Poly(c3A) (poly 3-deazaadenylic
acid) and poly(c3I) (poly 3-deazainosinic
acid) differ in
biological reactivity from their parent compounds
poly(A) and
poly(I) and from their 7-deaza counterparts poly(c7A) and poly(c7I). Three parameters of
biological reactivity were evaluated : (1 degree)
interferon induction, (2 degrees) anti-
complement activity, (3 degrees)
reverse transcriptase inhibition. Unlike
poly(A)-
poly(U),
poly(I)-
poly(C) and poly(I)-poly(br5C), the mixtures of poly(c3A) +
POLY(U), poly(c3I) +
poly(C), and poly(c3I) + poly(br5C) failed to elicit an
interferon response in "super-induced" primary rabbit kidney cells;
Poly(I) and its analogs poly(c3I) and poly(c7I) inhibited
hemolytic complement activity, whereas
poly(A) and its analogs poly(c3A) and poly(c7A) failed to do so. Both
poly(I) and poly(c7I), but not poly(c3I), lost their anti-
complement potency when annealed to either
poly(C) or
poly(A)-
poly(U). Similarly,
poly(I) and poly(c7I), but not poly(c3I), suppressed the
interferon inducing ability of
poly(A)-
poly(U), suggesting that both
poly(I) and poly(c7I), but not poly(c3I), added to
poly(A)-
poly(U) to form a triple-helical structure.
Poly(I), poly(C7I) and poly(c7A)exerted a distinct inhibitory effect on turine
leukemia virus, while under the same conditions poly(c3I) and poly(c3A) showed little, if any, inhibitory effect.