复制或者生活周期的影响更可能是通过间接的机制。
但是也有研究报道，HIV也可以感染肝细胞，因此HIV和HBV的直接相互作用存在理论上的可能。
本文在肝肿瘤细胞系中研究了HIV对HBV部分生活周期的影响。虽然具体的机制阐述不是很明确，但是其实验的设置，文章的逻辑性等还是值得我们学习。
期刊：J Virol. 2010 Mar 31. [Epub ahead of print
标题：Co-infection of hepatic cell lines with HIV-hepatitis B virus (HBV) leads to an
increase in intracellular hepatitis B surface antigen (HBsAg).
作者：Iser DM, Warner N, Revill PA, Solomon A, Wightman F, Saleh S, Crane M, Cameron PU, Bowden S, Nguyen T, Pereira CF, Desmond PV, Locarnini SA, Lewin SR.
单位：Department of Medicine, University of Melbourne, St. Vincent's Hospital,
Melbourne, Victoria, Australia; Infectious Diseases Unit, Alfred Hospital,
Melbourne, Victoria, Australia; Department of Research and Molecular Development,
Victorian Infectious Diseases Reference Laboratory, North Melbourne, Victoria,
Australia; Department of Medicine, Monash University, Melbourne, Victoria,
Australia; Centre for Virology, Burnet Institute, Melbourne, Victoria, Australia;
Monash Micro Imaging, Monash University, Victoria, Australia.
摘要：Liver-related mortality is increased in the setting of HIV-hepatitis B virus
(HBV) co-infection. However, interactions between HIV and HBV to explain this
observation have not been described. We hypothesised 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 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
CXCR4 or CCR5. 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 blot or nucleic acid signal
amplification. However, co-infection with HIV was associated with a significant
increase in intracellular HBsAg when measured by Western blot, quantitative HBsAg
and fluorescent microscopy. Conclusion: HIV infection of HBV-infected hepatic
cell lines significantly increased intracellular HBsAg, but not HBV DNA
synthesis. Increased intrahepatic HBsAg secondary to direct infection by HIV may
contribute to accelerated liver disease in HIV-HBV co-infected individuals.
全文链接：http://www.ncbi.nlm.nih.gov/pubmed/20357083
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