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Lymphoproliferative disease virus of turkeys (LPDV), a C-type retrovirus, was shown to contain 3 major [32 kilodaltons (kd, p 32), 26 kd, 22/21 kd] and 2 minor (41 kd and 12 kd) polypeptides. Preliminary evidence suggests a glycoprotein of 76 kd (GP 76) and a major doublet polypeptide of 13.5/13 kd to be also of viral origin. Of these GP 76 was susceptible to bromelain action implying its surface location in the virion, while p 32, p 26 and p 13.5/13 were the main constituents of viral cores. p 13.5/13 bound an RNA probe, suggesting it to be the main constituent of viral ribonucleoprotein. p 22/21 was not cleaved by bromelain, and was absent in viral cores suggesting its intramembrane location between virion envelope and core. The polypeptide profile of LPDV is distinct from those of avian sarcoma-leukosis viruses and avian reticuloendotheliosis viruses.

Northern pike from several locations in central Canada were observed to have two different types of hyperplastic epidermal lesions on the body and fins. One type of epidermal hyperplasia consisted of flat lesions, bluish-white in color with a granular or "gritty" appearance. Histological examination of this granular lesion showed the presence of grossly hypertrophied cells surrounded by normal sized epidermal cells. The enlarged nuclei in thin section contained many typical herpesvirus capsids measuring 100 nm in diameter. A large proportion of the cytoplasmic mass consisted of many dark staining inclusions in which were embedded numerous herpes-like virions. For this herpesvirus of pike the name esocid herpesvirus 1 is proposed in keeping with the herpesvirus nomenclature of Roizman et al. (19). The second type of epidermal hyperplasia was a smooth convex whitish translucent tissue mass consisting largely of a population of randomly oriented normal sized undifferentiated cells. Electron microscopic examination showed them to be associated with clusters of C-type retrovirus measuring 150 nm in diameter. The formation of these virus particles was by budding from the cytoplasmic membrane into the inter-cellular spaces. Neither the herpesvirus nor the C-type particles could be isolated in fish cell cultures.

The ultrastructural morphogenesis of squirrel monkey retrovirus (SMRV) and Mason-Pfizer monkey virus (MPMV) growth in cell culture were compared. Both viruses develop by a process that begins with the formation of intracytoplasmic A particles which are then enveloped at the plasma membrane during budding. SMRV also develops as a crescent-shaped nucleoid beneath a bulging plasma membrane, a development characteristic of type C oncornaviruses. Free extra-cellular mature SMRV was generally round with a centrally located electron-dense nucleoid enclosed by the viral envelope. In contrast, mature MPMV had a tubular-shaped nucleoid. Negative stained preparations of both viruses yielded head-tail forms with surface projections. By uranyl acetate/critical point drying, SMRV particles were usually round with an eccentric electron-dense nucleoid enclosed by the viral envelope, whereas MPMV particles were round and contained an electron-dense bar-shaped nucleoid. These morphological observations indicate that SMRV more closely resembles MPMV, presently the only member of genus oncornavirus type D, than other retroviruses species. However, since SMRV can be morphologically, biochemically, and immunologically distinguished from MPMV, it represents a new species within genus oncornavirus type D.

Retrovirus infectivity is the result of a cooperative interaction of three structural genes, gag, pol, and env. Since the L-cell endogenous retrovirus (LCV) lacks the env gene translation product, our aim was to study the biological and molecular basis of its non-infectiousness. Fusion experiments between LCV and homologous or heterologous cells demonstrated that virus production could be obtained only after LCV artificial penetration in murine cells and that the new progeny was still noninfectious. Northern blot analysis and heteroduplex mapping of the genomic RNA revealed a 0.99 kb deletion including the 3' region of the pol reading frame, the whole xenotropic and part of the ecotropic domain of the env gene. The results suggest that the observed deletion is responsible for the absence of the gp 70 and the gp 15 E molecules in the virion and seems therefore to be the molecular basis for the non-infectiousness of this retrovirus.

Biochemical and morphological evidence indicates that a type-C retrovirus is present in the blood of swine (both leukemic and nonleukemic) exposed to strontium-90 radiation. Nonexposed swine that were leukemic also had virus present. The virus was shown to contain an RNase-sensitive DNA polymerase activity with cation, detergent and template requirements similar to those of known viral reverse transcriptases. The buoyant density of the virus was 1.14 to 1.16 g/ml, which can be converted, by treatment with ether, to a virion core having a density of 1.20 to 1.23 g/ml. Linear regression analysis indicated a correlation between virus-associated DNA polymerase activity and the number of blast cells in the peripheral blood.

This paper presents some observations concerned with the growth of simian foamy virus and some modifications which should be introduced to the fluorescence assay of foamy virus. The modified procedure is the most sensitive method described for the titration of foamy virus. Examination of the optimal conditions for the growth and titration by fluorescence assay of simian foamy virus showed that the virus was particularly sensitive to changes in virus and cell concentration. At the low cell concentrations employed previously a "saturation-type" response was obtained with high titre virus and virus adsorption efficiency was decreased as input virus was diluted. Maximum virus production was obtained with high cell concentrations at input multiplicities of 5 and 10. At high multiplicities of infection more than 90 per cent of the cells adsorbed virus but only 45 per cent became infected, this appeared to be related to cell DNA synthesis.

Eel Virus (Berlin) is associated with the occurrence of skin tumors in European eels. The genome of the virus consists of two segments of double-stranded (ds) RNA. The agent is assembled exclusively in the cytoplasm. Isometric particles with a diameter of 61 nm and in addition tubular structures and smaller particles were observed. The virion has a single shell: its capsid is composed of 132 interconnected morphological units with T = 13 dextro symmetry. According to particle size and bipartite nature of the genome, this virus has to be assigned to the tentatively proposed group of bisegmented ds RNA animal viruses.

The mechanism of cell-fusion induced by caprine arthritis-encephalitis virus (CAEV) was investigated. Following infection with concentrated CAEV, cell fusion occurred prior to the production of infectious progeny virus. The time of initial detection of cell fusion was dependent on the multiplicity of infection and was not detected until 5 hours after infection. The virus-induced cell fusion was only partially inhibited by ultraviolet irradiation of the virus and was not inhibited by cytosine arabinoside. The results indicated that fusion by CAEV was a slow response to direct interaction of input virus with cells (fusion from without) and that virus replication was not required.

The replication of the avian osteopetrosis virus MAV-2-O was compared in chick embryo fibroblasts from two strains of chicken. These were G-B1 which is relatively resistant to MAV-2-O and CB which is susceptible. The production of MAV-2-O was delayed in G-B1 cells (compared with CB cells). The same result was observed after infection with Rous sarcoma viruses of subgroups B, C, and D. In addition, the transforming viruses induced foci on G-B1 fibroblasts 24 to 48 hours later than on CB fibroblasts. In G-B1 cells there was also a delayed kinetics of intracellular viral RNA production. Integrated and linear unintegrated MAV-2-O DNA species were also present in lower amounts in G-B1 than in CB fibroblasts at 3 days postinfection. In vivo studies confirmed the in vitro situation. There was a marked difference in the amount of virus present in the osteoid bone matrix and the osteocytic lacunae of osteopetrotic bones from susceptible and G-B1 chickens. In contrast to the bone lesions from susceptible animals, budding virus particles were not detectable in lesions from G-B1 chickens. There was no difference in the amount of virus in osteopetrotic and non-osteopetrotic bone of susceptible chickens suggesting that virus replication alone is not sufficient for induction of osteopetrosis and that an additional specific virus-cell interaction is required. The relative resistance of strain G-B1 may therefore, be a consequence of a reduced frequency of this interaction. Its basis may be the lower amount of integrated, as well as unintegrated, viral DNA.