Subject(s)
Bunyaviridae Infections/prevention & control , Bunyaviridae/classification , Hantavirus Infections/prevention & control , Orthohantavirus/classification , Animals , Bunyaviridae/isolation & purification , Bunyaviridae Infections/epidemiology , Bunyaviridae Infections/transmission , Disease Reservoirs , Global Health , Orthohantavirus/isolation & purification , Hantavirus Infections/epidemiology , Hantavirus Infections/transmission , HumansABSTRACT
EMC virus causes a lethal infection in baboon monkeys within 4-8 days following subcutaneous injection with 10(4)-10(8) pfu of virus. The infection is accompanied by viremia, invasion of heart muscle and of brain. Monkeys infected with 10(6) pfu of EMC virus were treated with human leukocyte interferon. The interferon was injected intramuscularly first 0, 0.5, 6 and 24 h post-infection, then twice daily with a dose of 3 X 10(6) units for 5 consecutive days. All the monkeys treated with interferon remained alive and healthy. Animals infected with EMC virus, but not treated with interferon died within 6 days with evidence of myocarditis. The EMC virus-interferon interaction in baboon monkeys seems to provide a useful primate model system for testing the prophylactic and therapeutic antiviral activity of interferons or other antiviral substances.
Subject(s)
Enterovirus Infections/therapy , Interferon Type I/therapeutic use , Animals , Disease Models, Animal , Encephalomyocarditis virus/drug effects , Enterovirus Infections/pathology , Enterovirus Infections/prevention & control , Interferon Type I/metabolism , Kinetics , PapioABSTRACT
Essential unsaturated fatty acids such as oleic, linoleic, or arachidonic were incorporated into the phospholipids of animal cells and induced in them a change in the fluidity of their membranes. Exposure of enveloped viruses such as arbo-, myxo-, paramyxo-, or herpesviruses to micromolar concentrations of these fatty acids (which are not toxic to animal cells) caused rapid loss of infectivity of these viruses. Naked viruses such as encephalomyocarditis virus, polio virus or simian virus 40 were not affected by incubation with linoleic acid. The loss of infectivity was attributed to a disruption of the lipoprotein envelope of these virions, as observed in an electron microscope.
Subject(s)
Fatty Acids, Unsaturated/pharmacology , Viruses/drug effects , Animals , Cell Membrane/drug effects , Fatty Acids, Unsaturated/metabolism , Hemolysis/drug effects , Linoleic Acids/pharmacology , Membrane Lipids/analysis , Mice , Viruses/metabolismABSTRACT
Adsorption of Sendai virus to HeLa cells induced in them an increased permeability to K+, Na+, Ca++, deoxyglucose, but not to fluorescein. The stimulation of uptake of 42K was temperature-dependent, did not occur below 15 degrees C, and was not inhibited by ouabain. The virus-induced increase in the uptake and release of 42K and of 3H deoxyglucose could not be mimicked by treatment of cells with linoleic acid, a procedure which increased the fluidity of the cellular membranes. The stimulatory effect of 0.5 mM ATP on the release of deoxyglucose was enhanced several fold in the presence of Sendai virus. These results seem to indicate the possible involvement of membranal enzymes such as e.g. protein kinase in the permeability changes induced by Sendai virus.
Subject(s)
Cell Membrane Permeability , Cell Transformation, Viral , HeLa Cells/metabolism , Calcium/metabolism , Cell Membrane/metabolism , Deoxyglucose/metabolism , Fluoresceins/metabolism , Humans , Parainfluenza Virus 1, Human , Potassium/metabolism , Sodium/metabolismABSTRACT
Unsaturated free fatty acids such as oleic, arachidonic or linoleic at concentrations of 5-25 microgram/ml inactivate enveloped viruses such as herpes, influenza, Sendai, Sindbis within minutes of contact. At these concentrations the fatty acids are inocuous to animal host cells in vitro. Naked viruses, such as polio, SV40 or EMC are not affected by these acids. Saturated stearic acid does not inactivate any viruses at concentrations tested. Though the mode of action of unsaturated fatty acids is not understood, electronmicrographs of enveloped viruses treated by them indicate that the inactivation is associated with disintegration of the virus envelope.
Subject(s)
Fatty Acids, Unsaturated/pharmacology , Herpesviridae/drug effects , Influenza A virus/drug effects , Paramyxoviridae/drug effects , Togaviridae/drug effects , Arachidonic Acids/pharmacology , Linoleic Acids/pharmacology , Oleic Acids/pharmacology , Sindbis Virus/drug effects , Stearic Acids/pharmacologyABSTRACT
Adsorption of Sendai virus at high multiplicity (500-1,000 HAU/10(6) cells) to HeLa cells grown in monolayers causes immediate changes in the ion barrier of the cell membrane, as well as changes in the morphology of the virus-treated cells. Within minutes of adsorption the cells begin to lose potassium and an extensive influx of ions into the cells occurs. Concomitantly with these changes, the cell membrane becomes depolarized, and the resting potential across its membrane decreases. Twenty to sixty minutes post adsorption the damage to the cell membrane is repaired, and both the potassium uptake and the resting potential return to their pre-exposure values. Scanning electron-micrographs of Sendai infected cells incubated at 37 degrees C show formation of bridging microvilli in a zipper-like fashion within two to five minutes post-adsorption; 30 to 60 minutes thereafter the majority of cells in the monolayer are fused. Biochemical changes induced by virus adsorption and the role of Ca++ ions in the observed effects are discussed.
