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)

The discovery of persistent transmissible agents by veterinarians has led to striking advances in the infectious cause of neuropathies of human beings. There is evidence for persisting infection in congenital rubella and the herpes group of viruses including cytomegalovirus infections. Hepatitis types A and B are candidates for inclusion in the category of persisting viral infections. The rubeola or measles virus is established as a persistent virus which causes elevated antibodies in the serum and cerebrospinal fluid of many patients with severe demyelinating disease such as subacute sclerosing panencephalitis and multiple sclerosis. Elevated antibodies against vaccinia virus have been found in the cerebrospinal fluid of some patients with multiple sclerosis and neuromyelitis optica, a rare form of multiple sclerosis.
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PMID:Persistent or slow viral infections and related diseases. 16 38

Several animal and human demyelinating diseases of the central nervous system (CNS) are associated with RNA or DNA viruses. These viruses infect CNS cells lytically or persistently. They mainly belong to the group of envelope viruses which derive their envelope partly from the host cell membrane. The process of virus release may result in the appearance of new antigens of virus-infected cells or the incorporation of cell membrane material into the viral envelope. These changes may lead to an immune response which selectively injures the CNS. These alterations of host cell membranes and host cell functions, together with the immune mechanism, are central to many of the hypotheses regarding virus-induced demyelination. The role of virus infection in progressive multifocal leukoencephalopathy, subacute sclerosing panencephalitis, visna and mouse hepatitis virus infections, is discussed in relation to the demyelinating process of these diseases.
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PMID:Virus infection in demyelinating diseases. 21 25

Methisoprinol (Isoprinosine), a purine derivative, has been shown to exert a number of immunopharmacological effects, both in vitro and in vivo, in animal and human studies. The agent, somehow mimicking the effects of thymic factors, induces the appearance of phenotypic markers of differentiation on immature precursor T cells; enhances the proliferative response of murine and human lymphocytes to mitogens or antigens, augments helper or suppressor T cell functions and increases the production of lymphotoxin a lymphokine. It has also been shown that this drug can potentiate the effects of macrophage activating factor to stimulate macrophage, and of interferon to protect mice against experimental viral and tumor challenges. In humans, beneficial results have been reported from clinical trials testing the effects of methisoprinol in a variety of diseases including subacute sclerosing panencephalitis (SSPE), acute viral encephalitis, recurrent mucocutaneous infections due to type I and II Herpes viruses as well as in immune restoration of cancer patients with immunodepression following radiotherapy. The drug is also being studied in immunopathological disorders such as rheumatoid arthritis, systemic lupus erythematosus. Sjogren's disease and type A hepatitis. The large spectrum of effects of methisoprinol on a number of immune parameters, the increasing evidence of its therapeutic value in several pathological conditions and its safety of use qualifies this drug as an interesting immunoregulating agent.
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PMID:A recent overview on in vitro and in vivo immunological activities of methisoprinol. 617 7

The review reflects the concerns of researchers of the "Stefan S. Nicolau" Institute of Virology who used electron microscopy techniques with a view to visualizing morphological features of virus structure (influenza, adeno, hepatitis, herpes, cytomegalic, Aujeszky, rabies viruses, etc.) and different aspects of the virus - host cell relationships (Sendai virus/Hep2 cells, influenza and adenovirus/mouse lung, subacute sclerosing panencephalitis/human brain or cell cultures, Coxsackie and foot-and-mouth disease virus/myofibrils, Rubarth hepatitis virus/chick embryo liver cells, a.o.). Morphological aspects of normal or tumoral cells and the influence of chemical agents (actinomycin D, EDTA), viruses, bacteria or parasites have also been studied. Mention is made of several original techniques used to obtain electron microscopy preparations.
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PMID:Contribution of the "Stefan S. Nicolau" Institute of Virology to the electron microscopic study of viruses. 639 66

Two different subpopulations of IgG antibodies to nucleic acids may be demonstrated: (1) IgG directed against single-stranded (ss) nucleic acids: they are found in normal human serum and increased in sera in subacute sclerosing panencephalities, multiple sclerosis and in other neurological diseases. Absent from normal cerebrospinal fluid, they can be synthetized inside the central nervous system during these diseases. Their only common antigenic determinant seems to be the polymeric single-stranded structure. No correlation can be demonstrated between their increase in sera and their local synthesis (inside the central nervous system) and between these data and the clinical stage. These facts suggest a "non-specific" reaction and not a pathogenic mechanism. (2) IgG antibodies directed against double-stranded (ds) nucleic acids: they were detected in cerebrospinal fluid during 3 neurological diseases only, all of proved viral etiology: subacute sclerosing panencephalitis, herpes meningoencephalitis and B hepatitis polyradiculoneuritis. These antibodies are also synthetized inside the central nervous system, and are distinct from antibodies to ss nucleic acids. The mechanism of production and the signification of these antibodies remains unknown, and their scarcity in MS patients must be stressed.
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PMID:Serum and cerebrospinal fluid antibodies to single-stranded and double-stranded nucleic acids in neurological diseases. 711 9

A number of viruses can initiate central nervous system (CNS) diseases that include demyelination as a major feature of neuropathology. In humans, the most prominent demyelinating diseases are progressive multifocal leukoencephalopathy, caused by JC papovirus destruction of oligodendrocytes, and subacute sclerosing panencephalitis, an invariably fatal childhood disease caused by persistent measles virus. The most common neurological disease of young adults in the developed world, multiple sclerosis, is also characterized by lesions of inflammatory demyelination; however, the etiology of this disease remains an enigma. A viral etiology is possible, because most demyelinating diseases of known etiology in both man and animals are viral. Understanding of the pathogenesis of virus-induced demyelination derives for the most part from the study of animal models. Studies with neurotropic strains of mouse hepatitis virus, Theiler's virus, and Semliki Forest virus have been at the forefront of this research. These models demonstrate how viruses enter the brain, spread, persist, and interact with immune responses. Common features are an ability to infect and persist in glial cells, generation of predominantly CD8(+) responses, which control and clear the early phase of virus replication but which fail to eradicate the infection, and lesions of inflammatory demyelination. In most cases demyelination is to a limited extent the result of direct virus destruction of oligodendrocytes, but for the most part is the consequence of immune and inflammatory responses. These models illustrate the roles of age and genetic susceptibility and establish the concept that persistent CNS infection can lead to the generation of CNS autoimmune responses.
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PMID:Virus demyelination. 1270 46