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 prevalence of feline calicivirus (FCV), feline leukaemia virus (FeLV) and feline immunodeficiency virus (FIV) antibodies were assessed in 78 British and 18 North American household cats with chronic stomatitis and in appropriate controls. In British cats, FCV was significantly (P less than 0.005) more prevalent in both hospital (92 per cent) and general practice (79 per cent) cases compared to their controls (19 per cent in both cases). A similar difference in prevalence of FCV was noted in North American cats where 50 per cent of cases were positive compared to 0 per cent of controls (P less than 0.01). FeLV prevalence was low in all chronic stomatitis populations. A significantly higher prevalence of antibody to FIV was found in British hospital cases (81 per cent) compared with time-matched controls (16 per cent) (P less than 0.001): a similar rate was found in the general practice cases (75 per cent) for which no controls were available. In the North American sample, FIV antibody status was similar in cases (54 per cent positive) and their age, sex and breed matched controls (50 per cent). The possible role of FCV and FIV in the pathogenesis of feline chronic stomatitis is discussed.
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PMID:Prevalence of feline calicivirus, feline leukaemia virus and antibodies to FIV in cats with chronic stomatitis. 254 29

The neplanocin A analogs, 3-deazaneplanocin A, 9-(trans-2',trans-3'-dihydroxycyclopent-4'-enyl)adenine (DHCA), and 9-(trans-2',trans-3'-dihydroxycyclopent-4'-enyl)-3-deazaadenine (DHCDA), all potent inhibitors of S-adenosylhomocysteine (AdoHcy) hydrolase, were studied for their broad-spectrum antiviral potential. 3-Deazaneplanocin A, DHCA, and DHCDA proved specifically effective against vesicular stomatitis virus, vaccinia virus, parainfluenza virus, reovirus, and rotavirus. Their selectivity was greater than that of neplanocin A, particularly against vesicular stomatitis virus and rotavirus. As could be expected from adenosine analogs that are directly targeted at AdoHcy hydrolase, 3-deazaneplanocin A, DHCA, and DHCDA were fully active in adenosine kinase-deficient cells, implying that their activity did not depend on phosphorylation by adenosine kinase. None of the AdoHcy hydrolase inhibitors showed selective activity against human immunodeficiency virus (type 1). 3-Deazaneplanocin A at a dose of 0.5 mg/kg per day conferred marked protection against a lethal infection of newborn mice with vesicular stomatitis virus.
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PMID:Broad-spectrum antiviral activities of neplanocin A, 3-deazaneplanocin A, and their 5'-nor derivatives. 255 6

A representative sample of the pet cat population of the United Kingdom was surveyed. Blood samples from 1204 sick and 1007 healthy cats of known breed, age and sex were tested for antibodies to feline immunodeficiency virus (FIV) and feline leukaemia virus (FeLV). The prevalence of FIV was 19 per cent in sick cats and 6 per cent in healthy cats, and the prevalence of FeLV was 18 per cent in sick cats and 5 per cent in healthy cats; both infections were more common in domestic cats than in pedigree cats. Feline immunodeficiency virus was more prevalent in older cats but FeLV was more prevalent in younger cats. There was no difference between the prevalence of FeLV in male and female cats but male cats were more likely to be infected with FIV than female cats. No interaction was demonstrated between FIV and FeLV infections. Of the cats which were in contact with FIV in households with more than one cat, 21 per cent had seroconverted. The prevalence of FeLV viraemia in cats in contact with FeLV was 14 per cent. The clinical signs associated with FIV were pyrexia, gingivitis/stomatitis and respiratory signs, and with FeLV, pyrexia and anaemia. It was concluded that both viruses were significant causes of disease, and that the cats most likely to be infected with FIV were older, free-roaming male cats and for FeLV, younger, free-roaming cats.
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PMID:Prevalence of feline leukaemia virus and antibodies to feline immunodeficiency virus in cats in the United Kingdom. 255 56

Mannan sulfate, a novel sulfated polysaccharide, was prepared and investigated for its activity against human immunodeficiency virus type 1 (HIV-1) in vitro. Mannan sulfate completely inhibited HIV-1-induced cell destruction and viral antigen expression in HIV-1-infected Molt-4 (clone 8) cells at a concentration of 4 micrograms/ml. The 50% antiviral effective doses obtained with mannan sulfate in Molt-4 (clone 8) cells and in MT-4 cells were 1.5 and 9.3 micrograms/ml, respectively. No toxicity for Molt-4 (clone 8) cells or MT-4 cells was observed at a concentration of 4,000 and 2,500 micrograms/ml, respectively. Mannan sulfate was also inhibitory to other enveloped viruses, i.e. herpes simplex virus types 1 and 2, vaccinia virus and vesicular stomatitis virus. These results suggest that mannan sulfate may be useful for the chemotherapy of various viral infections, including those causing and associated with AIDS.
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PMID:In vitro activity of mannan sulfate, a novel sulfated polysaccharide, against human immunodeficiency virus type 1 and other enveloped viruses. 256 84

Cell lines originally derived from malignant tumours of the brain were infected by diverse human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2) isolates. By surface immunofluorescence it was shown that susceptible cells did not bear the CD4 antigen. They were also non-permissive for the formation of plaques by vesicular stomatitis virus pseudotypes and did not form syncytia with HIV-producing cells. Virus production was of low titre, and reverse transcriptase and the p24 antigen were consistently undetectable in the culture supernatants. Output virus could be detected by cocultivation with a sensitive T cell line, C8166, by the culture of supernatant medium with T cells and by detection of proviral HIV DNA after amplification. A higher multiplicity of input virus was required to establish a brain cell infection than was required for T lymphocytes or monocytes. Some HIV-susceptible brain cells contained mRNA for CD4 but infection was not blocked by anti-CD4 antibodies. Apparently HIV infection of these cells does not involve CD4 as the cellular receptor.
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PMID:Infection of brain cells by diverse human immunodeficiency virus isolates: role of CD4 as receptor. 267 35

Serum samples from 557 individuals participating in studies from four separate lowland and highland populations in Papua New Guinea exhibited consistently false-positive results for human T lymphotropic virus (HTLV) type 1 (10%) and human immunodeficiency virus (HIV) type 1 (5%) antibody in direct antiglobulin and agglutination assays. All serum samples were negative in competitive ELISAs and radioimmunoassays for HTLV-1 and HIV-1; selected samples of reactive sera were negative in an HTLV-2 competitive ELISA. Immunofluorescent antibody tests using HTLV-1 infected cells correlated poorly with ELISA results. None of the sera from Papua New Guinea neutralized vesicular stomatitis virus pseudotypes of HTLV-1. By Western blot analysis, only three serum samples were weakly reactive to HTLV-1 gag proteins. These studies suggest there is as yet no firm evidence of HTLV-1, HTLV-2, or HIV-1 infection in Papua New Guinea, although there may be a low prevalence.
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PMID:HTLV-1 infection in Papua New Guinea: evidence for serologic false positivity. 272 52

We describe the identification, experimental transmission, and pathogenesis of a naturally occurring powerfully immunosuppressive isolate of feline leukemia virus (designated here as FeLV-FAIDS) which induces fatal acquired immunodeficiency syndrome (AIDS) in 100% (25 of 25) of persistently viremic experimentally infected specific pathogen-free (SPF) cats after predictable survival periods ranging from less than 3 months (acute immunodeficiency syndrome) to greater than one year (chronic immunodeficiency syndrome), depending on the age of the cat at time of virus exposure. The pathogenesis of FeLV-FAIDS-induced feline immunodeficiency disease is characterized by: a prodromal period of largely asymptomatic viremia; progressive weight loss, lymphoid hyperplasia associated with viral replication in lymphoid follicles, lymphoid depletion associated with extinction of viral replication in lymphoid follicles, intractable diarrhea associated with necrosis of intestinal crypt epithelium, lymphopenia, suppressed lymphocyte blastogenesis, impaired cutaneous allograft rejection, hypogammaglobulinemia, and opportunistic infections such as bacterial respiratory disease and necrotizing stomatitis. The clinical onset of immunodeficiency syndrome correlates with the replication of a specific FeLV-FAIDS viral variant, detected principally as unintegrated viral DNA, in bone marrow, lymphoid tissues, and intestine. Two of seven cats with chronic immunodeficiency disease that survived greater than 1 year after inoculation developed lymphoma affecting the marrow, intestine, spleen, and mesenteric nodes. Experimentally induced feline immunodeficiency syndrome, therefore, is a rapid and consistent in vivo model for prospective studies of the viral genetic determinants, pathogenesis, prevention, and therapy of retrovirus-induced immunodeficiency disease.
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PMID:Experimental transmission and pathogenesis of immunodeficiency syndrome in cats. 282 40

The efficacy of two heating cycles (90 sec at 103 degrees C and 10 hr at 65 degrees C) used during manufacture of a plasma-derived hepatitis-B vaccine was validated for the inactivation of 12 virus families. A period of 15 min warming up to 65 degrees C had already completely inactivated representatives of nine virus families, ie, poxvirus (vaccinia), picornavirus (encephalomyocarditis virus), togavirus (sindbis virus), coronavirus (mouse hepatitis virus), orthomyxovirus (influenza virus), rhabdovirus (vesicular stomatitis virus), herpes virus (cytomegalovirus), lentivirus (human immunodeficiency virus), and retrovirus (murine leukemia virus). After prolonged heating at 65 degrees C or heating for 90 sec at 103 degrees C, parvovirus (canine parvovirus) and the phage phiX174 were also completely inactivated. Papovavirus represented by simian virus 40 (SV-40) was the most heat-resistant virus evaluated. The infectivity of SV-40 was reduced by 10(4) Tissue Culture Infectious Doses (TCID50) per ml after 90 sec at 103 degrees C, but a marginal residual activity (less than 1.5 TCID50 per ml) was observed. Subsequent pasteurization for 10 h at 65 degrees C did not further reduce the infectivity of SV-40. This study shows that the two heat-inactivation steps used during the production of this vaccine kill a wide variety of viruses that might be present in human blood.
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PMID:Inactivation of 12 viruses by heating steps applied during manufacture of a hepatitis B vaccine. 282 25

Virus sterilization of blood plasma derivatives by addition of several naturally occurring fatty acids was evaluated using vesicular stomatitis virus and Sindbis virus as markers for lipid-enveloped virus inactivation and human immunodeficiency virus (HIV). Inactivation of greater than or equal to 10(4) tissue culture infectious doses (TCID50) of marker viruses added to antihemophilic factor (AHF) concentrates, with 60-100% retention of AHF activity, was achieved with oleic, 11-eicosenoic, linoleic, linolenic, palmitoleic and arachidonic acids. Elaidic, gamma-linolenic, palmitic, and arachidic acids and another fat-soluble compound previously reported to inactivate virus, butylated hydroxytoluene, were less effective. A long chain mono- but not a di- or triglyceride also displayed virucidal properties. Evaluation of the inactivation of HIV added to an immune globulin solution on exposure to 0.033% sodium oleate for 20 min indicated inactivation of greater than or equal to 10(3.4) TCID50. The degree of virus inactivation depended on the sample composition. A favorable balance was achieved between degree of virus inactivation and retention of protein function for AHF concentrate, prothrombin complex concentrate, antithrombin III concentrate, and immune globulin solution on incubation with 0.033% (w/v) sodium oleate at 24 degrees C for 4-6 h. Virus inactivation in whole plasma and plasma cryoprecipitate was not complete despite use of higher concentrations of sodium oleate and/or incubation at 37 degrees C. Reduced virus kill in these less purified derivatives probably is a consequence of their endogenous lipid and/or albumin.
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PMID:Inactivation of lipid-enveloped viruses in labile blood derivatives by unsaturated fatty acids. 283 69

Twenty-seven medicinal herbs reputed in ancient Chinese folklore to have anti-infective properties were extracted by boiling under reflux. The extracts were tested for inhibitory activity against the human immunodeficiency virus in the H9 cell line at concentrations nontoxic to growth of the H9 cells. Using a significant reduction (greater than 3 S. D. below the mean) in the percentage of cells positive for specific viral antigens in three successive assays as indicative of activity against the virus, 11 of the 27 extracts were found to be active. One of the extracts (Viola yedoensis) was studied in greater depth. At a subtoxic concentration, this extract shut off completely the growth of HIV in virtually all experiments. It did not inactivate HIV extracellularly, did not induce interferon and did not inhibit the growth of herpes simplex, polio or vesicular stomatitis viruses in human fibroblast culture. Chinese medicinal herbs appeared to be a rich source of potentially useful materials for the treatment of human immunodeficiency virus infection.
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PMID:Inhibition of growth of human immunodeficiency virus in vitro by crude extracts of Chinese medicinal herbs. 284 Aug 49


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