Abstract
In the previous paper the author reported that the 2-mecaptoethanol (2-ME) sensitive hemagglutination inhibition (HI) antibody appeared in the early immune stage of chickens infected with the avirulent strain of Newcastle disease virus (B1) and discussed its relationship to the protection against challenge.
The present paper deals with the molecular composition and the sensitivity against 2-ME of HI and neutralizing (SN) antibodies, using the gel filtration technique (Sephadex G-200).
The results are summarized as follows.
1) HI activity in IgM fraction appeared within 7 days, increased till about 9 days and then decreased to disappear between 21 to 28 days after the primary inoculation of virus. On the other hand, the activity in IgG fraction appeared 7 days and became higher in titer than that of IgM fraction 12 days after inoculation. The, activity in IgG fraction reached maximum about 12 days and 28 days after inoculation of avirulent and virulent strains, respectively.
2) The pattern of SN activity showed the same one as that of HI activity. However, the SN activity was remarkably lower in titer than the HI in IgM fraction. The SN activity in IgG fraction predominated over IgM 9 days after infection.
3) The response in chickens vaccinated with inactivated virus was principally similar to that in-ones infected with the virus. The HI activity, however, persisted in IgM fraction and kept the same level as that in IgG fraction even 70 days after vaccination.
4) No difference of antibody response was observed between IgM fractions following the primary and secondary inoculations, wheares the quicker and higher appearance of activity observat ed in IgG fraction after the secondary inoculation.
5) Antibody activities, both HI and SN, were completely inactivated by 2-ME treatment in IgM fraction and partially in IgG fraction at the early immune stage. They were, however, completely resistant at the later immune stage.
6) The pattern of HI activity coincided with that of SN in IgG fraction at the late immune stage, in which activities became resistant to 2-ME treatment.
