Disease relevance of Virus Inactivation

• Viral inactivation of vesicular stomatitis virus in normal human serum by cross-linked polyvinylpyrrolidone [1].
• Comparative study of mechanisms of herpes simplex virus inactivation by sodium lauryl sulfate and n-lauroylsarcosine [2].
• The rates of virus inactivation by 4-nitroquinoline 1-oxide (NQO) and 4-hydroxyaminoquinoline 1-oxide (HAQO) were compared and samples of cytomegalovirus (CMV)-infected cell lysates to which NQO had been added were examined for the presence of HAQO [3].
• Arenavirus Z protein as an antiviral target: virus inactivation and protein oligomerization by zinc finger-reactive compounds [4].
• BACKGROUND: Hepatitis C virus (HCV) RNA was measured in commercial factor VIII concentrates, that is, antihemophilic factor (human) (AHF), to allow the retrospective evaluation of the effect of various virus-inactivation procedures [5].

High impact information on Virus Inactivation

• APOBEC3G deaminates deoxycytidines in minus strand DNA to deoxyuridines, resulting in G to A hypermutation and viral inactivation [6].
• HBV may therefore be particularly vulnerable to the capsid-targeted viral inactivation approach [7].
• Viral inactivation was abolished by the addition of a synthetic disaccharide that contains the alpha-galactosyl epitope, indicating that virolysis is mediated by anti-alpha-galactosyl natural Ab [8].
• Furthermore, transmission of B19 infection was observed, indicating presence of the infectious virus despite routine viral inactivation/removal procedures during the manufacturing process [9].
• Pretreatment of cells with compound prior to addition of virus also demonstrated strong microbicidal activity with dextran sulfate and polystyrene sulfonate, but cellulose sulfate required several orders of magnitude more compound for virus inactivation [10].

Chemical compound and disease context of Virus Inactivation

• The role of DNA damage in PM2 viral inactivation by methylene blue photosensitization [11].
• The virus inactivation step incorporated into the manufacturing process (incubation with n-heptane at 60 degrees C for 20 hours) was shown to inactivate at least 8.6 logs of type 1 human immunodeficiency virus [12].
• The effect of the surfactin isoforms and methyl esters on erythrocyte hemolysis correlated with the virus-inactivation capacity [13].
• The recovery of poliovirus D-antigen after virus inactivation was studied for two inactivating agents (beta-propiolactone and formalin) using the three poliovirus types (Sabin types 1, 2 and 3) [14].
• While virus inactivation with TNBP/Tween 80 was slower, effective inactivation of Sindbis, HSV-1, VSV and human immunodeficiency virus type-1, i.e. 4.1-->6.3 log, occurred within 30 minutes [15].

Biological context of Virus Inactivation

• Since molecular changes of viral epitopes and the genome may indicate virus inactivation, we measured the alteration of these constituents with 0.065% peracetic acid (PAA) for exposure times up to 1 h [16].

Anatomical context of Virus Inactivation

• Erythrocyte damage, virus inactivation and photooxidation of reduced glutathione (GSH) and histidine were all enhanced if light was delivered at 100 W/m2 as compared to 500 W/m2 [17].
• The procedure, which is fully compatible with modern plasma fractionation schemes, includes anion-exchange chromatography on DMAE-Fractogel EMD, viral inactivation by solvent-detergent treatment, adsorption on SO3-Fractogel EMD and viral removal by nanofiltration on 35- and 15-nm pore size membranes [18].
• Photodynamic virus inactivation of thrombocyte concentrates by phenothiazine dyes [19].
• However, the virus inactivation by alveolar macrophages was modified only slightly by Y-19995 treatment [20].

Associations of Virus Inactivation with chemical compounds

• The virucidal properties of compound 1 were confirmed by virus inactivation assays [21].
• BACKGROUND: Photodynamic virus inactivation of plasma with methylene blue significantly decreases the recovery of fibrinogen and coagulation factors V and VIII [22].
• BACKGROUND: Virus inactivation of plasma can be achieved by photodynamic methods in the presence of phenothiazine dyes such as methylene blue (MB) [23].
• The influence of various factors on the rate of virus inactivation also was studied by modifying the composition of the IgG solutions with respect to IgG, sucrose, and NaCl content [24].
• To protect RBCs from photodynamic damage, type I free radical quenchers, such as mannitol, which did not affect virus inactivation, were added [25].

Gene context of Virus Inactivation

• We have investigated the effect of virus inactivation procedures on FVIII function by preparing experimental concentrates from the same starting cryoprecipitate with the following procedures: none (N); dry heat (DH); pasteurisation (P); solvent/detergent (SD); solvent detergent + dry heat (SDDH); solvent detergent + pasteurisation (SDP) [26].
• Pharmacokinetic studies on Wilfactin, a von Willebrand factor concentrate with a low factor VIII content treated with three virus-inactivation/removal methods [27].
• The generation of hmw TNF alpha mRNA required exposure to fully infectious influenza A virus, since virus inactivation at 56 degrees C induced only regular and not hmw TNF alpha mRNA [28].
• STUDY DESIGN AND METHODS: Virus inactivation was monitored by decrease of infectivity and loss of capsid integrity [29].
• Methylene blue (MB), riboflavin (RB) and psoralen sensitizers (4' aminomethyl-4,5',8-trimethylpsoralen [AMT] and derivatives) are under study as sensitizers of viral inactivation of blood products such as plasma proteins, platelets and red cells, all of which lack genomic nucleic acid [30].

Analytical, diagnostic and therapeutic context of Virus Inactivation

• Leucocytes can be eliminated from plasma by filtration prior to viral inactivation with methylene blue [31].
• Indirect evidence of virus inactivation was obtained by examining the decrease in HBV-associated DNA polymerase and HBcAg activities after treatment with increasing concentrations of disinfectant [32].
• Using a combination of Cohn ethanol fractionation, virus inactivation, glycine and sodium chloride precipitation, and lysine-Sepharose affinity chromatography, a unique and rapid simplified method was developed to obtain highly purified fibrinogen for diagnostic use with both biological (Clauss method) and immunological (Jacobsson method) activity [33].

References