Premium
Further studies by immunofluorescence of the monoclonal antibodies associated with experimental non‐A, non‐B hepatitis in chimpanzees and their relation to D hepatitis
Author(s) -
Shimizu Yohko K.,
Purcell Robert H.,
Gerin John L.,
Feinstone Stephen M.,
Ono Yasushi,
Shikata Toshio
Publication year - 1986
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840060618
Subject(s) - immunoelectron microscopy , hepatitis , antibody , monoclonal antibody , virology , immunofluorescence , liver biopsy , hepatitis b virus , virus , hepatitis b , hepatitis a , biopsy , biology , pathology , medicine , immunology
To further investigate the specificity of the monoclonal antibodies (48‐1 and S‐1) associated with non‐A, non‐B hepatitis, extensive immunofluorescence studies were performed on liver biopsy specimens from chimpanzees with experimental hepatitis A, B, non‐A, non‐B or δ, or from normal chimpanzees. Both 48‐1 and S‐1 antibodies reacted in the same manner with liver biopsy specimens from 47 of 50 (94%) chimpanzees with acute or chronic non‐A, non‐B hepatitis and 15 of 18 (83%) chimpanzees with type D hepatitis. Examinations of serial liver biopsy specimens revealed that the duration of expression of the antigen reacting with the antibodies in hepatocytes of chimpanzees infected with non‐A, non‐B viruses appeared to be longer than that of chimpanzees infected with the hepatitis δ‐virus. By thin‐section electron microscopy, the presence of the microtubular aggregates, identical to those previously described for chimpanzees with non‐A, non‐B hepatitis and shown by immunoelectron microscopy to react with the antibodies, was noted in hepatocytes during the acute phase of hepatitis δ‐virus. The antibodies did not react with liver biopsy specimens from chimpanzees acutely or chronically infected with hepatitis B virus or hepatitis A virus, or from normal chimpanzees. The present results confirm our previous observations with the 48‐1 and S‐1 antibodies. Furthermore, the finding that these two antibodies were also associated with hepatitis D would support the possibility that non‐A, non‐B agents and the hepatitis δ‐virus may have a similar nature or may elicit a similar host response.