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Biomedical subjects

E A Kvetkova

Publications and source records attributed to E A Kvetkova.

15 recordsLinked to original sources
PubMed1995

Antibodies against tick-borne encephalitis virus (TBEV) non-structural and structural proteins in human sera and spinal fluid.

Western immunoblotting of the serum and spinal fluid of patients with tick-borne encephalitis (TBE) revealed the presence of antibodies against non-structural and internal virion proteins. Antibodies against different viral proteins have been shown to appear 8 days postinfection and to circulate for more than 2 months in case of acute TBE. Antibodies against structural glycoprotein E and non-structural glycoprotein NS1 do not prevail over antibodies against other kinds of viral proteins. The large viral non-structural proteins NS5 and NS3 and small hydrophobic proteins NS2A and NS4B can cause an effective immune response as well. There is no strong correlation between immune response spectrum and fever or meningitis forms of disease. However, sera of patients with chronic TBE contained IgM antibodies to virus-specific proteins more than 1 year later and IgG antibodies with very low titers (if any).

Adolescent↗
PubMed1991

Identification of RNA replicase subunits responsible for initiation of RNA synthesis of tick-borne encephalitis virus by affinity labelling.

Porcine embryo kidney cells infected by tick-borne encephalitis virus (TBEV) were fractionated into nuclear, membrane, and cytoplasmic fractions. To identify proteins involved in the initiation of RNA replication at different stages of infection a highly specific affinity labelling technique was used. In samples of the nuclear fraction taken from cells 45 h after infection (late stage), affinity labelling with aldehyde-containing derivatives of ATP and elongation of this label with [alpha-32P]GTP identified a polypeptide with a molecular mass of about 69 kDa. By means of affinity labelling with aldehyde-containing analogues of GMP, GDP, and GTP as initiation substrates and [alpha-32P]ATP as the elongation substrate, a polypeptide of 100 kDa was selectively modified in the nuclear fraction of cells at the early stages of infection (8 h). These proteins were immunostained with TBEV-specific antibodies, and were identified as the nonstructural TBEV proteins NS3 and NS5, respectively. It was concluded that NS3 and NS5 take part in the initiation of TBEV genome replication at the late and early stages of infection, respectively.

Animals↗
PubMed1990

Mapping of the region of the tick-borne encephalitis virus replicase adjacent to initiating substrate binding center.

Affinity labelling with aldehyde-containing analogs of initiation substrates of nuclear fraction of tick-borne encephalitis virus (TBEV) infected cells results in a labelling of a single polypeptide with a molecular mass of 68 kDa which was immunologically identified as TBEV NS3 protein. A single-hit hydroxylamine hydrolysis, using limited and long-term CNBr cleavages allowed one to identify Lys1800 and/or Lys1803 as the label attachment sites. These amino acid residues are situated in the proximity of the 'B'-site of NTP-binding motif of viral RNA replicase.

Adenosine Triphosphate↗
PubMed1990

[Replication complex of tick-borne encephalitis complex. I. Identification of a nuclear fraction protein responsible for the initiation of RNA synthesis using affinity labeling].

The pig embryo kidney cells infected by tick-borne encephalitis virus were fractionated into nuclear-associated, cytoplasmic and membrane fractions. The main part of the virus replicase activity was associated with the nuclei. The replication complex is able to synthesize full-length viral RNAs in vitro. To identify proteins involved in the initiation of the replication at the late stages of the infection, the highly specific affinity labelling technique was used. It was shown that with aldehyde-containing derivatives of ATP, ADP and AMP and [alpha-32P]GTP the target of labelling is a polypeptide having molecular weight about 69 kDa. The same protein is immunostained with TBE virus specific antibodies after blotting onto nitrocellulose. The conclusion is made that nonstructural protein NS3 takes part in virus replication at the late stage of the infection.

Animals↗
PubMed1984

[Clinico-immunologic correlations in epilepsy].

In 51 epileptic patients with frequent attacks, the clinical manifestations were correlated with some parameters of immune responsiveness. The authors determined the content of plasma globulins of the main classes, cerebral antibodies, T and B lymphocytes, the rate of the inhibition of the leukocyte migration with respect to the cerebral antigen. Epilepsy was shown to run its course in the presence of immune responsiveness depression. A certain relationship existed between the duration of the disease, the endogenic factors, the nature of fits and some immunologic indices. With the development of the disease, the initial deficiency of the B lymphocyte immunity was coupled with the progressive dysfunction of the T lymphocyte immunity.

Autoantibodies↗
PubMed1982

[Cerebrospinal fluid immunoglobulins in patients with acute tick-borne encephalitis].

Data characterizing the quantitative parameters and the spectrum of basic non-specific and specific immunoglobulins (IgA, IgG, IgM) in the cerebrospinal fluid (CSF) of patients with acute tick-borne encephalitis are presented. Statistically significant differences in the intensity and character of the changes in the protein constituents of the CSF were revealed in patients with the subclinical form and forms accompanied with the brain affection. On the basis of evaluating the cerebral microcirculation in the patients with tick-borne encephalitis, and determining the correlation between the content of immunoglobulins in the CSF and the serum an idea is suggested that of a certain significance for the rise of the immunoglobulin levels is (in addition to their local synthesis in the CNS) the phenomenon of protein filtration through the damaged hematoencephalic barrier in the acute period of the infection.

Acute Disease↗
PubMed1976

[Study of delayed hypersensitivity in experimental tick-borne encephalitis].

Experiments were conducted on albino mice. With the aid of the test of inhibition of splenocyte migration in the agar medium it was shown that the tick-borne encephalitis virus caused the state of hypersensitivity of delayed type (HDT) expressed from the 3rd day after the infection and persisting up to the appearance of the clinical signs of the disease; in latent infection the HDT state persisted for a period of up to 50 days (observation period). At the same time the experimental animals displayed a weak splenocyte sensitization with the brain tissue chiefly observed in cases of an acute infection and expressed inconstantly in the latten course of tick-borne encephalitis.

Animals↗
PubMedDate not supplied

[Comparison of 3 express-methods of detection of tick-borne encephalitis virus].

Comparative studies of the diagnostic value of three express methods for detection of tick-borne encephalitis virus in ticks (fluorescent antibody technique (FAT) enzyme immunoassay (EIA), and molecular hybridization of nucleic acids) and the traditional method (bioassay in white mice) showed all the three express methods to be rapid, specific, sensitive, and useful for large-scale epidemiological surveys. Notable was the high effectiveness of the method of nucleic acids hybridization which was not inferior to bioassays in suckling mice and exceeded FAT and EIA. The results of the latter seem to be affected by antigenic variations among tick-borne encephalitis virus strains.

Animals↗
PubMedDate not supplied

[Development of cellular immunity in experimental tick-borne encephalitis].

The development of cellular immunity was investigated in mice infected experimentally with tick-borne encephalitis virus strains (TBE) isolated from patients. In the presence of strain variants of the response, two main trends in the dynamics of cellular immunity induced by different virus strains were established: a rapid increase in the level of sensitization of lymphoid cells in the first days after virus inoculation followed in the stage of paralysis by the desensitization phenomenon (the dynamics of the waning type), and a gradual increase in the level of cellular response in the course of the infectious process (the dynamics of progressive type). The type of the dynamics and the level of immune response correlate with the clinical forms of TBE in man. A possible mechanism of the effect of the immunosuppressing properties of the virus on the immune response pattern in infected mice and the significance of the latter in TBE pathogenesis are discussed.

Animals↗
PubMedDate not supplied

[The morphogenesis of tick-borne encephalitis in light of the new data on virus replication].

The analysis of the RNA virus spread of tick encephalitis in the course of infection has been performed. The virus RNA is detectable first, (as early as one day after the infection) in the lymph nodes. Later it is retained in the cells of T-dependent areas. Viral RNA is also the first to be detected in the vascular structures and ventricular system of the brain. The correlation between the time of the viral RNA replication and specific initial damage in the lymphoid tissue and central nervous system is established. The question is raised on the role of the lymphocyte recirculation in the spread of the virus in the body.

Acute Disease↗