Interspecies reactivity of type C and D retrovirus p 15E and p 15C proteins.
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Biomedical subjects
Publications and source records attributed to T J Matthews.
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The potent capacity of B6 anti-AD755a tumor cell serum to protect mice against challenge with large doses of the homologous tumor cells has been shown to reside in the IgG2a antibody subclass. Despite their inability to protect in vivo, other IgG subclass antibodies obtained from the anti-AD755a serum demonstrated serologic reactivities in vitro comparable to those obtained with the protective IgG2a fraction. The specificity of serum protection is linked to the oncornavirus associated with the AD755a tumor and the serum immunoprecipitates only virus structural proteins from the tumor cell surface. Removal of these antibodies by specific immunoadsorbent resins eliminated nearly all of the in vitro serologic reactivity of unfractionated serum and the IgG2a subclass, but it had absolutely no effect on their protective capacity in vivo. Further target cell-binding studies suggest that nonprotective antibodies in the anti-AD755a serum bind more efficiently to the target cell in vitro than the protective fraction and have raised the possibility that the latter antibodies may only have weak affinity for the target cell itself.
Low m.w. extracts from three known oncogenic viruses, Friend, Moloney, and Rauscher, inhibited the accumulation of macrophages at sites of delayed inflammatory reactions in mice. The potential biologic significance of these proteins is suggested by their potency: as little as 1.2 ng of viral protein inhibited (p less than 0.02) macrophage accumulation when injected at a site distant to the inflammatory reaction. A virus envelope protein fraction of 15,000 daltons (p15E) was likewise found to inhibit macrophage accumulation and may in part represent the active factor of the virus extracts. Certain oncogenic viruses may thus exert their immunosuppressive activity by release of potent inhibitors of systemic macrophage function.
Pigeons' key pecks were maintained by variable-ratio or variable-interval schedules of food reinforcement. For pairs of pigeons in one group, variable-ratio reinforcement was arranged for one pigeon's pecks; for the second pigeon, reinforcement was arranged according to a variable-interval schedule yoked to the interreinforcement times produced by the first pigeon. For pairs of pigeons in another group, variable-interval reinforcement was arranged for one pigeon's pecks; for the second pigeon, reinforcement was arranged according to a variable-ratio schedule yoked to the interreinforcement responses produced by the first pigeon. For each pair, the yoking procedure was maintained for four or five consecutive sessions of 50 reinforcements each. In more than three-quarters of the pairs, variable-ratio response rates were higher than variable-interval rates within two sessions; in all cases, the rate difference developed within four sessions.
Pulse-chase kinetics and extensive pactamycin mapping studies show that the translation of rhinovirus 1A proceeds in the order: initiate-P1-S-P2-terminate, where P1 is the precursor to the capsid proteins, S is a stable primary gene product, and P2 is the precursor to a family of noncapsid products. Initial examination of the molar stoichiometry of the families of rhinoviral proteins in infected cells suggested that both the P1 and P2 regions were translated more frequently than the S region. However, we show that this apparent asymmetry in translation is an artifact arising from two phenomena: (i) ambiguous cleavage sites which result in two alternative products from the S region, having apparent molecular weights of 47,000 and 38,000, and (ii) several fates for the P2 precursors, including degradation of 35 to 45% of the P2 family to small unidentifiable products. Another artifact, a time-dependent shift in the pactamycin mapping position of polypeptide r-39, was traced to a selective inhibition of the rate of cleavage of its precursor (peak 76). The processing rate of the capsid precursor (peak 92) was not retarded by pactamycin.
Of thirty-nine patients with Klippel-Feil syndrome, twenty-five (64 per cent) had significant genitourinary-tract anomalies demonstrated by intravenous urogram and physical examination. The incidence of these anomalies in Feil's three types of the syndrome was essentially the same, unilateral renal agenesis being the most common. A routine intravenous urogram is indicated in patients with this syndrome.
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