Jilbert A R, Botten J A, Miller D S, Bertram E M, Hall P M, Kotlarski J, Burrell C J
Infectious Diseases Laboratories, Institute of Medical and Veterinary Science, Adelaide, Australia.
Virology. 1998 May 10;244(2):273-82. doi: 10.1006/viro.1998.9095.
Experimental inoculation of naive ducks with duck hepatitis B virus (DHBV) can lead to one of three outcomes, namely, persistent viremia, transient infection with or without viremia, or no evidence of infection. The ability of individual ducks to resolve DHBV infection was found to be linked to the age of the duck at the time of inoculation and the dose of inoculated virus. (1) In recently hatched ducks inoculated intravenously (i.v.) with 4 x 10(4) DHBV DNA genomes, a switch from persistent viremia to transient antibody appearance was seen at an age of inoculation between 7 and 14 days. A 25-fold increase in the dose of virus (1 x 10(6) DHBV genomes) delayed this switch by 7 days. (2) When 4-month-old ducks were inoculated i.v. with different doses of virus, only those receiving the highest dose (2 x 10(11) DHBV genomes) showed viremia and extensive viral replication and histological changes in the liver; 2/3 ducks in this group had a transient infection, while the third duck had viral replication and histological changes in the liver that were still present at day 120 postinoculation (p.i.). In all ducks receiving lower doses (1 x 10(3), 1 x 10(6), 1 x 10(9) DHBV genomes) antibodies to viral surface and core antigens developed without detectable viral replication in the liver on days 6, 9, or 12 p.i. (3) When 10- to 16-month-old ducks were inoculated i.v. with 2 x 10(11) DHBV genomes, all showed extensive viral replication in hepatocytes and mild to moderate histological changes in the liver on days 4 or 6 p.i. In 4/5 ducks viremia was not detected, anti-surface antibodies were first detected on day 8 p.i., and viral DNA and antigen were cleared from the liver by days 35-47 p.i. The remaining duck became viremic with persistence of virus in the liver until at least day 46 p.i. The findings of the study are consistent with a model for noncytopathic viruses (R. M. Zinkernagel (1996) Science 271, 173-178).
用鸭乙型肝炎病毒（DHBV）对未感染的雏鸭进行实验性接种可导致三种结果之一，即持续性病毒血症、伴有或不伴有病毒血症的短暂感染，或无感染迹象。发现个体雏鸭清除DHBV感染的能力与接种时雏鸭的年龄以及接种病毒的剂量有关。（1）在7至14日龄时静脉内（i.v.）接种4×10⁴个DHBV DNA基因组的刚孵出的雏鸭中，在接种年龄为7至14天时，可观察到从持续性病毒血症向短暂抗体出现的转变。病毒剂量增加25倍（1×10⁶个DHBV基因组）会使这种转变延迟7天。（2）当对4月龄的雏鸭静脉内接种不同剂量的病毒时，只有那些接受最高剂量（2×10¹¹个DHBV基因组）的雏鸭出现病毒血症、广泛的病毒复制以及肝脏的组织学变化；该组中2/3的雏鸭有短暂感染，而第三只雏鸭在接种后第120天（p.i.）肝脏中仍存在病毒复制和组织学变化。在所有接受较低剂量（1×10³、1×10⁶、1×10⁹个DHBV基因组）的雏鸭中，在接种后第6、9或12天出现了针对病毒表面和核心抗原的抗体，且肝脏中未检测到病毒复制。（3）当对10至16月龄的雏鸭静脉内接种2×10¹¹个DHBV基因组时，所有雏鸭在接种后第4或6天肝脏中均出现广泛的病毒复制以及轻度至中度的组织学变化。在4/5的雏鸭中未检测到病毒血症，在接种后第8天首次检测到抗表面抗体，并且在接种后第35至47天肝脏中的病毒DNA和抗原被清除。其余一只雏鸭出现病毒血症，病毒在肝脏中持续存在直至至少接种后第46天。该研究结果与非细胞病变病毒的模型一致（R. M. 津克纳格尔（1996年）《科学》271卷，第173 - 178页）。
