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)

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)
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PMID:Viral safety of solvent/detergent-treated blood products. 774 45

We report here the results of our evaluation of virus inactivation during the manufacturing steps of two intravenous immunoglobulin (IGIV) preparations. Virus inactivation and/or removal by processing steps, such as ethanol fractionation and polyethylene glycol precipitation, and deliberate virucidal steps, such as solvent/detergent treatment and pasteurization, were tested on a variety of human pathogenic and experimental model viruses, including human immunodeficiency, Hepatitis C, Mumps, Vaccinia, Chikungunya, Vesicular Stomatitis, Sindbis, and ECHO viruses. All viruses were successfully inactivated and/or eliminated by the processing steps studied. In some cases, however, multiple steps were required. We conclude that the incorporation of steps deliberately designed to inactivate or remove viruses during the production of IGIV provides an extra measure of viral safety.
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PMID:Inactivation and elimination of viruses during preparation of human intravenous immunoglobulin. 786 23

Cationic phthalocyanines with either aluminum or silicon as the central metal were evaluated for their ability to inactivate viruses in red blood cell concentrates (RBCC) photodynamically. In addition, the virucidal potential of a substituted anionic phthalocyanine, aluminum dibenzodisulfophthalocyanine hydroxide (A1N2SB2POH) was evaluated and compared with that of the much studied anionic aluminum tetrasulfophthalocyanine hydroxide (A1PcS4OH). Based on the rate of inactivation of the lipid-enveloped vesicular stomatitis virus (VSV), the virucidal potential of these phthalocyanines was: HOSiPcOSi(CH3)2(CH2)3N+(CH3)3I- (Pc 5) = SiPc[OSi(CH3)2-(CH2)3N+(CH3)3I-]2 (Pc 6) > A1PcOSi(CH3)2(CH2)3N+(CH3)2(CH2)11CH3I- (Pc 21) = A1N2SB2POH = A1PcS4 > HOSiPc[OSi(CH3)2(CH2)3N+(CH3)2(CH2)11CH3I-]2 (Pc 14) > A1PcOSi(CH3)2(CH2)3N+(CH3)3I- (Pc 2). Phthalocyanine ligand 14 and Pc 21 are new phthalocyanines, made by quaternizing known amino analogues. Compared to VSV, the rate of inactivation of Sindbis virus (another model lipid-enveloped virus) was identical when treated in red blood cells (RBC) with Pc 5 and slightly higher when treated with Pc 6 and A1PcS4OH. Treatment of RBCC containing cell-free human immunodeficiency virus (HIV-1) with Pc 5 or A1PcS4OH required 15 min of irradiation to inactivate (> 5 log10 reduction) the virus. The extent of HIV-1 inactivation with A1N2SB2POH was 3.7 log10 after 60 min of red light exposure. The RBC integrity after photosensitization was measured by the ability of the cells to bind to plates coated with poly-L-lysine, (which reflects the retention of the RBC surface negative charges) and hemolysis of the cells over a 7 day storage period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New phthalocyanines for photodynamic virus inactivation in red blood cell concentrates. 793 15

As the scope of the acquired immunodeficiency syndrome (AIDS) epidemic grows to include increasingly larger proportions of heterosexual adults and children, there has also been a change in the severity of human immunodeficiency virus (HIV)-related periodontal conditions at one San Francisco clinic. The cases of HIV-associated gingivitis, now called linear gingival erythema, HIV-associated periodontitis (or necrotizing ulcerative periodontitis), and necrotizing stomatitis have been less severe, despite an increase in overall HIV caseload. No clear basis for this trend has been established, but possible explanations include: biased population samples, increased immunosuppression as the disease matures, use of antimicrobial therapy, or a change in patient demographics. Several studies have failed to identify a single causative organism. This article presents a review of HIV-related periodontal complications and points out that the condition can be treated with local and systemic antibiotics and that dental professionals throughout the world can expect a tremendous increase over the next several years in HIV-infected patients with special clinical complications.
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PMID:Periodontal complications of HIV infection. 803 7

Four hundred and thirty-nine feline serum samples from cats with different living conditions in the north of Italy were tested for antibodies to feline immunodeficiency virus (FIV) and for antigen of Feline Leukemia Virus by enzyme-linked immunosorbent assay. A Western blot technique was also used on the positive sera in order to confirm the presence of specific antibodies to FIV. The Western blot enabled the detection of a false positive serum. The prevalence of FIV infection in this population was 12.5% and among the seropositive cats a greater proportion was male (74.5%) than female (25.5%). A correlation between the clinical status and the evolution of the pathology is described together with a score based on the severity of the stomatitis in infected cats. The Western blot patterns of positive samples were then compared with the stage of the pathology. Statistical analysis on the distribution of FIV in stray cats, cats with garden and courtyard access and strictly house-confined cats showed a highly significant risk of the infection in the first group.
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PMID:Seroepidemiological and clinical survey of feline immunodeficiency virus infection in northern Italy. 804 81

Cats naturally infected with feline immunodeficiency virus (FIV) develop an AIDS-like syndrome whereas experimentally infected cats do not. To investigate the role of cofactors in the development of this disease in cats, 7 specific pathogen-free (SPF) and 12 random-source (RS) cats were infected with FIV. Over 4 years, infected cats developed similar phenotypic and functional immune abnormalities characterized by early and chronic inversion of CD4+:CD8+ cell ratios and significantly decreased mitogen responses compared with controls. Beginning 18-24 months after infection, 10 RS cats developed chronic clinical disease typical of feline AIDS, including stomatitis and recurrent upper respiratory disease; 4 SPF cats also developed chronic clinical disease, 2 with neurologic disease and 2 with B cell lymphomas. Thus, immunologic background is important in the type of disease that develops in cats infected with FIV, and FIV represents a promising animal model for studying the immunopathogenesis of AIDS in humans.
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PMID:Development of clinical disease in cats experimentally infected with feline immunodeficiency virus. 807 11

The human peripheral blood mononuclear cells responsible for IFN-alpha production in response to viral stimuli have been most often described as either monocytes (as typified by the response to Sendai virus) or as a light density, HLA-DR+ population which is negative for most cell surface markers characteristic of mature T cells, B cells, monocytes, or natural killer cells (as typified by the response to Herpes simplex virus (HSV)). The frequency of IFN-alpha-producing cells (IPC) responding to Sendai virus is typically 10-fold or more higher than those responding to HSV. In the current study, we have used ELISpot assays to determine the frequency of IPC responding to DNA and RNA viruses including HSV, Sendai, vesicular stomatitis virus, cytomegalovirus, adenovirus, SV40, influenza, measles, mumps, Newcastle disease virus (NDV) and human immunodeficiency virus (HIV). The enveloped viruses but not the nonenveloped viruses (adenovirus and SV40) elicited an IFN-alpha response. The frequency of IPC for each of the other viruses was more similar to the low frequency HSV-responding population than to the higher frequency Sendai virus response. These included several viruses in the same family as Sendai virus, namely the paramyxo viruses measles, mumps, and NDV. IPC were also tested for sensitivity to the lysosomotropic drug chloroquine, which diminishes IFN-alpha produced in response to HSV but not Sendai virus. With the exception of Sendai virus, chloroquine treatment abrogated the majority of IFN-alpha produced and IPC against each of the viruses. We conclude that low frequency, nonmonocytic NIPC account for the majority of IFN-alpha production in response to different viruses.
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PMID:Viral induction of low frequency interferon-alpha producing cells. 809 44

The small membrane protein Vpu of human immunodeficiency virus type 1 stimulates rapid degradation of CD4 molecules that are retained in the endoplasmic reticulum. To analyze the domain(s) of CD4 involved in Vpu-stimulated degradation, we examined degradation of hybrid proteins made between the vesicular stomatitis virus glycoprotein (VSV G) and CD4. Vpu expression stimulated rapid degradation of a hybrid consisting of the extracellular domain of VSV G linked to the transmembrane and cytoplasmic domains of CD4. Analysis of additional hybrids showed that both the cytoplasmic and transmembrane domains of CD4 were required for this Vpu-stimulated degradation. This conclusion is in apparent conflict with a recent study showing that the cytoplasmic domain of CD4 alone is sufficient to cause Vpu-stimulated degradation of a CD8-CD4 hybrid protein. The apparent conflict may be explained by the presence of related sequences or structures in the transmembrane domains of CD4 and CD8 that are involved in binding Vpu directly or that interact with the Vpu-stimulated degradation system.
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PMID:Stimulation of heterologous protein degradation by the Vpu protein of HIV-1 requires the transmembrane and cytoplasmic domains of CD4. 809 84

Incorporation of human immunodeficiency virus type 1 (HIV-1) envelope proteins into vesicular stomatitis virus (VSV) particles was studied in a system that allows expressed envelope proteins to rescue phenotypically a temperature-sensitive mutant of VSV (tsO45). This mutant exhibits defective transport of its own envelope glycoprotein (G) and can be rescued by simultaneous expression of wild-type G protein from cDNA. We report here that a hybrid HIV-1-VSV protein containing the extracellular and transmembrane domains of the HIV-1 envelope protein fused to the cytoplasmic domain of VSV G protein was able to rescue the tsO45 mutant lacking the G protein, while the wild-type HIV-1 envelope protein was not. The VSV(HIV) pseudotypes obtained infected only CD4+ cells and were neutralized specifically by anti-HIV-1 sera. Our results indicate that the cytoplasmic tail of the VSV glycoprotein contains an independent signal capable of directing a foreign protein into VSV particles. The VSV(HIV) pseudotypes generated here were prepared in the absence of HIV-1 and should be useful for identifying molecules that block HIV-1 entry.
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PMID:Cytoplasmic domain requirement for incorporation of a foreign envelope protein into vesicular stomatitis virus. 809 20

Experimental infection with the Mt. Airy isolate of feline immunodeficiency virus (FIVMA), a lentivirus isolated from a domestic cat exhibiting signs of an immunodeficiency-like syndrome, results in transient lymphadenopathy, fever, stomatitis, enteritis, neurologic abnormalities, and immunosuppression. The effects of FIVMA infection on neutrophil and natural killer cell (NK) function were examined in vitro. Suppression of neutrophil chemiluminescence (CL) responses, as well as reduction in NK-mediated cytotoxicity were demonstrated. Neutrophil CL was decreased by 50% in infected cats when compared to control values. This loss of CL was present through 6 months after infection. In addition, NK-mediated cytotoxicity was approximately 50% less in FIVMA infected cats than in controls. Loss of innate immunity was paralleled with inversion in feline CD4/CD8 lymphocyte ratios and decreases in lymphocyte mitogenesis seen as early as 5 weeks after infection. These results suggest that FIVMA infection induces an immunodeficiency disorder in infected cats similar to that seen in human immunodeficiency virus infections.
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PMID:Loss of neutrophil and natural killer cell function following feline immunodeficiency virus infection. 810 92


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