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Gibbon ape leukemia virus-Hall's Island (GaLV-H), a type C virus related to previous isolates of GaLV and simian sarcoma virus, was isolated from a gibbon ape with lymphocytic leukemia from a small colony of free-ranging gibbon apes on Hall's Island near Bermuda. We show here by molecular hybridization experiments that GaLV-H is approximately 60% related to three previous isolates of GaLV (GaLV-SF, GaLV-SEATO, and GaLV-Br) and is less closely related to simian sarcoma virus. The oligopyrimidine pattern of a transcript of the terminal 135 ± 5 nucleotides of the viral RNA of GaLV-H is similar to that of GALV-Br but distinct from that of GaLV-SF and simian sarcoma virus. GaLV-H thus represents a fifth distinct strain of the infectious primate type C viruses, which among the previously described isolates of GaLV is most closely related to GaLV-Br.

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Treatment with 5-iodo-Z'-deoxyuridine (IdUrd) of BALB/3T3 cells non-productively transformed with Kirsten murine sarcoma virus (K-BALB) results in the induction of extracellular t y p e 4 virus production with a concomitant appearance of intracellular reverse transcriptase. Production of BALB virus-2 (v-2) and i t s Kirsten sarcoma virus pseudotype, occurring 2-3 days after IdUrd treatment, is inhibited and stimulated by interferon and dexamethasone, respectively, By contrast, and as pre-. viously reported, neither compound affects synthesis of N-tropic virus (BALB virus-1) which i s produced later (5-7 days) after IdUrd treatment. The stimulatory and inhibitory activities of these compounds are partially antagonistic since: (1) the simultaneous presence of both dexamethasone and interferon results i n a virus production level between those observed with either compound alone; and (2) increasing the dexamethasone concentration at a fixed interferon concentration increases virus production. However, the effects of these two compounds on the appearance of an intracellular viral protein (reverse transcriptase) after IdUrd treatment were unexpected. The post-induction appearance of intracellular reverse transcriptase i s inhibited by interferon but is not affected by dexamethasone. This suggests that dexamethasone stimulates a step after protein synthesis, and that interferon inhibits an earlier step (translational or pre-translational) or that it enhances degradation of viral proteins. When interferon and dexamethasone are both present, no inhibition of the appearance of reverse transcriptase is observed. Thus, dexamethasone has a second effect on virus production, namely t o prevent the inhibition by interferon of the appearance of intracellular reverse transcriptase. Since dexamethasone completely overcomes the inhibitory effect of interferon on intracellular reverse transcriptase levels, but only partially reverses the inhibition by interferon of virus production, interferon (in the presence of dexamethasone) must also inhibit a post-translational step i n virus production. This step may or may not be the same as the late dexamethasone-sensitive step. Thus, both dexamethasone and interferon appear t o have both translational (or pre-translational) and post-translational effects on the production of xenotropic (v-2) mouse t y p e 4 virus. This suggests that BALB/c mouse cells restrict the production of xenotropic endogenous virus at two distinct sites.Clones of mouse BALB/3T3 fibroblasts infected with Kirsten murine sarcoma virus contain the sarcoma virus genome, but they do not produce detectable extracellular virions (Aaronson and Weaver, 1971) or gs antigen (Aaronson, 1971). Despite the lack of virus production, these cells are morphologically transformed (Aaronson and Weaver, 1971), contain relatively high levels of Kirsten virusspecific RNA (Benveniste and Scolnick, 1973 ;Wu et al., 1974), and can be induced by treatment with 5-iodo-2'-deoxyuridine (IdUrd) to produce extracellular virus (Aaronson, 1971). Viru...

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