Age-Related Differences in Amplification of Covalently Closed Circular DNA at Early Times after Duck Hepatitis B Virus Infection of Ducks

ABSTRACT Inoculation of 3-day-old (3D) or 3-week-old (3W) ducklings with duck hepatitis B virus results in chronic or transient infection, respectively. We previously showed that rapid production of neutralizing antibody following inoculation of 3W ducklings prevents virus from spreading in the liver and leads to a transient infection (Y.-Y. Zhang and J. Summers, J. Virol. 78:1195-1201, 2004). In this study we further investigated early events of viral infection in both 3D and 3W ducks. We present evidence that a lower level of virus replication in the hepatocytes of 3W birds is an additional factor that probably favors transient infection. We suggest that lower virus replication is due to a less rapid covalently closed circular DNA amplification, leading to lower viremias and a slower spread of infection in the liver, and that the slower spread of infection in 3W ducks makes the infection more sensitive to interruption by the host immune responses.

[1]  J. Summers,et al.  Rapid Production of Neutralizing Antibody Leads to Transient Hepadnavirus Infection , 2004, Journal of Virology.

[2]  S. Litwin,et al.  Single-cell analysis of covalently closed circular DNA copy numbers in a hepadnavirus-infected liver , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[3]  J. Summers,et al.  Low Dynamic State of Viral Competition in a Chronic Avian Hepadnavirus Infection , 2000, Journal of Virology.

[4]  J. Summers,et al.  Acute liver injury following infection with a cytopathic strain of duck hepatitis B virus , 1999, Hepatology.

[5]  J. Summers,et al.  Competition in vivo between a cytopathic variant and a wild-type duck hepatitis B virus. , 1998, Virology.

[6]  E. Bertram,et al.  Characterization of age- and dose-related outcomes of duck hepatitis B virus infection. , 1998, Virology.

[7]  D. Miller,et al.  Kinetics of duck hepatitis B virus infection following low dose virus inoculation: one virus DNA genome is infectious in neonatal ducks. , 1996, Virology.

[8]  J. Summers,et al.  Construction of avian hepadnavirus variants with enhanced replication and cytopathicity in primary hepatocytes , 1994, Journal of virology.

[9]  J. Summers,et al.  Coordinate regulation of replication and virus assembly by the large envelope protein of an avian hepadnavirus , 1994, Journal of virology.

[10]  T. Wu,et al.  Rapid resolution of duck hepatitis B virus infections occurs after massive hepatocellular involvement , 1992, Journal of virology.

[11]  J. Summers,et al.  Morphogenetic and regulatory effects of mutations in the envelope proteins of an avian hepadnavirus , 1991, Journal of virology.

[12]  A. Horwich,et al.  Hepadnavirus envelope proteins regulate covalently closed circular DNA amplification , 1990, Journal of virology.

[13]  J. Summers,et al.  In hepatocytes infected with duck hepatitis B virus, the template for viral RNA synthesis is amplified by an intracellular pathway. , 1990, Virology.

[14]  J. Summers,et al.  Infection and uptake of duck hepatitis B virus by duck hepatocytes maintained in the presence of dimethyl sulfoxide. , 1989, Virology.

[15]  P. Tiollais,et al.  Hepatitis B virus. , 1991, Scientific American.

[16]  R. Sprengel,et al.  Replication strategy of human hepatitis B virus , 1987, Journal of virology.

[17]  J. Summers,et al.  Formation of the pool of covalently closed circular viral DNA in hepadnavirus-infected cells , 1986, Cell.

[18]  T R Bender,et al.  Acute hepatitis B virus infection: relation of age to the clinical expression of disease and subsequent development of the carrier state. , 1985, The Journal of infectious diseases.

[19]  R. Miller,et al.  Hepatitis B virus DNA forms in nuclear and cytoplasmic fractions of infected human liver. , 1984, Virology.

[20]  J. Summers,et al.  Experimental transmission of duck hepatitis B virus. , 1983, Virology.

[21]  J. Taylor,et al.  Asymmetric replication of duck hepatitis B virus DNA in liver cells: Free minus-strand DNA. , 1982, Proceedings of the National Academy of Sciences of the United States of America.

[22]  J. Summers,et al.  Replication of the genome of a hepatitis B-like virus by reverse transcription of an RNA intermediate , 1982, Cell.

[23]  D. Shafritz,et al.  Evidence for supercoiled hepatitis B virus DNA in chimpanzee liver and serum dane particles: Possible implications in persistent HBV infection , 1982, Cell.

[24]  J. Summers Three recently described animal virus models for human hepatitis B virus , 1981, Hepatology.

[25]  J. Summers,et al.  Virus of Pekin ducks with structural and biological relatedness to human hepatitis B virus , 1980, Journal of virology.

[26]  C E Stevens,et al.  The e antigen and vertical transmission of hepatitis B surface antigen. , 1977, American journal of epidemiology.

[27]  M. Imai,et al.  e antigen and anti-e in the serum of asymptomatic carrier mothers as indicators of positive and negative transmission of hepatitis B virus to their infants. , 1976, The New England journal of medicine.

[28]  A. Redeker Viral hepatitis: clinical aspects. , 1975, The American journal of the medical sciences.

[29]  R. Beasley,et al.  Vertical transmission of hepatitis B antigen in Taiwan. , 1975, The New England journal of medicine.