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)

Prevention of EBV-associated lymphoproliferative diseases in immune deficient individuals is preferred; however, standard therapy for the B cell lymphomas has been successful. Chemotherapy must be given cautiously lest further immune compromise result in opportunistic infections. Recently, Acyclovir has decreased morbidity of patients with acute infectious mononucleosis in immune competent persons. In contrast, immunodeficient patients with X-linked lymphoproliferative (XLP) syndrome do not seem to respond favorably. Hence, a prospective study is underway using prophylactic immunoglobulin containing (EBV)-specific antibodies. The mortality rate is 85% following EBV infection in XLP due to fatal infectious mononucleosis associated with fulminant hepatitis and virus-associated hemophagocytic syndrome, acquired hypogammaglobulinemia or malignant B cell lymphoma. We can detect XLP by noting failure of switching from IgM to IgG antibody production on secondary challenge with bacteriophage phi X174. Also, linkage studies with the XLP locus using restriction fragment length polymorphisms are being done to detect affected males pre-EBV infection. Our rationale for prevention of phenotypes of XLP is based on observations that infants in tropical Africa and males with XLP do not develop EBV-induced diseases while neutralizing maternal antibodies are present. An EBV vaccine will be used, when available, in seronegative males with XLP. Prevention of acquired immune deficiency by screening blood for human immune deficiency virus, encouraging prudent life styles, development of specific immunosuppressive agents, development of new antiviral agents (i.e., DHPG), and identification of high risk seronegative patients offer possibilities for preventing life-threatening EBV-induced diseases.
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PMID:Prevention and treatment of Epstein-Barr virus (EBV)-associated lymphoproliferative diseases in immune deficient patients. 243 95

Some generalizations can be drawn from a review of virus-associated bone marrow failure. The story of B19 parvovirus illustrates that viral infection may be an occult cause of marrow failure. Although the epidemiology of transient aplastic crisis suggested a viral aetiology, the implication of a single virus was surprising; the sporadic appearance of chronic bone marrow failure in immunosuppressed persons has had none of the features of a viral illness. The incrimination of parvovirus in these cases required development of specific immunological and molecular assays. Human and animal retrovirus studies have shown that small changes in the virus genome can have dramatic effects on the biology of the infectious agent and its pathogenicity in infected hosts. In Epstein-Barr virus infection, the host's immune response may play a more important role in mediating disease than virus cytotoxicity. Finally, the association of aplastic anaemia with hepatitis may be underestimated because of the inability to diagnose virus infection without obvious liver disease. The true spectrum of bone marrow disease due to virus infection is not known.
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PMID:Viruses and bone marrow failure. 253 67

In the last years it has been suggested that idiopathic obstructive cholangiopathy is a pathologic process with evolutive studies: extrahepatic biliary atresia and neonatal hepatitis. The possibility of a viral agent as the inciting factor has been investigated. This report shows four male and one female with confirmed idiopathic obstructive cholangiopathy with different clinical picture. There was evidence of cytomegalovirus infection in two patients, rubella infection in one patient, hepatitis B virus infection in one patient and Epstein-Barr virus infection in one patient. While other causes of neonatal cholestasis were excluded, we suggest that those viruses has an etiologic role in the initial injury and the progression of the disease.
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PMID:[Viral infection and obstructive cholangiography in children]. 271 22

Two patients with mononucleosis, one due to cytomegalovirus (CMV), and the other due to Epstein-Barr virus (EBV), presenting with high fever, malaise and hepatitis, had granulomas in the bone marrow but not in the liver. In patients who have unexplained fever, bone marrow granulomas may be a clue to CMV or EBV infection and need not initially raise the fear of prognostically more severe illness.
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PMID:Bone marrow granulomas in mononucleosis. 282 52

Hepatic fibrin-ring granulomas were the main histological finding in the liver of a 38-year-old man with Epstein-Barr virus primary infection. The patient presented with fever, hepatomegaly, icterus, abnormal liver tests, autoimmune hemolytic anemia, and mononucleosis syndrome. There was neither enanthema nor lymphadenopathy or splenomegaly. Serologic tests disclosed an Epstein-Barr primary infection profile: anti-viral capsid antigen IgM antibodies and anti-early antigen antibodies were present, whereas anti-Epstein-Barr nuclear antigen antibodies were absent. There was no evidence for Q fever, Hodgkin's disease, or allopurinol-induced hepatitis, which are recognized causes of hepatic fibrin-ring granulomas. It is suggested that Epstein-Barr virus infection might be an additional cause of these peculiar hepatic granulomas.
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PMID:Epstein-Barr virus infection and hepatic fibrin-ring granulomas. 283 98

Among the many different manifestations of Epstein-Barr virus (EBV) infection, neurologic disturbances are less frequently observed, and they are diverse in nature. A young woman was admitted with acute hyperthermia, mydriasis, nystagmus, respiratory insufficiency, muscular hypertonia, evolving to decerebrate posturing, and bilateral facial epileptic contractions. The appearance of atypical blood lymphocytes, hepatitis, migrating skin rash, positive heterophile antibody tests, and specific serologic tests for EBV led to a diagnosis of EBV encephalitis. Under treatment with intravenously administered acyclovir, the patient recuperated almost completely. This case illustrates a less frequent manifestation of EBV infection.
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PMID:Coma as a presenting sign of Epstein-Barr encephalitis. 283 58

We describe a severe multisystem Coxsackie virus type B3 infection in a previously healthy 14-year-old girl who presented with a mononucleosis-like syndrome (MS). Initial observations included a prominent cervical lymphadenopathy, exudative pharyngitis and leucocytosis with atypical lymphocytosis. At the end of the 2nd week of illness the patient developed meningoencephalomyelitis and haemolytic anaemia. Subclinical myocarditis was also recorded. Prolonged hepatitis recrudescing at the time of recovery coincided with serological evidence of a reactivated Epstein-Barr virus infection. The diagnosis was based on a significant rise in serum antibody titres against Coxsackie virus type B3, using the neutralization test. Intrathecal synthesis of antibodies to Coxsackie virus type B3 was also demonstrated. Generalized Coxsackie virus infections in adolescence are rare and an MS has not, to our knowledge, been associated with Coxsackie virus type B3 infection.
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PMID:Mononucleosis-like syndrome associated with a multisystem Coxsackie virus type B3 infection in adolescence. 284 Feb 91

Viral infections that occur in patients with primary immunodeficiencies are summarized. These viral infections include: Echovirus, poliovirus, varicella zoster, non-A non-B hepatitis and hepatitis B. Cases of X-linked lymphoproliferative syndrome associated with Epstein-Barr virus infection and congenital rubella syndrome are also reviewed. In the second part of the paper, retrovirus (HIV) isolations from blood mononuclear cells of 3 out of 31 patients with common variable hypogammaglobulinemia are reported. This supports the concept that some of the non-familial "primary" immunodeficiencies may be due to retrovirus infections.
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PMID:Viruses and antibody deficiency syndromes. 284 58

A continuous cell line of chimpanzee lymphocytes producing an antibody specifically associated with non-A, non-B hepatitis (NANB) was established. Peripheral blood lymphocytes of a chimpanzee convalescent from experimental infection with NANB hepatitis were transformed in vitro by Epstein-Barr virus infection into lymphoblastoid cell lines. Supernatants of the cell cultures were screened by immunofluorescence for antibody activity against the liver tissue of a chimpanzee with NANB hepatitis. Nineteen of the 1402 cultures were found to be positive for the activity. Ten of these 19 gave cytoplasmic reactions and the remaining 9 gave nuclear reactions in hepatocytes. One culture (48-1) stably producing the antibody was further characterized. The antibody produced in 48-1 was IgM and gave granular cytoplasmic reactions in hepatocytes. Cloning of 48-1 was performed by the soft agar method and cloned cell lines stably producing the antibody were obtained. The 48-1 antibody reacted with liver biopsy specimens from 12 chimpanzees obtained during the acute or chronic phase of hepatitis caused by five different NANB strains, but not with biopsy specimens from chimpanzees with hepatitis A or B or from normal chimpanzees. In addition, examinations of serial liver biopsy specimens obtained from 2 chimpanzees experimentally infected with NANB hepatitis demonstrated that the antibody reacted with the biopsies obtained during the preacute, acute, and chronic hepatitis, but not with those obtained before inoculation, early incubation period, or during convalescence. The present results indicate the specific association of the antibody with NANB hepatitis. Immunoelectron microscopy revealed that the antibody reacted with the microtubular aggregates identical to those previously described in a patient and chimpanzees with NANB hepatitis.
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PMID:Production of antibody associated with non-A, non-B hepatitis in a chimpanzee lymphoblastoid cell line established by in vitro transformation with Epstein-Barr virus. 298 83

Monoclonal antibody-secreting cell lines were isolated after transformation of peripheral blood leukocytes with Epstein-Barr virus. Blood samples were obtained from human donors having circulating antibodies against hepatitis viruses (HAB, HBV), rubella, or rabies virus and from a chimpanzee infected with HAV. Dextran-isolated leukocytes were submitted to Epstein-Barr virus infection at low cell concentrations (1 X 10(4) cells X ml-1). Proliferating clones could be observed in 50-100% of the cultures within 4-6 weeks. Out of 1 ml blood (1 X 10(6) leukocytes) 1-10 stable clones were isolated, secreting specific anti-viral antibodies. These clones were fused with an aminopterin-sensitive, ouabain-resistant, non-immunoglobulin producing mouse-human hybridoma (Org MHH.1). From such fusions 10-90% of the cultures yielded viable hybridomas of which 45% produced antibodies with the same specificity as of the parental EBV transformant. Immunoglobulin production of both EBV transformants and hybridomas was shown to be stable for more than 6 months and at a concentration up to 100 micrograms X ml-1 X 48 h-1. Chimpanzee EBV-transformed lymphocytes proliferated excellently in vitro. Mouse-human hybridomas, however, could be more easily cultivated, cloned and scaled up than the parental EBV-transformed lymphocytes. In conclusion, stable, monoclonal antibody-secreting cell lines of either human or chimpanzee origin could be isolated with an efficiency that exceeds by 10-100-fold standard murine hybridoma technology.
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PMID:Human and chimpanzee monoclonal antibodies. 298 74


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