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It was for the first time that complementation between the human and simian adenoviruses in human cells as well as the ability of the human adenovirus Ad2 (HADv2) genome to transform completely into the simian adenovirus SA7(C8) (SADv15) capsid (transcapsidation) was demonstrated. A defective adeno-adeno hybrid (recombinant) between the above viruses is described; the recombinant has the SA7(C8) capsid and Ad2 genome with a 10% insertion of SA7(C8) in the central region. Defective hybrid virions are able to replicate both in human and simian cells by using the SA7(C8) virus as helper. The hybrid virions help the above virus to replicate in human cells: they form a mutually complementing virion pair.

A highly oncogenic monkey adenovirus SA7(C8) facilitates the reproduction of human adenovirus type 2 (Ad2) in monkey cells. Upon mixed infection of monkey cells with both viruses, these viruses recombine producing defective adeno-adeno hybrids Ad2C8 serologically identical to Ad2 and capable of assisting Ad2 to reproduce in monkey cells. Ad2C8 and Ad2 form an intercomplementary pair inseparable in monkey cells. Unlike oncogenic SA7(C8), Ad2C8 is a nononcogenic virus for hamsters but is able to induce tumor antigens of this virus (T and TSTA). Molecular genetic analysis of 68 clones of adeno-adeno hybrids revealed that the left part of their genome consists of Ad2 DNA, and the right part contains no less than 40% of the viral SA7(C8) genome where E2A, E3, and E4 genes are located. Apparently, the products of these genes contribute to the composition of adenoviral tumor antigens, while the E4 gene is involved in complementation of monkey and human adenoviruses and makes a contribution to host range determination of these viruses.

Trials of the first Soviet live recombinant smallpox-hepatitis B vaccine (SHBV) in volunteers (20 men aged 18-20 years) showed its safety, good "take"-rate, and lower reactogenicity as compared with the standard smallpox vaccine (LIVP strain). Smallpox virus-neutralizing antibodies in response to SHBV were produced as well as in response to the smallpox vaccine. Revaccination of human subjects with smallpox vaccine and SHBV 45 days after the previous vaccination resulted in antibody booster to vaccinia virus. After two inoculations of SHBV at an interval of 45 days no anti-HBsAg antibodies were found for 3 months after the last vaccination. However, even a single vaccination with SHBV induced priming to HBsAg. This could be demonstrated after inoculation of the subjects vaccinated with SHBV with one dose of plasma hepatitis vaccine. In the subjects vaccinated with SHBV antibody in response to the plasma vaccine formed more frequently and in higher titres than in those prevaccinated with smallpox vaccine or placebo.

The method for biological testing of growth factors (GF) produced by transformed cells is described. The method is suitable for studying the ability of donor cells to release GF that stimulate colony formation of test-cells. Donor cells and test-cells are placed into different semisolid agar layers and separated by intermediate agar layer. The method provides a much more efficient testing of GF biological activity than the use of conditioned cultural fluids of transformed cells. It permits the assessment of GF dialyzation and the role of donor cell proliferation in the production of GF.

Immune sera to Mason-Pfizer virus (M-PMV) are capable of precipitating type C viruses of mice (NIH-MuLV, G-MuLV, and to a lower degree R-MuLV), cats (FeLV, RD-114), and monkeys (SSV-1, GALV, BEV). The immune sera to RD-114, BEV, SSV-1 and GALV viruses can precipitate M-PMV virions. The adsorption analysis suggests that cross-reactions between M-PMV, RD-114, NIH-MuLV, and G-MuLV viruses depend on common virus-specific antigenic determinants in the envelopes of the virions. The relationship between M-PMV and type C viruses decreases in the series RD-114--NIG-MuLV--G-MuLV. Type C viruses of mammals have common envelope antigenic determinants lacking in M-PMV. No common antigenic determinants with M-PMV have been found in the envelope of virions of bovine leukemia virus, type B virus of mice (MMTV), or type C avian virus (Pr-RSV).

A progene hypothesis has been proposed earlier to explain the mechanism of origin of the self-reproducing genetic system. Progenes (precursors of the genetic system) are mixed anhydrides of an amino acid and deoxyribotrinucleotide at the 3'-gamma-terminal phosphate (NpNpNppp-AA); they are produced from dinucleotides (NpNp) and 3'-gamma-aminoacylnucleotidylates (Nppp-AA) as a result of specific interaction between amino acid and dinucleotide. The postulated mechanism of progene formation accounts for the selection of substances, including chirality, the origin of the genetic code as well as for the mechanisms of formation, self-reproduction and evolution of the simpliest genetic system ("gene--polypeptide"). A stereochemical analysis of the progene formation mechanism has allowed us to support the main statements of the hypothesis that relate to the origin of the genetic code and to selection of substances. Atomic groups that could be responsible for the specificity of interaction between dinucleotides and amino acids in progene formation have been revealed. Stereochemical evidence for the physicochemical basis of the origin of the existing genetic code have been produced: 1) a special role of the second nucleotide in the codon is demonstrated in amino acid coding by the progene hypothesis principle; 2) an advantage of T against U in such coding is demonstrated; 3) for 16 amino acids out of 20 an agreement has been obtained between the optimal dinucleotide as revealed by the stereochemical analysis and the codon dinucleotides; 4) an explanation for the third nucleotide selection mechanism is offered. A restoration of the prebiotic code, based on these results, has indicated that the code contains 32 codons, is statistical and group-wise. It encodes 7 groups of isofunctional amino acids: 3 overlapping groups of non-polar amino acids 1) medium-size hydrophobic amino acids (chiefly Val, n-Val and a-But), 2) small and medium-size non-polar amino acids (chiefly Ala Val, n-Val a-But and Gly), 3) small non-polar amino acids (Gly, Ala, a-But) and 4 groups of polar amino acids--1) hydroxy--+dicarbonic (Asp, Glu, Ser and Thr), 2) dicarbonic (Asp and Glu), 3) hydroxy (Ser and Thr) and 4) basic (Arg and Lys). The code includes about 20 amino acids among which are 15-17 canonical and a few common non-canonical. The prebiotic code explains many properties of the existing genetic code and is capable of evolving into the latter by way of a gradual replacement of the physicochemical coding mechanism by the enzymatic coding mechanism.

The modern concepts of tumorigenic virus oncogenes are discussed. The available literature data on the identification of oncogenes of polyoma-, adeno- and oncoviruses and the corresponding protein the products of oncogenes, are reported. Under consideration is the idea of the cellular origin of virus oncogenes. It is suggested that the study of virus oncogenes would offer some new methodical approaches to the identification of cell genes, which impairment results in cell malignification.

A comparative analysis of the results of bovine sera examinations by three methods for the detection of antibody to bovine leukemia virus (BLV): VSV BLV pseudotype neutralization test (PTNT), gel immunodiffusion using BLV glycoprotein antigen (GIDgp) and BLV 125I-p24 radioimmunoprecipitation (RIPp24), was performed. The results of all the three methods were in good correlation. The PTNT sensitivity was shown to exceed essentially all the other methods of BLV antibody detection. There was a definite correlation between the serum titer in PTNT and the possibility of antibody detection in RIPp24 and GIDgp. The potentials of these methods for diagnosis of BLV infection in animals are discussed.

A new heterologous system of radioimmunoassay (p24 of bovine leukemia virus--antiserum to Rous sarcoma virus) has been developed which demonstrated for the first time the existence of a common antigenic determinant in the major inner protein of unrelated oncoviruses: avian leukemia-sarcoma virus, bovine leukemia virus, mammalian type C viruses (mouse, hamster, monkey) and type D viruses (simian Mason-Pfizer virus). These data suggest a common origin of unrelated oncoviruses and open new approaches for the search of unknown agents associated with human and animal neoplastic diseases.

The capacity of leukovirus RD-114 to replicate in human embryo lung diploid cell cultures and continuous human angiosarcoma cell cultures (AS and 709 lines). Differences in the capacity to support the virus reproduction were observed in the two strains of human embryo lung cells (HEL-1 and HEL-3) and the two continuous angiosarcoma cell lines. No virus reporduction was observed in mouse and rat cell cultures. No cytopathic or transformation changes were caused by the virus in any of the systems examined.