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HIV-1 virions are as immature noninfectious particles lacking a central core. Shortly after budding, virions temporally mature and acquire cores and infectious activity. The cause of maturation remains poorly studied. We have revealed that the virions produced early after infection following 24-36 hours, never mature and remain noninfectious, and only virions produced 48-72 hours after infection mature. The mature virions contain 3 times more genomic viral RNA than "early" virus. The "early" virions contain the same proteolytically cleaved Gag proteins as mature virions in contrast to the accepted version. The virus protease inhibitor Indinavir sulfate (IS) fully blocks infectivity when added early after infection. The early proteolysis of Gag precursor in the infected cells and inclusion into the virions of cellularly cleaved matrix protein (cMA) are shown in the IS-treated cells. cMA is associated with genomic viral RNA.

Three proteins, namely: "core" protein C and glycoproteins E1 and E2, are main structural proteins forming a hepatitis C vius (HCV) virion. The virus structure and assembly, a role of the structural proteins in virion morphogenesis remain unknown because of the lack of an efficient culture system for HCV to be grown in vitro. Using recombinant baculoviruses expressing HCV structural protein genes in insect cells the specific structural proteins at the level of 25-35% relative to a common cell protein content, heterodimers of the glcoproteins, and HCV-like particles have been obtained. It has been demonstrated that recombinant proteins C, E1, and E2 go through the posttranslation modification, the glycoproteins form the non-covalent heterodimer, and HCV-like particles are located in endoplasmatic reticulum membrains of infected cells. An ability of the expressed proteins for forming E1E2 dimers and HCV-like particles was used for studying the role of E1 protein glcosylation upon expression and processing of the glycoproteins.

A mathematical model of the intracellular reproduction of the influenza virus has been constructed, which describes the regulation of transcription, translation, replication, and assembly of the virus in a sensitive noninterferonogenic cell. A structural and parametric verification of the model has been performed, which involves an analysis of alternative mechanisms of regulation of the key events of the reproduction of the influenza virus at the stages of the primary and secondary transcription. It was shown that the dynamics of the concentrations of the system components is in qualitative agreement with the experimental data. An analysis of the model parameters showed a high sensitivity of the model to changes in the parameters that control the efficiency of the binding of the viral polymerase to virus-specific RNAs at the stages of initiation and elongation of transcription and replication of the viral genome. The results obtained suggest that the stages of the virus reproduction sensitive to changes in the parameters are potential targets for drugs. Using the model, a minimal multiplicity of infection at which the formation of viral particles is observed was predicted.

The ultrastructure of endothelial cells and fibroblasts infected with VHL/E or AD169 strains was examined. The cells producing the virus 25 days after infection with VHL/E strains (0.01 PFU/cell) contain numerous cytoplasmic-located filament-associated capsids in addition to standard infectious and noninfectious viral particles. Only single filament-contacting capsids were found in the cytoplasm of the cells producing the virus 20 days after infection with AD169 strain (0.001 PFU/cell). In situ DNA hydridization on the VHL/E-infected cells has indicated that the capsid-contacting filament is human cytomegalovirus DNA. The findings suggest that premature release of viral DNA from the capsids occurs during their maturation in the cytoplasm.