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The comparison of interepidemic influenza viruses with the pathogens of resultant influenza epidemics has revealed that they belong to the same type (subtype) of influenza virus. A definite correlation has been found between the antigenic specificity of haemagglutinin of epidemic and interepidemic strains. The antigenic structure of the interepidemic viruses and the pathogens of further epidemics of influenza B viruses have been found to be completely identical. The interepidemic A(H1N1) isolates have been shown to be antigenic analogues of the causative agents of influenza A(H1N1) during the previous epidemics. Despite the time and place of their isolation, as well as the etiology of the previous and subsequent epidemics, the interepidemic influenza A(H3N2) viruses have been ascertained to be similar to the reference A/Bangkok/1/79.

Simultaneous circulation of different subtypes of influenza A viruses provides conditions for reassortant strains formation. A comparative investigation of genome of 47 influenza A virus strains (H1N1, H2N2, and H3N2) was carried out by competitive dot hybridization technique and sequence analysis of some of cDNA-copies of the virus genes. All the genes of 43 strains encoding nonglycolysed proteins corresponded to the serum subtype of surface glycoproteins. The reassortant pattern of genome for some genes of core proteins was revealed in 4 viruses. All the dot hybridization data were completely confirmed by sequence analysis of the genes.

A molecular analysis was made of genomes of influenza A (H1N1) virus strains, the causative agents of an epidemic in Leningrad, 1986. The primary structure of hemagglutinin gene of two of these strains, A/Leningrad/624/86 and A/Leningrad/621/86, was established, as well as partial primary structure of PB1 gene of certain current strains of the A (H1N1) subtype. A hypothesis of a "shift" of PB1 gene in 1950-1957 is suggested.

The hemagglutinin gene primary structure of influenza virus A/Riga/9977/86 (H3N2) belonging to the "Coen/84" antigenic subgroup was determined by primer sequencing. A comparative analysis confirmed that the reversions of amino acids in the late stages of the H3 influenza virus subtype antigenic drift became more frequent and the antigenic variants remained in epidemic circulation longer. The possible role of some mutations is discussed.

A complex study of samples obtained from patients with influenza and other acute respiratory diseases has revealed that the laboratory methods used in this study can be rated in the following order according to their sensitivity: isolation of the virus in chick embryos, analysis of seroconversions in the hemagglutination inhibition test, immunofluorescent determination of viral antigens, determination of viral antigens by enzyme immunoassay (EIA), detection of RNA-containing viral structures by means of molecular hybridization. From the point of view of the possibility of documenting influenza A in patients, the best results are achieved by the combination of molecular hybridization and EIA techniques: 90% and more of all cases. A rational scheme for the examination of samples obtained from patients with a view to epidemiological study, including both traditional and new rapid diagnostic methods, is proposed.

The results of virological and serological study of the influenza epidemic of 1976 revealed a further antigenic drift of hemagglutinin and neuraminidase in current influenza A viruses. One of the features of the A/76 epidemic strains was a marked weakening of antigenic relationships with viruses of the A/Port Chalmers group and a marked relation to chronologically more remote ancestor of the current epidemic subcycle, A/Victoria/72 virus. This gives grounds to consider the new viruses to be the progeny of the latter and not of A/Port Chalmers/73 viruses. The strains of influenza A virus isolated 1 1/2-2 months before the outbreak (November-December, 1975) were typical members of the A/Port Chalmers group and differed markedly from the agents in the epidemic of 1976. This evidence indicates the exogenic, imported origin of the causative agents of the influenza epidemic in 1976 in the USSR.

Examinations by the HI test of 652 sera from children aged from 9 months to 13 years revealed antibodies to A/Singapore/1/57 (H2N2) in 0.9% and A/PR/8/34 (H0N1) in 1.2% of the children. The specific nature of the activity of the sera was proved by neutralization tests and by treatment of the sera with Staphylococcus aureus adsorbing IgG class antibodies. Antineuraminidase antibodies to these viruses were also detected. Examinations of 247 paired sera from children revealed seroconversion to hemagglutinin and neuraminidase of A/Singapore/1/57 and A/PR/8/34 in 2% and 0.4%, respectively. These results testify to continuing circulation in the human population of influenza A virus subtypes of no current epidemiological importance.

Three epidemics of influenza A (H1N1) occurring in 1977, 1979 and 1981 were studied. These epidemics were found to be gradually dying down, which was manifested by progressively decreasing morbidity rate, the frequency and intensity of seroconversions, as well as by a decrease in the duration of the epidemic period. Changes in the biological properties of influenza A (H1N1) virus were accompanied by changes in its antigenic properties. The drift of neuraminidase in the influenza A (H1N1) virus of 1981 towards increased relationship with neuraminidase in the virus of 1952 was observed, while hemagglutinin in the strains of each of these two groups retained its individual character.

Investigations of the antigenic and biological properties of the causative agents of the 1977 influenza epidemic revealed their appurtenance to the old subtype A1 of influenza virus which had disappeared from circulation 20 years ago. A comparative study of A1 viruses isolated in 1947--1956 and A1/77 established closer relationship of the latter to the causative agents of 1949 and 1950 epidemics. The "old" and newly isolated viruses 4ere also closely related biologically. The similarity of influenza A1/77 viruses with the agents of the pandemic cycle of A1 in 1947--1956 is a convincing confirmation of the hypothesis of Francis-Davenport and Smorodintsev-Luzyanina.

Influenza viruses with different degrees of virulence for the human being produced various reactions of the lymphoid-macrophagal elements in the peritoneal exudate of guinea pigs inoculated intraperitoneally. The higher the virulence of the strain for the human being -- the deeper the inhibition of the lymphoid and macrophagal cells of guinea pigs. Low virulent strains of influenza virus induced a considerable functional activity of macrophages, but were devoid of the lympholytic activity. Because of close corrleation between the virulence of the virus and the cellular content of the exudate the lymphocytic-macrophagal reaction in the animals resistant to influenza virus could serve for determination of the toxic activity of the viruses under study.

The novelty of influenza epidemics of 1972-1973 in Leningrad and other towns of the Soviet Union was due to changes in the antigenic profile of influenza viruses neuraminidase which was found to be closely related to that of A/Victoria/35/72 virus according to the results of neuraminidase activity inhbition test. The epidemic influenza A virus strains isolated in 1972-1973 were also found to be sensitive to thermostable inhibitors of mouse serum which was not typical for the Hong Kong group of viruses.