Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The microviscosity of the hydrophobic region of the membrane of infectious hematopoietic necrosis virus was determined using fluorescence depolarization analysis of the probe 1,6-diphenyl-1,3,5-hexatriene and was found to be much lower at 37 C than that of another rhabdovirus, vesicular stomatitis virus. However, the microviscosity of this fish virus at 18 C, the temperature at which it was grown, corresponded to the microviscosity of vesicular stomatitis virus at 37 C. Data obtained with the fish virus host cell (chinook salmon embryo cells) grown at 18 C suggest that its membranes have a lower microviscosity than either L-929 or BHK-21 cells (the vesicular stomatitis virus host cells) grown at 37 C.
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PMID:Comparative membrane microviscosity of fish and mammalian rhabdoviruses studied by fluorescence depolarization. 18 97

The fluorescence probe 1,6-diphenyl-1,3,5-hexatriene was used to study and compare the dynamic properties of the hydrophobic region of vesicular stomatitis virus grown on L-929 cells, plasma membrane of L-929 cells prepared by two different methods, liposomes prepared from virus lipids and plasma membrane lipids, and intact L-929 cells. The rate of penetration of the probe into the hydrophobic region of the lipid bilayer was found to be much faster in the lipid vesicle bilayer as compared with the intact membrane, but in all cases the fluorescence anisotropy was constant with time. The L-cell plasma membranes, the vesicles prepared from the lipids derived from the plasma membranes, and intact cells are found to have much lower microviscosity values than the virus or virus lipid vesicles throughout a wide range of temperatures. The microviscosity of plasma membrane and plasma membrane lipid vesicles was found to depend on the procedure for plasma membrane preparation as the membranes prepared by different methods had different microviscosities. The intact virus and liposomes prepared from the virus lipids were found to have very similar microviscosity values. Plasma membrane and liposomes prepared from plasma membrane lipids also had similar microviscosity values. Factors affecting microviscosity in natural membranes and artificially mixed lipid membranes are discussed.
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PMID:Enveloped viruses as model membrane systems: microviscosity of vesicular stomatitis virus and host cell membranes. 18 11

Interaction with excess unilamellar phosphatidylcholine (PC) vesicles resulted in depletion of as much as 90% of the cholesterol from the membrane of intact vesicular stomatitis (VS) virus. The cholesterol depletion was not significantly influenced by the proteolytic removal of virion glycoprotein spikes, but it was temperature dependent. Cholesterol depletion caused substantial reduction in anisotropy of the VS virion membrane as measured by fluorescence depolarization of the lipophilic probe 1,6-diphenyl-1,3,5-hexatriene; residual adsorbed vesicles represent a significant factor in this apparent increase in virion membrane fluidity. Interaction with PC vesicles resulted in a substantial loss of VS viral infectivity as measured by plating efficiency on L-cell monolayers. Reduction in infectivity appeared to be related to temperature-dependent depletion of virion cholesterol by PC vesicles. Interaction of VS virions with cholesterol-containing PC vesicles resulted in significantly less decline in infectivity, but attempts to restore cholesterol and infectivity to depleted VS virions were unsuccessful. Depletion of virion cholesterol apparently results through collision with PC vesicles rather than movement of cholesterol monomers or micelles through the aqueous phase, because PC vesicle-virion interaction in the presence of cholesterol oxidase did not result in substantial oxidation of translocated cholesterol.
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PMID:Interaction of vesicular stomatitis virus with lipid vesicles: depletion of cholesterol and effect on virion membrane fluidity and infectivity. 21 Dec 63

Cholesterol was depleted from the membrane of vesicular stomatitis virus by exposing virion suspensions to serum lipoproteins enriched with phospholipids. Unlike the reaction of virions with phospholipid vesicle, nonspecific adherence of lipoproteins and exogenous lipids to the envelope of the virus was found to be minimal. The extent of cholesterol depletion was dependent upon the type of phospholipid complexed with interacting lipoprotein; sphingomyelin and dipalmitoyllecithin were found to be highly effective depleters of cholesterol compared to egg phosphatidylcholine, phosphatidylethanolamine, or phosphatidylserine. Similar depletion of cholesterol from the virion membrane was also observed when vesicular stomatitis virus was exposed to a complex of poly(vinylpyrrolidone) and bovine serum albumin coated with egg phosphatidylcholine or dioleoylphosphatidylcholine. Cholesterol depletion was found to alter the morphology but not the membrane integrity of the virus. Directly correlated with depletion of cholesterol was a substantial loss in the anisotropy of the viral membrane as determined by fluorescence depolarization of the lipophilic probe 1,6-diphenyl-1,3,5-hexatriene. Interaction with poly(vinylpyrrolidone) complexed with albumin, phosphatidylcholine, and cholesterol resulted in exchange of cholesterol from the virion membrane which following biphasic kinetics with a rapid and a slow phase; these data indicate that 75-85% of viral membrane cholesterol is present in the outer monolayer, and 15-25% is located in the inner monolayer. Depletion of cholesterol from the virion membrane resulted in a significant drop in the infectivity of the virus as measured by plating efficiency on L-cell monolayers. Such an effect was not observed when virion cholesterol was exchanged without net reduction in the concentration of viral membrane cholesterol. Part of the loss in infectivity following depletion of cholesterol could be restored by reincorporation of cholesterol in the membrane, thus demonstrating that membrane cholesterol partly contributes to the infectivity of vesicular stomatitis virus.
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PMID:Depletion and exchange of cholesterol from the membrane of vesicular stomatitis virus by interaction with serum lipoproteins or poly(vinylpyrrolidone) complexed with bovine serum albumin. 626 Jan 33

The vesicular stomatitis virus glycoprotein (G) was reconstituted into dipalmitoylphosphatidylcholine (DPPC) vesicles by detergent dialysis. The DPPC gel to liquid-crystalline phase transition of the DPPC-G protein vesicles was monitored by the fluorescence anisotrophy of trans-paranaric acid, 16-(9-anthroyloxy)palmitoylglucocerebroside, 1,6-diphenyl-1,3,5-hexatriene, and 4-heptadecyl-7-hydroxycoumarin. The DPPC transition temperature measured by all four fluorescent probes was lowered in the presence of the G protein and the DPPC gel state was disordered by the G protein as evidenced by a decreased fluorescence anisotropy for all four probes below the phase-transition temperature. A possible ordering of the DPPC liquid-crystalline state by the G protein was indicated by an increased anisotropy of trans-paranaric acid and 16-(9-anthroyloxy)palmitoylglucocerebroside in the liquid-crystalline state of DPPC-G protein vesicles. The G protein in addition affected the ionization of the 4-heptadecyl-7-hydroxycoumarin in lipid vesicles, increasing the apparent pK of the probe from 9.05 to 9.45.
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PMID:Fluorescence studies of dipalmitoylphosphatidylcholine vesicles reconstituted with the glycoprotein of vesicular stomatitis virus. 626 45