No abstract

The reactions between purified anti-poly A. poly U and-poly I. poly C. antibodies (IgG and IgM)

Immunization of rabbits with the double-stranded polynucleotide complex poly G·poly C adsorbed to methylated bovine serum albumin produced antibodies that reacted with RNA. These antibodies were specific for ribosomal RNA from animal cells and RNA from certain viruses.

DBA/2 mice immunized with poly(A)·poly(U) complexed with methylated bovine serum albumin and emulsified in Freund's complete adjuvant were protected against challenge with Friend leukemia virus. There was no correlation between the level of antibody to the immunogen in the prechallenge serum and induced resistance to the virus. Although prechallenge sera of mice given the same amount of the duplex in a single inoculum bound 9.7% of poly(A)·poly([ 3 H]U) input, as compared to 45.3% bound by the prechallenge sera of mice given the immunogen in divided doses, both groups of mice were equally resistant to infection. Immunization with two other nonviral agents, bovine serum albumin fraction V or dinitrophenylated keyhole limpet hemocyanin, induced the same level of protection. A sparing effect of approximately 10 1.5 in infectivity was afforded the immunized mice. Immunization with either poly(A)·poly(U) alone or with the carrier methylated bovine serum albumin was ineffective. In addition to antibodies to the respective immunogens, the prechallenge sera of the immunized mice also contained antibody to Friend leukemia virus gp71. The presence of such viral antibodies was not always related to resistance to infection by Friend virus. Some immunized mice that survived infection did not have gp71 antibody in their serum before challenge, and mice immunized with poly(A)·poly(U) alone were susceptible to infection, although their prechallenge sera contained antibody to gp71. The mechanism involved in the induction of resistance to infection is not known. The effect may be mediated through a modification of the expression of both endogenous and exogenous type C viruses and affect immunological mechanisms controlling cellular responses.

Summary. Leukocyte migration inhibition tests (LMIT)were