Autoimmune nature of influenza atherogenicity.

It has been observed during influenza epidemics and in a number of population and clinical trials that this prevalent viral infection was associated with increased death rates from cardiovascular diseases. The clinical and experimental data that may explain accelerated coronary atherosclerosis in influenza infection with implications involving autoimmune mechanisms are analyzed in this article. Both cellular and humoral autoimmune modes could be proposed to participate in the onset or progression of atheromatous lesions due to influenza infection.

[Influenza viruses and atherosclerosis: the role of atherosclerotic plaques in prolonging the persistent form of influenza infection].

It was established that viral particles, like low-density lipoproteins (LDLP), when subjected to some modification changes, lost their ability to be internalized by tissue somatic cells and acquired tropism to macrophage cells. The data, obtained by us by using the polymerase chain reaction (PCR) method, made it possible to assert that atherosclerotic plaques, isolated from vessels of patients with ischemic heart disease (IHD) who underwent coronary bypass, contained RNA of the A(HINI) and AH3N3) influenza viruses. Whereas, the vessel portions, undamaged by atherosclerosis, did not contain any genetic substances of influenza viruses.

[Influenza virus infection in progressing atherosclerosis].

Aim: To study relationship between influenza virus infection and activity of clinical presentations of atherosclerosis.

Methods And Results: Average blood level of IgG to influenza A virus was significantly higher in patients with progressing forms of ischemic heart disease then in patients without objective signs of exacerbation of atherosclerotic process. Mean titles of antibodies to parainfluenza virus and adenoviruses were similar in both groups of patients.

[The use of cycloferon in the therapy of experimental herpetic keratitis].

The cycloferon efficacy was investigated in the treatment of experimental herpesvirus kerato-conjunctivitis in rabbits. The model was demonstrated to reflect the main aspects of herpesvirus eye lesions in humans. Cycloferon application similarly to that of known interferon inducer poludan has been shown to enhance processes of inflammation and subsequent regeneration of eye tissues as well as to decrease mortality of animals due to the generalization of infection.

[Reticuloendothelial system and persistence of influenza virus in the body].

The method of in situ transcription was used to detect influenza virus genome in the organs of infected mice. Virus-specific RNA was found in the alveolar macrophages 5 months after infection, this confirming the capacity of the virus to persist in vivo in these cells for a long time. Evidence in favor of influenza virus modification in an infected host body is presented, which fact dramatically affects virus interactions with macrophages.

[Study of the nature and mechanism of action of virus neutralizing inhibitors of the blood].

Low-density lipoproteins (LDL, d 1.0.40-1.

[The receptor-mediated endocytosis of influenza viruses and low-density lipoproteins by tissue cells].

The experimental data obtained by immunological, immunomorphological, biochemical, and virological methods are presented which substantiate a concept that various strains of influenza virus under study may penetrate tissue cells at sites of high affinity usually meant for low-density lipoproteins (LDLP) providing the cells with cholesterol for construction of outer and inner membranes. A computer analysis of a bank of data on the primary structure of proteins (the package of GENBER programme) revealed significant similarity of amino acid sequences between the area of viral hemagglutinin site attachment to cells and corresponding amino acids comprising apoB LDLP. The presented proofs are a convincing example of virus particles mimicry realized at the molecular level and give new concepts concerning the mechanisms of virus penetration into body cells which are important for the development of a principally new approach to creation of highly effective antiviral compounds.

[The effect of microwave irradiation on the peroxide modification of low density lipoproteins in human blood serum].

In experiments in vitro the electromagnetic field of 2375 mHz, 500 microW/cm2 was shown to influence peroxide modification of low density lipoproteids. It was also shown that this modifying effect was prevented by high density lipoproteids that decreased the level of lipid peroxidation.

[Protective effect of high density lipoproteins, their subfractions and lecithin-cholesterol-acyltransferases on the peroxidation modification of low density lipoproteins].

The role of high density lipoproteins (HDL), their subfractions (HDL2 and HDL3) and lecithin: cholesterol acyltransferase (LCAT) on peroxidative modification of low density lipoproteins (LDL) in vitro was studied. Peroxidative modification was estimated by the formation of malonic dialdehyde (MDA) and LDL aggregates during LDL incubation at 37 degrees C for several days without Fe2+ or for 2 hours in the presence of Fe2+ in EDTA-free media. It was shown that the addition of HDL3 (but not HDL2) markedly decreases the formation of both MDA and LDL aggregates.

Accumulation of cholesteryl esters in macrophages incubated with human lipoprotein-antibody autoimmune complex.

The interaction of mouse peritoneal and human pericardial macrophages with lipoprotein (LP)-antibody (Ab) immune complex isolated from the serum of ischemic heart disease (IHD) patients has been studied. It is shown that the Ab of the autoimmune complex belongs to IgG class, and the antigen is the LP with d less than 1.063 g/ml.

[Antioxidant effect of high-density lipoproteins in the peroxidation of low-density lipoproteins].

It has been shown that in the solution of low density lipoproteins (LDL) during their incubation at 37 degrees C the turbidity and concentration of malondialdehyde was increased, as compared to that observed at 4 degrees C. Both parameters were slowed down by the addition of high density lipoproteins (HDL) into the medium. The protective effect of HDL depended on the time of incubation and the concentration of HDL added.

Lipoprotein-antibody immune complexes. Their catabolism and role in foam cell formation.

Immune complexes consisting of human [125I]LDL or [125I]VLDL and anti-apo B IgG were prepared in vitro. After intravenous administration of these complexes or free LDL to normal rabbits the elimination rate for complexes was 2-3-fold higher than for free lipoproteins. The liver/spleen radioactivity ratio after administration of immune complexes was 34% less than after administration of free lipoproteins.

[Capture of native and in vivo modified 125I-low density lipoproteins by fibroblasts and macrophages. Effect of high density lipoproteins on this process].

Unspecific interaction was analyzed between native 125I-lipoproteins of low density (LDL) as well as 125I-LDL, maintained in rabbit circulation during 4 hrs, and fibroblasts and macrophages. Alterations in properties of the LDL, occurred in blood, were accompanied by an increase in their affinity towards macrophages and a decrease in the affinity to fibroblasts. In vivo effect of HDL on catabolism of LDL was manifested as inhibition of extracellular modification of LDL and elimination of them from circulation, and in vitro--as inhibition of the native LDL capture by fibroblasts and, especially, by macrophages.

[Ultrastructural characteristics of macrophage transformation in foam cells in in vitro experiments].

Ultrastructural features of lipid vacuole formation in foam cells were studied in a mouse macrophage culture on the use of aggregated low density lipids (a-LDL) and fibroblast-modified LDL (fm-LDL). Modification of LDL properties is a factor which induces rapid transformation of macrophages to foam cells. Catabolism of a-LDL and fm-LDL and lipid vacuole formation is carried out in two ways: with and without involvement of lysosomes.

Effect of high density lipoproteins on permeability of rabbit aorta to low density lipoproteins.

A study was made on the effect of high density lipoproteins (HDL) on the permeability of rabbit aorta to low density lipoproteins (LDL) after intravenous administration of human HDL and human [125I]LDL to normal and hypercholesterolemic rabbits. Evaluation of radioactivity in plasma and aorta has shown that the administration of a large dose of HDL decreased the aorta permeability rate for [125I]LDL on an average by 19% in normal rabbits, and by 45% in rabbits with moderate hypercholesterolemia. A historadiographic study showed that HDL also decreased the vessel wall permeability to [125I]LDL in normal and particularly in hypercholesterolemic animals.

[Effect of high-density lipoproteins on the permeability of the rabbit aorta for low-density lipoproteins].

After administration of high doses of high density lipoproteins (HDL) into control rabbits the index of aorta permeability for 125I-low density lipoproteins (LDL) was decreased by about 19%. This index was decreased by 45% if HDL was administered into animals with hypercholesterolemia. Historadiographic assays showed that presence of 125I-LDL in circulation simultaneously with the exogenous HDL caused a decrease in the vessel wall permeability for LDL both in control rabbits and, especially, in hypercholesterolemic animals.

[Nonreceptor interaction of low-density lipoproteins with human fibroblasts].

An analysis was made of catabolism of low density lipids (LDL) labeled in the protein or lipid moieties with cultivated human fibroblasts under inhibition of receptor-mediated endocytosis of LDL. The results have shown that under these conditions, only part of LDL uptaken by the cells are catabolized in the cells for 24 h. A considerable part account for a slow-metabolized intracellular pool.

[Changes in the size and properties of lipoprotein particles in the extracellular medium during incubation of low density lipoproteins with human fibroblasts].

Electron microscopy, disc electrophoresis in polyacrylamide gel, and microzonal electrophoresis on acetate cellulose were used to examine the changes in the properties of low density lipoproteins (LDL) in extracellular medium during incubation with human fibroblasts. It was established that as a result of LDL interaction with fibroblasts there appeared lipoprotein particles less in size, with higher aggregation ability and electrophoretic mobility. The data obtained indicate that LDL undergo physicochemical changes due to non-specific interaction with fibroblasts.

[Alteration in content of lipids and lipoproteins in blood of rabbits with experimental allergic polyneuritis and encephalomyelitis].

Experimental allergic encephalomyelitis an polyneuritis were caused in male rats of 2.5-3.0 kg body mass of the Shinshilla strain by means of administration into the foot of the animals pads of homogenous basic protein myelin from bovine spinal cord and myelin from bovine sciatic nerve as a mixture containing complete Freund's adjuvant.

[Blood lipids and lipoproteins in rabbits with experimental allergic polyneuritis].

Experiments were carried out using 69 rabbit males with a body mass of 2.5-3.0 kg.

[Hexokinase and lactate dehydrogenase activity and isoenzymatic makeup of the smooth gastric muscle in intact and sympathectomized rabbits].

After immunological sympathectomy in rabbits activity and isoenzyme spectra of hexokinase (HK) and lactate dehydrogenase (LDH) were studied in smooth muscle of stomach. Activity of KH in the muscles was statistically significant due to increase in content of a single isoenzyme of HK occurring in the tissue. Activity o LDH was unaltered.

[Hexokinase and lactate dehydrogenase activity and isoenzymatic makeup of the soluble fraction of dissimilarly functioning rabbit muscles normally and in experimental allergic encephalomyelitis].

Only one isozyme of hexokinase (type I) was found in a soluble fraction of smooth muscle of rabbit stomach using column chromatography and polyacrylamide gel electrophoresis. By the pattern of metabolism the smooth muscle of rabbit stomach accupies an intermediate position between rapidly and slowly contracting sceletal muscles, approaching to musculus soleus by the activity and isozyme spectra of hexokinase and lactate dehydrogenase (LDH). Activity of these enzymes was altered not uniformly in dissimilarly functioning muscles of rabbits with experimental allergic encephalomyelitis: it was increased in musculus gastrocnemius of rabbits and decreased in soleus or in smooth muscles.