Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heat treatment at 60 degrees C for 10 h in solution (pasteurization) was introduced into the manufacturing process of antihemophilic cryoprecipitate (AHC) and factor VIII concentrates (F VIII) to reduce the risk of transmission of hepatitis to hemophiliacs. Since the acquired immunodeficiency syndrome (AIDS) may also be transmitted to hemophiliacs by antihemophilic plasma protein preparations, we have investigated inactivation of the AIDS virus HTLV III by pasteurization in AHC or F VIII and included in this study cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus (HSV), poliovirus and vaccinia virus. Each of these viruses was efficiently inactivated by pasteurization although considerable differences were observed between the different viruses HTLV III was rapidly inactivated, becoming nondetectable within 30-60 min. Our findings indicate that pasteurized AHC or F VIII should have a high margin of safety regarding the transmission of AIDS or any other infectious disease caused by viruses such as those tested.
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PMID:Inactivation of the AIDS-causing retrovirus and other human viruses in antihemophilic plasma protein preparations by pasteurization. 301 43

A model for monitoring the accumulation of natural killer cell/large granular lymphocytes (NK/LGL) at a site of virus replication was studied by using mice infected i.p. with either lymphocytic choriomeningitis virus (LCMV), murine cytomegalovirus (MCMV), mouse hepatitis virus (MHV), Pichinde virus, or vaccinia virus. An i.p. but not i.v. infection resulted in a localized increase in NK/LGL cell number (a fourfold to greater than 20-fold increase) and augmentation (a 10- to 20-fold increase) of NK cell activity associated with virus-induced peritoneal exudate cell (PEC) populations. An increase in NK/LGL cell number was detected as early as 12 hr postinfection (p.i.) and peaked at 3 days p.i. with MHV. The initial LGL recruited into the peritoneal cavity at 1 to 3 days p.i. were nonadherent to plastic and were demonstrated to have an NK cell phenotype: asialo GM1+, Thy-1.2 +/-, Lyt-2.2-, and J11d-. The peak number of LGL appeared at 7 days after infection with the NK cell-resistant virus, LCMV. This LGL population had been previously demonstrated to contain cytotoxic T lymphocyte/LGL (CTL/LGL) as well as NK/LGL. During an MHV infection the number of LGL decreased between days 3 and 7 p.i., suggesting that the second wave of CTL/LGL was absent. These findings may explain the absence of a good MHV-CTL model. Virus-induced, activated NK/LGL responded to chemotactic signals by migrating in a unidirectional manner across two 5-microns pore size polycarbonate filters during 7 hr in vitro chemotaxis assays. Wash-out fluid obtained from the peritoneal cavity contained chemotactic activity for NK/LGL as well as for other cell types. We conclude that production and/or release of chemotactic factors at sites of virus replication are at least partially responsible for the accumulation of NK/LGL at these sites.
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PMID:Accumulation and chemotaxis of natural killer/large granular lymphocytes at sites of virus replication. 302 67

The pathogenesis of mousepox due to infection with ectromelia virus strain NIH-79 was characterized in genetically susceptible (BALB/cAnNCr) and genetically resistant (C57BL/6NCr) mice. BALB/c mice inoculated subcutaneous (s.c.) or intranasally (i.n.) had high mortality. Most mice died within 7 days from severe necrosis of the spleen and liver. Necrotic foci in livers of BALB/c mice that survived beyond 7 days often were accompanied by mononuclear cell infiltrates and by hyperplasia of lymphoid tissues. C57BL/6 mice inoculated by either route remained asymptomatic and necrotic lesions were mild or absent, whereas focal non-suppurative hepatitis and lymphoid hyperplasia were prominent. Infectious virus and viral antigen were distributed widely in tissues of BALB/c mice, but had limited distribution in C57BL/6 mice. Both mouse strains had infection of the respiratory tract, genital tract, oral tissues and bone marrow, and BALB/c mice also had infection of the intestines. Both strains also developed serum antibody to vaccinia virus antigen after infection. The results show that ectromelia virus occurs in tissues conducive to mouse to mouse transmission and that the severity and character of mousepox lesions correlate directly with resistance and susceptibility to infection. They also support the concept that cellular immunity contributes to survival from infection.
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PMID:Mousepox in inbred mice innately resistant or susceptible to lethal infection with ectromelia virus. II. Pathogenesis. 303 74

A considerable amount of information has accumulated during the past 10 years in the search for antiviral agents. Ribavirin and inosiplex are 2 interesting developments to come out of this search. Ribavirin, a synthetic nucleoside, has an unusually wide spectrum of antiviral activity, especially when tested in vitro. A large number of RNA and DNA viruses are sensitive, especially herpes viruses, poxvirus, influenza, parainfluenza, reovirus, togavirus, and RNA tumour viruses. The in vivo antiviral spectrum of activity is much narrower, with activity against herpes virus, influenza, parainfluenza, measles and adenoviruses. However, controlled clinical trials have not been uniformly successful in treating influenza, hepatitis, herpes simplex and herpes zoster. Inosiplex has been shown to have antiviral activity in vivo against influenza, herpes simplex, rhinovirus and vaccinia virus infections. However, antiviral activity has not been consistently demonstrated, and this observation led to further studies which revealed its immunomodulating effects. The accumulated evidence has indicated that inosiplex is more a prohost agent rather than an antiviral drug. Immune functions which are depressed during viral infection can be restored to normal by inosiplex therapy. At present, neither ribavirin nor inosiplex alone has been shown to be uniformly successful in the treatment of human viral diseases. Nevertheless, their potential place in chemotherapy should not be neglected, although further data are needed to determine what this place will be. Whether combining them with other antiviral agents such as interferon, acyclovir, Ara-A, and so on, would produce a potentiation of action and improved antiviral chemotherapy, will be an interesting area for further study.
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PMID:Ribavirin and inosiplex: a review of their present status in viral diseases. 616 18

Young BALB/c mice inoculated intraperitoneally with herpes simplex virus type 2 develop focal necrotizing hepatitis. After infection, the livers of these mice show increasing virus titers, which reach a maximum on day 3 after infection; this is followed by a dramatic decrease in the amount of virus recovered on days 4 and 5. This decrease in virus content is accompanied by a progressive infiltration of the lesions with mononuclear leukocytes and an apparent resolution of the lesions. Adoptive transfer of immune spleen cells from mice infected 6 days earlier accelerated this process. When 50 x 10(6) to 100 x 10(6) immune spleen cells were transferred 24 h after infection, the inflammatory response and the clearance of virus from the livers were advanced by almost 2 days. As few as 12 x 10(6) immune spleen cells accelerated the healing process, whereas fewer immune cells, disrupted immune cells, or normal spleen cells did not have an effect. The protection conferred by herpes simplex virus type 2-sensitized immune spleen cells was specific since mouse cytomegalovirus- or vaccinia virus-sensitized immune spleen cells had no effect on the course of infection with herpes simplex virus type 2, whereas some cross-reactivity was observed between herpes simplex virus types 1 and 2. This model seems to be suitable for examining the immunological mechanisms that are active during recovery from visceral herpes simplex virus infections.
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PMID:Recovery of mice from herpes simplex virus type 2 hepatitis: adoptive transfer of recovery with immune spleen cells. 626 98

An epizootic of mousepox in two colonies of mice was described. Clinical signs, morbidity and mortality rates, and necropsy lesions were substantially influenced by husbandry practices, intercurrent diseases (Sendai pneumonia, mouse hepatitis virus), and total body x-irradiation. In one colony, 54 mice were necropsied; 19 mice had cutaneous or visceral lesions of mousepox although none had combined visceral and cutaneous lesions. In the other colony, 20 mice were necropsied, and 10 mice had cutaneous lesions; none had visceral lesions. Sera from 24 mice with the cutaneous form of the disease had no demonstrable HI antibody titer. Experimental mice injected with spleen/liver homogenates from infected colony mice developed typical visceral lesions with numerous poxvirus profiles on electron micrographs and positive HI titers. Mice immunized with vaccinia virus were not susceptible to the disease.
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PMID:Clinical, pathologic, and serologic features of an epizootic of mousepox in Minnesota. 628 60

The role of natural killer (NK) cells in the natural resistance of mice to infections by several viruses was examined. Mice were specifically depleted of NK cells by i.v. injection of rabbit antiserum to asialo GM1, a neutral glycosphingolipid present at high concentrations on the surface of NK cells. Control mice were left untreated or were injected with normal rabbit serum. Four to 6 hr later, these mice were infected with lymphocytic choriomeningitis virus (LCMV), mouse hepatitis virus (MHV), murine cytomegalovirus (MCMV), or vaccinia virus. The mice were sacrificed 3 days post-infection and assayed for virus in liver and spleen, spleen NK cell activity, and plasma interferon (IFN). All mice treated with anti-asialo GM1 antibody had drastically reduced NK cell-mediated lysis. Correlating with NK cell depletion, these mice had significantly higher (up to 500-fold) titers of MCMV, MHV, or vaccinia virus in their livers and spleens as compared to control mice. NK cell-depleted MCMV and MHV-infected mice had higher levels of plasma IFN than controls, correlating with the higher virus titers. These NK cell-depleted, virus-infected mice had more extensive hepatitis, assayed by the number of inflammatory foci in their livers, as compared to control virus-infected mice; these foci were also larger and contained more degenerating liver cells than those in control mice. In contrast to the results obtained with MHV, MCMV, and vaccinia virus, NK cell depletion had no effect on virus titers in the early stages of acute LCMV infection or during persistent LCMV infection. Mice depleted of NK cells had similar amounts of LCMV in their spleens and similar plasma IFN levels. Because this antibody to asialo GM1 does not impair other detectable immunologic mechanisms, these data support the hypothesis that NK cells act as a natural resistance mechanism to a number of virus infections, but suggest that their relative importance may vary from virus to virus.
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PMID:Natural killer cell depletion enhances virus synthesis and virus-induced hepatitis in vivo. 630 65

Hepatitis B virus (HBV) is an important human pathogen responsible for over 200 million cases of chronic infection, many of which progress to hepatocellular carcinoma. Although HBV cannot be propagated in tissue culture, highly effective subunit vaccines obtained from the plasma of chronically infected patients have been developed and licensed. Such vaccines are safe but their expense and limited quantities make them unavailable to most Third World countries. Other approaches to vaccine construction, including purification of the HBV surface antigen (HBsAg) from genetically engineered eukaryotic cells and the synthesis of peptides predicted from the nucleotide sequence of the HBsAg gene, are still under evaluation. Another potential application of recombinant DNA technology to vaccine development is the use of live virus vectors to express foreign genes. An infectious vaccinia virus recombinant that expressed the HBsAg in animal cells and which stimulated the production of antibody to HBsAg (anti-HBs) in rabbits represented a novel candidate vaccine of this class. As a continuation of our earlier study, we now present evidence that chimpanzees vaccinated with a live recombinant vaccinia virus protected against hepatitis following challenge with HBV.
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PMID:Live recombinant vaccinia virus protects chimpanzees against hepatitis B. 647 64

The use of a pasteurization step (heating in solution to 60 degrees C for 10 h) makes it possible to inactivate viruses, thus increasing the safety of the preparations. Using Factor XIII concentrate solution, it can be shown that hepatitis B virus and 10 other virus species are inactivated. Pasteurized Factor XIII was produced from starting material containing a total of 10(5.7) CID50 hepatitis-B virus (10(3.5) CID50/ml; CID = chimpanzee infectious dose). This Factor XIII preparation was injected in 4 chimpanzees; they remained healthy over an observation period of 37 weeks, whereas the 2 chimpanzees that received nonheated starting material developed hepatitis B. Furthermore, Rous-sarcoma, Epstein-Barr, cytomegalo, herpes simplex, measles, and rubella virus added to Factor XIII solution are inactivated by pasteurization within 2 h, mumps virus within 8 h, and adeno, polio, and vaccinia virus within 10 h. Pasteurizing of clotting factor preparations during the manufacturing process is a suitable for inactivating viruses and thereby increasing the safety of the preparations.
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PMID:[Inactivation of viruses in Factor XIII concentrate by pasteurization]. 654 27

The protection of mice against experimental infections with three different viruses (herpes simplex, vaccinia and mouse hepatitis) by Propionibacterium granulosum strain KP-45 and isolated cell walls was investigated. Pretreatment of NMRI mice with P. granulosum strain KP-45 3-7 days prior to HSV intranasal infection resulted in lowering of mortality rate (herpes encephalitis) from about 95% in controls to 15-30%. Pretreatment of NMRI mice prior to vaccinia virus infection also caused a significant decrease of the number of specific tail lesions. Infection of BALB/c mice with mouse hepatitis virus type 3 (MHV-3) resulted in development of acute infection with lethality in 4-6 days, while in fairly resistant C3H mice chronic infection manifested by loss of weight, uncoordination followed by paralysis and death in few months was observed. Pretreatment of BALB/c mice 3-7 days prior to MHV-3 infection lowered the mortality rate to about 25-30% while no effect was observed in animals injected with P. granulosum KP-45 on the day of virus inoculation. In chronic MHV-3 infections treatment with P. granulosum KP-45 was started 2 weeks after virus inoculation and was continued every 10 days. This resulted in a significant lowering of the number of paralysed mice and in a decrease of the mortality rate. Titre of MHV-3 recovered from livers of infected mice 4 months after virus inoculation was also significantly lower in animals treated with P. granulosum KP-45 or isolated cell walls.
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PMID:Protection and therapy of mice with acute and chronic experimental virus infections with propionibacterium granulosum kp-45. 722 26


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