Rizzetto M, Canese M G, Gerin J L, London W T, Sly D L, Purcell R H
J Infect Dis. 1980 May;141(5):590-602. doi: 10.1093/infdis/141.5.590.
Inoculation of hepatitis B surface antigen (HBsAg)-positive sera from patients with chronic liver disease and intrahepatic delta (delta) into chimpanzees susceptible to infection with hepatitis B virus (HBV) resulted in type B hepatitis and delta markers (delta antigen and antibody to delta) in recipient animals. A dilution (10(-8)) of serum induced type B hepatitis without delta markers in another HBV-susceptible animal. HBV infection and delta markers did not develop in animals with preexisting titers of antibody of HBsAg. In chimpanzees with circulating HBsAg at the time of inoculation, synthesis of delta occurred earlier and its extent and duration were greater than in animals previously unexposed to HBV; coincident with synthesis of delta, hepatitis occurred in chronic HBsAg carriers, and synthesis of preexisting HBV gene products (HBsAg and hepatitis B core antigen) was diminished. Delta appears to be a marker of a transmissible pathogenic agent, either an HBV variant or another agent that requires the helper functions of HBV, that is defective and interferes with HBV replication.
将慢性肝病患者的乙型肝炎表面抗原(HBsAg)阳性血清以及肝内δ因子(δ)接种到对乙型肝炎病毒(HBV)感染易感的黑猩猩体内,结果在受者动物中引发了乙型肝炎以及δ标志物(δ抗原和δ抗体)。一份血清稀释液(10⁻⁸)在另一只对HBV易感的动物中引发了无δ标志物的乙型肝炎。在具有预先存在的HBsAg抗体滴度的动物中未发生HBV感染和δ标志物。在接种时具有循环HBsAg的黑猩猩中,δ的合成更早出现,其程度和持续时间比先前未接触过HBV的动物更大;与δ的合成同时,慢性HBsAg携带者发生了肝炎,并且先前存在的HBV基因产物(HBsAg和乙型肝炎核心抗原)的合成减少。δ似乎是一种可传播病原体的标志物,该病原体要么是HBV变体,要么是另一种需要HBV辅助功能的病原体,它有缺陷并干扰HBV复制。