Expression of the gene for the delta9 acyl-lipid desaturase in the thermophilic cyanobacterium.

A single-copy gene resembling the gene for the delta9 acyl-lipid desaturase (desC) was cloned from the thermophilic cyanobacterium Synechococcus vulcanus. Expression of desC in Escherichia coli confirmed that it encodes the delta9 desaturase. The nucleotide sequence of the desC was characterized by high G+C content that is typical of the sequences of thermophilic bacteria. The deduced amino acid sequence exhibited low Cys content and high Arg/Lys ratio that are the attributes of thermostable enzymes. A low level of the desC mRNA was detected in the cells grown at 55 degrees C, the optimum growth temperature for S. vulcanus. About a 10-fold increase was observed in the levels of the transcript and the protein during the shift in temperature from 55 to 45 degrees C. At 35 degrees C the amount of the desC mRNA and of the enzyme accumulated in the cells, was 3 to 4 times smaller than at 45 degrees C. At both temperatures, however, lipids were desaturated at similar rates. These results suggest that in S. vulcanus the conversion of stearic acid into oleic acid may be controlled not only by the de novo synthesis of the delta9 desaturase but, possibly, by the activation of the pre-existing enzyme.

[The early detection of allergic dermatoses and mycoses of the feet in workers in contact with phenol-formaldehyde resins]. / Rannee vyiavlenie allergicheskikh dermatozov i mikozov stop u rabochikh, kontaktiruiushchikh s fenolformal'degidnymi smolami.

Hypersensitivity to phenolformaldehyde resins was detected in 16.2% of workers exposed to them, allergic dermatitis and eczemas in 21.5%, mycoses of the soles in 13.5%, premorbid shifts in half of the examinees. Mycoses of the soles prevailed in subjects with a history of dermatitis and in patients suffering from allergic dermatoses.

Study on West Nile virus persistence in monkeys.

Experiments in M. rhesus showed persistence to be a typical property of West Nile virus. This property was exhibited by strains belonging to different antigenic types, and varying in virulence and in the isolation area (U.S.S.R., Uganda, India). The duration of persistence was at least 5 1/2 months in asymptomatic infection and in convalescence after encephalitis or a febrile disease. The virus isolated within the first 2 weeks after inoculation of monkeys has the standard properties. The virus persisting for 2 months retains its cytopathic and antigenic activity, however, is non-pathogenic for white mice. After 5 1/2 months of persistence the virus has no neurovirulence or cytopathic properties but is capable of infecting the susceptible cells and induces in them the synthesis of virus-specific antigen detectable by immunofluorescence. The persisting virus has been isolated by cocultivation of trypsinized monkey organ cells and cells of the indicator culture. This virus was located mostly in the cerebellum, cerebral subcortical ganglia, lymph nodes, and kidneys. The monkeys experiencing encephalitis, febrile, or asymptomatic infection showed in morphological examinations a subacute inflammatory-degenerative process in the central nervous system. The results suggest that West Nile virus, one of the most widely spread arboviruses in Africa, Asia, and Europe, may be implicated in the etiology of subacute diseases of the CNS.

[Effect of dehydrocorrine-cobalt complex on mitochondria]. / Vliianie degidrokorrinovogo kompleksa kobal'ta na mitokhondrii.

The effects of the decamethyloctadehydrocorrine-cobalt complex (Co-C) on respiration and the ATP-synthetase activity of rat liver mitochondria were investigated. The Co-C complex was found to be an effective shunt of the respiratory chain. It accepts electrons from ubiquinone and donates them directly to O2. The Co-C complex inhibits the ATPase and ATP-synthetase activities of mitochondria.

[Persistence of the Sindbis virus in cultures producing oncornavirus]. / Persistentsiia virusa Sindbis v kul'turakh, produtsiruiushchikh onkornavirus.

Continuous lines were obtained from primary cultures of BALB/C mouse embryo cells which were found by electron microscope and reverse transcriptase reaction to produce permanently oncoronavirus type C after exogenous infection with Rauscher leukemia virus (RLV). Sindbis virus (SV) was inoculated into virogenic cultures 398 days after infection with RLV. The system in characterized by rapid (3-21 days) disappearance of the infectious arbovirus from the medium and the cells, long-term (over 5 months) persistence on SV noninfectious antigen and signs of stimulation of oncornavirus activity. The level of reverse transcriptase activity in cultures in the presence of persisting arbovirus was 1.5-3.3-fold higher than in cultures infected with RLV alone. Two variants of the course of mixed chronic infection of the cultures with oncornavirus and arbovirus differing in the rate of transition of the arbovirus into the noninfectious form and inhibition or stimulation of oncornavirus functions are discussed.

[Persistence of Sindbis virus in cultures either non-producing or irregularly producing oncornavirus]. / Persistentsiia virusa Sindbis v kul'turakh, ne produtsiruiushchikh i nereguliarno produtsiruiushchikh onkornavirus.

Persistence of Sindbis virus (SV) was studied for 9 months in two lines of mouse cell cultures (BALB/C) in one of which the genome of endogenous ecotropic oncornaviruses was repressed. The other lines was exogenously infected at the level of plimary culture with Rauscher leukemia virus (RLV) and SV and showed gradual inhibition of oncornavirus functions. The presence of oncornavirus type C was not the necessary condition for the development of persistent SV infection, however it influenced the character of persistence. In both systems, sequential loss of the hemagglutinating and interferon-inducing activities, then infectivity of SV (61--82 days), and persistence of the noninfectious antigen of the arbovirus for 9 months were observed. The differences consisted in the time of appearance of homologous interference to SV: in the presence of oncornavirus earlier (40 days), under conditions of repressed oncornavirus genome later (179 days). Electron microscopic examinations showed that in the system infected with RLV and SV there occurred in the course of persistence a sharp activation of phagosome-lysosome complex accompanied by incorporation into phagocytolysomes of numerous intact and partially destroyed virions of SV and RLV and their release from cell with cytoplasmic fragments. Possible mechanisms of inhibition of functions of the oncogenic and infectious viruses in the reported model of mixed chronic infection are discussed.

[Interaction of the Sindbis virus and Rauscher and Friend leukoviruses in primary cultures and subcultures of mouse fibroblasts in the early stages of persistence]. / Vzaimodeistvie virusa Sindbis i leikovirusov Raushera i Frend v pervichnykh kul'turakh i subkul'turakh myshinykh fibroblastov na rannikh étapakh persistentsii.

The interaction between Friend and Raucher leukoviruses and Sindbis togavirus was studied in primary cultures of mouse fibroblasts and subcultures passaged for 77 days. In primary cultures, two types of virus interactions were observed: neutralism and interference. In interference, the release of the infectious Sindbis virus from the cells is blocked. According to electron microscopic observations, its reproduction terminates by formation of virus nucleocapsid. The blocking of the togavirus maturation is stable in primary cultures but reversible upon subcultivation of the cells infected with oncorna- and togavirus. Rauscher and Sindbis viruses are capable of joint persistence in subcultures with a gradual decrease of the infectivity of togavirus and the leukemogenic activity of oncornavirus.

Study on the mechanism of interference between Friend leukemia and Sindbis viruses in tissue culture.

Some mechanisms of interference developing in BALB/c mouse embryo fibroblast culture (MEC) infected with Friend leukemia virus (FLV) and 48 hours later superinfected with Sindbis virus (SV) was studied. In FLV-infected cells the amount of SV antigen formed was 2-3 times lower than in SV monoinfection, as indicated by immunofluorescence and cytofluorimetry. Electron microscopic examination showed that in mixed infection the number of newly formed SV particles decreased markedly (by 90%) despite the presence of compact aggregates of viral nucleocapsids in the cytoplasm. When the cells were initially infected with arbovirus and then superinfected with FLV, formation of virus antigen and virions of both viruses was not disturbed. Pre-treatment of cell monolayer with dactinomycin (0.2 mug/ml) blocked interferon production in MEC culture and inhibited interference between FLV and SV. It is assumed that interference between FLV and SV is associated with known mechanisms of interferon action as well as with disturbance of the stage of SV particles assembly and their release from the cell. Due to incomplete cycle of SV reproduction interrupted at the stage of ribonucleoprotein formation, productive type of its interaction with MEC cells is disturbed.