Defective mutants of hepatitis B virus in the circulation of symptom-free carriers.
A total of 75 clones of hepatitis B virus (HBV) DNA were isolated from the plasma of 4 symptom-free carriers. Each set of clones from a carrier all possessed at least one complete genome, for which the entire nucleotide sequence was determined. A deletion of nucleotide sequence, spanning from 13 to 1071 base pairs, was detected in 17 clones (23%). As many as 16 of them had a deletion in the C gene, with or without the involvement of the P and X genes. The remaining one clone had a deletion restricted to the pre-S region. Accordingly, these defective mutants could not replicate themselves without help from complete HBV co-infecting the same hepatocyte. Defective mutants would have developed during the replication of HBV by reverse transcription of an RNA intermediate, and provide another evidence for a close similarity of HBV with retroviruses.
Immunology Division, Jichi Medical School, Tochigi-ken, Japan.
H
H
Okamoto
F
F
Tsuda
M
M
Mayumi
D002872:Chromosome Deletion; D002908:Chronic Disease; D003001:Cloning, Molecular; D004279:DNA, Viral / Q000235:genetics; D003673:Defective Viruses / Q000235:genetics*; D005814:Genes, Viral; D006509:Hepatitis B / Q000382:microbiology*; D006515:Hepatitis B virus / Q000235:genetics*; D006801:Humans; D009154:Mutation; D014762:Viral Interference
D004279:DNA, Viral