UMLS:C0038362 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

Query: UMLS:C0038362 (stomatitis)
8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fresh frozen plasma (FFP) is prepared in blood banks world-wide as a by-product of red blood cell concentrate preparation. Appropriate clinical use is for coagulation factor disorders where appropriate concentrates are unavailable and when multiple coagulation factor deficits occur such as in surgery. Viral safety depends on donor selection and screening; thus, there continues to be a small but defined risk of viral transmission comparable with that exhibited by whole blood. We have prepared a virus sterilized FFP (S/D-FFP) by treatment of FFP with 1% tri(n-butyl)phosphate (TNBP) and 1% Triton X-100 at 30 degrees C for 4 hours. Added reagents are removed by extraction with soybean oil and chromatography on insolubilized C18 resin. Treatment results in the rapid and complete inactivation of greater than or equal to 10(7.5) infectious doses (ID50) of vesicular stomatitis virus (VSV) and greater than or equal to 10(6.9) ID50 of sindbis virus (used as marker viruses), greater than or equal to 10(6.2) ID50 of human immunodeficiency virus (HIV), greater than or equal to 10(6) chimp infectious doses (CID50) of hepatitis B virus (HBV), and greater than or equal to 10(5) CID50 of hepatitis C virus (HCV). Immunization of rabbits with S/D-FFP and subsequent adsorption of elicited antibodies with untreated FFP confirmed the absence of neoimmungen formation. Coagulation factor content was comparable with that found in FFP. Based on these laboratory and animal studies, together with the extensive history of the successful use of S/D-treated coagulation factor concentrates, we conclude that replacement of FFP with S/D-FFP, prepared in a manufacturing facility, will result in improved virus safety and product uniformity with no loss of efficacy.
...
PMID:Solvent/detergent-treated plasma: a virus-inactivated substitute for fresh frozen plasma. 131 64

The treatment of plasma with organic solvent/detergent mixtures at the time of plasma collection or pooling could reduce the exposure of technical staff to infectious viruses and enhance the viral safety of the final product. Treatment of plasma for 4 hours with 2-percent tri(n-butyl)phosphate (TNBP) at 37 degrees C, with 1-percent TNBP and 1-percent polyoxyethylensorbitan monooleate (Tween 80) at 30 degrees C, or with 1-percent TNBP and 1-percent polyoxyethylene ethers, (Triton X-45) at 30 degrees C resulted in the rapid and complete inactivation of greater than or equal to 10(4) tissue culture-infectious doses (TCID50) of vesicular stomatitis and Sindbis viruses, which are used as surrogates. Treatment of plasma with TNBP and TNBP and Tween-80 was shown to inactivate greater than or equal to 10(4) TCID50 of human immunodeficiency virus. TNBP treatment of plasma contaminated with 10(6) chimpanzee-infectious doses (CID50) of hepatitis B virus and 10(5) CID50 of non-A,non-B hepatitis virus prevented the transmission of hepatitis to chimpanzees. Immediately after treatment of plasma with 2-percent TNBP, the recovery of factors VIII, IX, and V and antithrombin III was 80, 90, 40, and 100 percent, respectively. Recovery of all factors was greater than or equal to 90 percent after treatment with TNBP and detergent mixtures. Treated plasma was fractionated by standard techniques into antihemophilic factor and prothrombin complex concentrates, immune globulin, and albumin. Prior treatment with TNBP or TNBP and detergent did not affect the separations of desired proteins. Therefore, it appears possible to inactivate viruses in plasma before the execution of standard fractionation procedures.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:The use of tri(n-butyl)phosphate detergent mixtures to inactivate hepatitis viruses and human immunodeficiency virus in plasma and plasma's subsequent fractionation. 175 94

More than 10(4) plaque-forming units (pfu)/ml of HIV are inactivated during the alcohol fractionation step from plasma to fraction (Fr)-II+III, greater than 10(4) pfu/ml is inactivated from Fr-II+III to Fr-II and greater than 10(4) pfu/ml is inactivated during the polyethylene glycol (PEG) fractionation process from Fr-II+III to intravenous IgG (IVIG). The total inactivation rate from plasma to IVIG via Fr-II+III or Fr-II was calculated to be greater than 10(8) or 10(12), respectively. The PEG fractionation method produces an intact and unmodified IVIG. In addition, the PEG fractionation method at a low ionic strength was found to be effective for the elimination of greater than 10(5) units of other viruses, including hepatitis B, vesicular stomatitis and Sindbis viruses.
...
PMID:Elimination of viruses (human immunodeficiency, hepatitis B, vesicular stomatitis and Sindbis viruses) from an intravenous immunoglobulin preparation. 282 31

Recent advances in molecular genetics have led to the possibility of using large DNA viruses, such as vaccinia virus, as a biological delivery system for immunizing man against unrelated disease-causing agents. When live vaccinia virus recombinants expressing the hepatitis B virus surface antigen (HBsAg), the influenza A virus haemagglutinin, the herpes simplex virus (HSV) type 1 D glycoprotein, the rabies virus G glycoprotein and the vesicular stomatitis virus G glycoprotein were used for immunization, animals were protected upon challenge with the appropriate pathogenic agent. A major concern with using such vaccines, however, stems from the previously documented vaccinia virus-associated post-immunizing complications. We present here experimental evidence that thymidine kinase-negative (TK-) vaccinia virus recombinants, constructed by inserting a variety of DNA coding sequences into the vaccinia virus tk gene, are less pathogenic for mice than wild-type virus.
...
PMID:Decreased virulence of recombinant vaccinia virus expression vectors is associated with a thymidine kinase-negative phenotype. 405 85

Recombinant DNA technology appears to be on the verge of producing safe and effective protein vaccines for animal and human diseases. The procedure is applicable to most viruses because their isolated surface proteins generally possess immunogenic activity. Strategies used for the preparation and cloning of the appropriate genes depend on the characteristics of the viral genomes: whether DNA or RNA; their size, strandedness, and segmentation; and whether messenger RNA are monocistronic or polycistronic. Cloned surface proteins of foot-and-mouth disease and hepatitis B viruses are being tested for possible use as practical vaccines. Two doses of the cloned foot-and-mouth disease viral protein have elicited large amounts of neutralizing antibody and have protected cattle and swine against challenge exposure with the virus. Surface proteins have also been cloned for the viruses of fowl plague, influenza, vesicular stomatitis, rabies, and herpes simplex. Cloning is in progress for surface proteins of viruses causing canine parvovirus gastroenteritis, human papillomas, infectious bovine rhinotracheitis, Rift Valley fever, and paramyxovirus diseases. In addition, advances in recombinant DNA and other facilitating technologies have rekindled interest in the chemical synthesis of polypeptide vaccines for viral diseases. The bioengineering of bacterial vaccines is also under way. Proteinaceous pili of enterotoxigenic Escherichia coli are being produced in E coli K-12 strains for use as vaccines against neonatal diarrheal diseases of livestock.
...
PMID:Recombinant DNA technology for the preparation of subunit vaccines. 612 35

The oligosaccharide processing and secretion of hepatitis B surface antigen (HBsAg) was studied in Chinese hamster ovary cells stably transfected with the gene coding HBsAg. HBsAg was secreted from cells with a relatively long half time (ca. 5 h). This appeared to be a characteristic of HBsAg itself, since HBsAg-producing cells infected with vesicular stomatitis virus transported the viral envelope glycoprotein to the cell surface with normal kinetics (half time of ca. 30 min). The secreted HBsAg was comprised of both the unglycosylated (P20) and the glycosylated (G25) polypeptides, characteristic of HBsAg isolated from human serum or secreted from other cell lines (C. W. Crowley, C.-C. Liu, and A. D. Levinson, Mol. Cell. Biol. 3:44-55, 1983; M. F. Dubois, C. Pourcel, S. Rousset, C. Chang, and P. Tiollais, Proc. Natl. Acad. Sci. U.S.A. 77:4549-4553, 1980; C.-C. Liu, D. Yansura, and A. D. Levinson, DNA, 1:213-221, 1982; G. M. Macnab, J. J. Alexander, G. Lecatsas, E. M. Bey, and J. M. Urbanocvicz, Br. J. Cancer, 24:509-515, 1976; A. M. Moriarity, B. H. Hoyer, J. W.-K. Shih, J. L. Gerin, and D. H. Hamer, Proc. Natl. Acad. Sci. U.S.A. 78:2606-2610, 1981; D. L. Peterson, J. Biol. Chem., 256:6975-6983, 1981). The glycosylated polypeptide (GP25) contained complex oligosaccharide chains. Cell-associated HBsAg also was comprised of both an unglycosylated and a glycosylated polypeptide; however, the glycosylated form (GP23) contained only high-mannose oligosaccharide chains. No oligosaccharide processing of the high-mannose chains could be detected within the cells. Thus, most of the time before secretion of HBsAg from cells must have been spent in a pre-Golgi or early Golgi compartment. Glycosylation was inhibited completely by tunicamycin, although unglycosylated particles were still secreted from cells and were antigenic. The secretion and oligosaccharide processing of HBsAg were inhibited with high concentrations of monensin, but at lower concentrations of monensin HBsAg was still secreted, although only half of the oligosaccharide chains were processed to the complex form.
...
PMID:Intracellular transport and secretion of hepatitis B surface antigen in mammalian cells. 674 60

Laboratory research that began in 1982 led to the licensing in the USA of a solvent/detergent (SD)-treated factor VIII concentrate in 1985. The licence was granted on the basis of several factors. First, studies had demonstrated the inactivation of several marker viruses (vesicular stomatitis virus, Sindbis virus, Sendai virus) and other viruses such as human immunodeficiency virus (HIV), hepatitis B virus (HBV), and non-A, non-B hepatitis virus (NANBHV; now known principally to be hepatitis C virus) added to the factor VIII concentrate just before treatment. Secondly, it had been realized that the relevant viruses in transfusion (e.g. HIV, HBV, NANBHV) all had lipid envelopes. Finally, laboratory, preclinical and clinical evidence indicated that factor VIII and other proteins present in the preparation were unaffected by SD treatment. The applicability of the SD method to a wide range of products and preparations, high process recoveries and a growing body of viral safety information linked with the failure of several other virus-inactivation methods to eliminate hepatitis transmission fostered the adoption of SD technology by more than 50 organizations worldwide. SD mixtures are now used in the preparation of a diverse array of products. Numerous laboratory and clinical studies suggest that coagulation-factor concentrates and other SD-treated products prepared from plasma pools are now safer than the individual units from which they were derived. Also, a large body of evidence indicates that hepatitis A virus (HAV) is not typically transmitted by blood and blood products.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Viral safety of solvent/detergent-treated blood products. 774 45

Laboratory research commencing in 1982 led to licensing in the United States in 1985 of a solvent/detergent (SD)-treated anti-haemophilic factor (AHF) concentrate. Licensing was based on (a) studies demonstrating the inactivation of several marker viruses [vesicular stomatitis virus (VSV), Sindbis virus, Sendai virus], human immunodeficiency virus (HIV), hepatitis B virus (HBV), and non-A, non-B hepatitis virus [NANBHV; now known to be principally hepatitis C virus (HCV)] added to AHF just before treatment, (b) the realization that the principal viruses of concern in a transfusion setting (e.g. HIV, HBV, NANBHV) were all lipid-enveloped, and (c) laboratory, preclinical and clinical evidence indicating that AHF and other proteins present in the preparation were unaffected. The applicability of the SD method to a wide range of products and preparations, high process recoveries, and a growing body of viral safety information linked with the failure of several other virus inactivation methods to eliminate hepatitis transmission fostered the adoption of SD technology by more than 50 organizations world-wide. SD mixtures are now used in the preparation of products as diverse as intermediate purity and monoclonal antibody purified AHF and other coagulation factor concentrates, fibrin glue, normal and hyperimmune IgG and IgM preparations including those derived from tissue culture, plasma for transfusion, and various diagnostic controls. Over four million doses of SD-treated products have been administered, and numerous laboratory and clinical studies designed to assess virus safety have been conducted. SD treatment has been shown to inactivate > or = 10(9.2) tissue culture infectious doses (TCID50) of VSV, > or = 10(8.8) TCID50 of Sindbis virus, > or = 10(6.0) TCID50 of Sendai virus, > or = 10(7.3) duck infectious doses of duck HBV, > or = 10(11.0) degrees TCID50 of HIV-1, > or = 10(6.0) TCID50 of HIV-2, > or = 10(6.0) chimpanzee infectious doses (CID50) of HBV, > or = 10(5.0) CID50 of HCV, > or = 10(6.0) TCID50 of cytomegalovirus, > or = 10(5.8) TCID50 of herpes simplex virus type 1, > or = 10(4.0) TCID50 of PI-1, > or = 10(6.0) TCID50 of murine leukemia virus (Mov-3), > or = 10(4.0) TCID50 of murine xenotropic virus, and > or = 10(2.0) TCID50 of Rauscher murine leukemia ecotropic virus. Moreover, in ten prospective clinical studies, 0/53, 0/427, and 0/455 patients susceptible to HBV, NANBHV (HCV), and HIV became infected on follow-up.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Viral safety of solvent-detergent treated blood products. 817 97

Certain large DNA viruses (e.g. herpesviruses and poxviruses) encode proteins related to cellular protein-serine/threonine kinases, and Hepatitis B virus and vesicular stomatitis virus may encode structurally different protein kinases. Other viruses activate cellular protein kinases, e.g. interferon-induced eukaryotic initiation factor-2 kinase, growth factor-induced kinases and protein kinases that regulate mitosis. Protein phosphatases are encoded by vaccinia virus and bacteriophage lambda and must also play a role in viral infection--as do cellular protein phosphatases. The functions of many of these viral enzymes remain to be determined, but they represent possible new targets for anti-viral therapy.
...
PMID:Viral protein kinases and protein phosphatases. 830 96

Hepatitis delta virus (HDV) is a defective virus requiring the hepatitis B virus (HBV) to provide hepatitis B surface antigens as the envelope protein. The hepatitis B surface antigens are posttranslationally modified by N-linked glycosylation, and its significance in HDV assembly was investigated with a cotransfection system using human hepatoma cell line Huh-7. After the N-linked glycosylation of HBsAg was blocked by tunicamycin treatment, the packaging of HDV in the culture system could be suppressed to a level as low as 5-10% of the untreated control. The extent of inhibition correlated with the increased concentrations of tunicamycin. In contrast, the loss of HBsAg glycosylation did not affect the efficiency of assembly of HBV particles. When the N-linked glycosylation site of small HBsAg at amino acid 146 was mutated from asparagine to glutamine, the mutant HBsAg packaged only a modest amount of HDV particles. The quantity and kinetics of formation of HDV particles in culture system were reduced by the depletion of HBsAg glycosylation. Therefore HDV, similar to influenza and vesicular stomatitis viruses, depends on glycosylation of the envelope proteins as a signal for envelope protein maturation and for virion formation.
...
PMID:N-linked glycosylation of hepatitis B surface antigens is involved but not essential in the assembly of hepatitis delta virus. 865 25

1 2 3 4 Next >>