Farci P, Karayiannis P, Lai M E, Marongiu F, Orgiana G, Balestrieri A, Thomas H C
Academic Department of Medicine, St. Mary's Hospital School of Medicine, London, England.
J Med Virol. 1988 Nov;26(3):279-88. doi: 10.1002/jmv.1890260308.
In a large population of patients, chronic hepatitis delta virus (HDV) infection was usually associated with absence of hepatitis B virus (HBV) replication. However, acute HDV superinfection progressing to chronic HDV infection in two hepatitis B e antigen (HBeAg)-positive HBV carriers and coinfection in two other patients who progressed to chronic HBV (HBeAg-positive) and HDV infection was associated with continuing high-level HBV replication for several years. Thus HDV infection does not always inhibit HBV replication. The hypothesis that the different effects of HDV coinfection and superinfection on HBV replication may stem from variability in the capacity of the host to produce and respond to interferon is discussed.
在大量患者群体中，慢性丁型肝炎病毒（HDV）感染通常与乙型肝炎病毒（HBV）复制缺失相关。然而，两名乙肝e抗原（HBeAg）阳性的HBV携带者发生急性HDV重叠感染并进展为慢性HDV感染，另外两名进展为慢性HBV（HBeAg阳性）和HDV感染的患者发生HDV合并感染，均伴有持续数年的高水平HBV复制。因此，HDV感染并不总是抑制HBV复制。本文讨论了一种假说，即HDV合并感染和重叠感染对HBV复制的不同影响可能源于宿主产生和应答干扰素能力的差异。
