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)

Porcine circoviruses (PCV) are small nonenveloped DNA viruses containing a unique single-stranded circular genome. Previously, no recognized link was found between PCV infection of pigs and disease, and PCV was considered a nonpathogenic agent. Over the last 5 years, a "novel" PCV, designated PCV2, has been associated with various disease syndromes in pigs, primarily postweaning multisystemic wasting syndrome (PMWS). Pigs with PMWS have a variety of clinical signs, including debility, dyspnea, palpable lymphadenopathy, diarrhea, and pallor or icterus. Lesions associated with the presence of PCV2 in a variety of cell types include lymphohistiocytic to granulomatous interstitial pneumonia, hepatitis, nephritis, myocarditis, enteritis, and pancreatitis. The lesions of PMWS have been reproduced experimentally after inoculation of piglets with PCV2 cell culture isolates, although the full expression of the disease syndrome may require the presence of other agents such as porcine parvovirus or porcine reproductive and respiratory syndrome (PRRS) virus. Recent reports have linked PCV2 to other disorders in pigs, ranging from abortion and reproductive failure to "atypical" PRRS. Available data indicate high seroprevalence of antibodies to PCV2 worldwide. The diagnosis of PCV2-associated disease is based on the direct demonstration of PCV2 antigens or nucleic acid in affected tissues. PCV2 is now regarded as an important emerging pathogen. Although vertical transmission has been documented, the epidemiology of PCV2 infections is poorly understood, as is the role of the immune response in controlling or augmenting disease.
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PMID:Porcine circoviruses: a review. 1069 Jul 69

The sequential tissue distribution of virus was investigated using virus isolation and immunofluorescence tests in 1-day-old piglets inoculated with porcine circovirus 2 (PCV2) and/or porcine parvovirus (PPV). Enlarged mesenteric lymph nodes were seen in the pig inoculated with PCV2 alone and killed at 26 days post-inoculation (PI). One of the pigs inoculated with PCV2 and PPV and killed at 21 days PI had an enlarged liver. The pig killed at 26 days PI in this group had enlarged liver, kidneys and heart. Histopathological changes were seen in lymphoid tissues of the pigs inoculated with PCV2 alone and killed at 14 and 26 days PI. Similar, but more severe, lesions were observed in the pigs infected with PCV2 and PPV and killed from 10 days PI onwards. Histological lesions of nephritis, pneumonia and hepatitis were also apparent in these animals. Mild nephritis was also seen in the pigs infected with PPV alone and killed at 14 and 26 days PI. Moderate amounts of PPV antigen were detected in tissues from the pigs inoculated with PPV alone and killed at 14 days PI. Low levels of PCV antigen were detected, mainly in lymphoid tissues, in the pigs inoculated with PCV alone and killed at 14 days PI. Low to moderate amounts of PCV antigen were detected in a wider range of tissues in the pig in this group killed at 26 days PI. In the pigs inoculated with both viruses, PPV antigen was detected in tissues of pigs killed from 3 to 26 days PI with maximal amounts detected between 6 and 14 days PI. PCV2 antigen was detected in low to moderate amounts in the tissues of pigs killed at 14 days PI. Large amounts of PCV2 antigen were detected in most of the tissues from pigs in this group killed between 17 and 26 days PI. Virus isolation results for PCV2 generally correlated well with the results for immunofluorescent staining. PPV was isolated from almost all tissues from pigs inoculated with PCV2 and PPV, a much higher incidence of positive tissues than observed for immunofluorescent staining.
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PMID:A sequential study of experimental infection of pigs with porcine circovirus and porcine parvovirus: immunostaining of cryostat sections and virus isolation. 1076 76

TTV is a new virus which was identified in the serum of a patient with non-A-G post-transfusion hepatitis in Japan. The original workers aimed to account for the small number of post transfusion hepatitis cases found in their clinical practice. Subsequent work has attempted to determine the properties and unravel the natural history of the new agent. The original study applied representational difference analysis to detect foreign DNA sequences which were present only during the acute phase of illness. Subsequent studies have used PCR to study the agent in serum liver and faeces. This review summarises the published data from clinical and epidemiological studies in different countries. The inclusion of the virus in the parvovirus family seems premature because its size is unknown, its reported density is too light and its sequence lacks the characteristic long terminal repeats. The agent can be found in 1-40% of health blood donors in different countries and also in faeces. TTV is ubiquitous but its taxonomic identity and disease load remain to be determined.
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PMID:TTV - a virus searching for a disease. 1081 32

The purpose of our study was to confirm reports of an association of human papillomavirus (HPV) with neonatal giant cell hepatitis (GCH) and biliary atresia (BA), and to expand these studies to include cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesvirus 6 (HHV6), and parvovirus B19 (PVB19). Frozen hepatic tissue was available for polymerase chain reaction (PCR) analysis in 19 cases of GCH or BA and 8 controls. Nested PCR to detect HPV types 6, 16, 18, and 33 was followed by 32P hybridization with generic probes. PCR followed by hybridization with a digoxigenin-labeled probe was used for all other viruses. HPV, EBV, and PVB19 were not detected in cases or controls. Two cases of GCH and 1 case of BA were PCR positive for CMV; controls were negative. HHV6 was detected in 6 cases: 2 GCH, 2 BA, and 2 controls. We conclude that HPV is not associated with GCH or BA. Detection of CMV in BA and GCH confirms other reports of this association. HHV6 requires further study to determine the significance of a positive PCR test in the livers of infants.
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PMID:Cytomegalovirus and human herpesvirus 6, but not human papillomavirus, are present in neonatal giant cell hepatitis and extrahepatic biliary atresia. 1089 Feb 52

Human parvovirus B19 is common and widespread. Major manifestations of B19 infection are transient aplastic crisis, erythema infectiosum, hydrops fetalis, acute and chronic rheumatoid-like arthropathy and, in the immunocompromised host, chronic or recurrent bone marrow infection. Less common presentations include skin eruptions, isolated cytopenias, vasculitis, hepatitis, and neuropathies. Increasing awareness of the clinical manifestations of B19 infection makes parvovirus B19 an emerging virus. B19 may persist in healthy or immunocompromised individuals. B19 has been suggested as a candidate agent in rheumatic diseases.
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PMID:Infection with Parvovirus B19. 1109 99

Viral infection has been shown to induce aplastic anemia, unidentified types of hepatitis being the most common cause for aplastic anemia-associated viral hepatitis. The survival rate for this group of patients after bone marrow transplantation with stem cells from an HLA-matched sibling is not well known. The aim of this study was to determine the prevalence of hepatitis G virus (HGV) and transfusion transmitted virus (TTV) infection in non-A, non-B, non-C hepatitis associated-aplastic anemia (HAAA) patients, and to define the role of bone marrow transplantation (BMT) as a therapeutic modality for this disease. Sixty-eight patients (43 males and 25 females) with aplastic anemia, underwent allogeneic BMT at the Hadassah University Hospital between 1981 and 1997. Onset of hepatitis was defined as jaundice and elevated alanine aminotransaminase (ALT) levels. Onset of aplastic anemia was defined as the first date on which varying degrees of pancytopenia occurred: hemoglobin level below 10 g/dl, WBC below 2 x 10(9)/l and low platelet count 10 x 10(10)/l. Serial serum samples from HAAA patients were assayed for virological and/or serological markers of hepatitis A, B, C, D, E, G viruses, TTV and parvovirus B19. Seventeen of the 68 patients with aplastic anemia (25%) suffered from hepatitis, 12 males and five females, ages 5 to 36 years. The mean interval between onset of hepatitis and first indication of aplastic anemia was 62 days (range 14-225 days). The development of aplastic anemia was unrelated to age, sex or severity of hepatitis. Ten of the 17 patients (59%) achieved complete ALT recovery prior to the diagnosis of aplastic anemia. Serum samples were available for 15 patients; none had evidence of acute or active hepatitis A, B, C, D, E, G and TTV virus infection at the time of diagnosis. Parvovirus B19 DNA sequences were not detectable in 10 of 12 tested cases; two positive results were detected in serum samples obtained after blood transfusion, making the analysis of these positive results difficult. All 17 patients underwent BMT. The mean post-BMT follow-up period was 38 months (range 1 day-123 months), five patients (30%) died 1 to 160 days post BMT, and 12 (70%) are alive 31 to 123 months after BMT. Relapsing hepatitis was not observed in any of the patients. In conclusion, HAAA is a disease of the young and the etiologic agent associated with HAAA remains unknown. HGV, TTV and parvovirus B19 sequences were not detected in any of the HAAA cases. The survival rate after BMT with stem cells from an HLA-matched sibling is similar to that for patients with non-hepatitis-associated aplastic anemia.
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PMID:Lack of known hepatitis virus in hepatitis-associated aplastic anemia and outcome after bone marrow transplantation. 1128 88

Syncytial giant cell hepatitis in the neonatal period has been associated with many different etiologic agents and may present initially as cholestasis. Infectious causes are most common and include: (1 ) generalized bacterial sepsis, (2) viral agents, (3) toxoplasmosis, (4) syphilis, (5) listeriosis, and (6) tuberculosis. Viral hepatitis may be due to cytomegalovirus, rubella virus, herpes simplex, HHV-6, varicella, coxsackievirus, echovirus, reovirus 3, parvovirus B19, HIV, enteroviruses, paramyxovirus, and hepatitis A, B, or C (rare). Giant cell hepatitis may result in fulminant liver failure with massive hepatocyte necrosis and severe liver dysfunction leading to death, resolution with severely compromised liver function, or liver transplantation. The authors report a 6-week-old male who had an unremarkable perinatal period, became jaundiced after developing diarrhea, and subsequently developed liver dysfunction with massively increased liver enzymes and a coagulopathy. Open wedge and core liver biopsies were performed to determine if the patient should be listed for liver transplantation. Giant cell hepatitis with a significant mixed lymphocytic and neutrophilic infiltrate was present on both the wedge and core biopsies. The residual 60% of hepatocytes had ballooning degeneration and many possessed pyknotic nuclei. The hepatocytes were arranged in a pseudoacinar pattern. Electron microscopy showed paramyxoviral-like inclusions in the giant cells, characterized as large inclusions with fine filamentous, beaded substructures (18-20 nm). Paramyxoviridae are nonsegmented, negative-sense, single-stranded RNA viruses. This family is divided into the Paramyxovirinae subfamily containing respirovirus (Sendai virus, parainfluenza virus type 3), rubulavirus (mumps, parainfluenza virus type 2), and morbillivirus genera (measles); and Pneumovirinae subfamily (pneumovirus genus [respiratory syncytial virus]). Supportive care to determine if hepatic function resolves following the viral episode, liver transplantation with fulminant liver failure, and ongoing evaluation in those who recover to assess chronic liver disease are necessary. Ultrastructural evaluation may unmask the etiologic agent for hepatitis and direct therapy.
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PMID:Neonatal syncytial giant cell hepatitis with paramyxoviral-like inclusions. 1129 22

The health of coyotes (Canis latrans) in urban areas has not been studied. Our objectives were to assess the health of coyotes in Tucson (Arizona, USA) by determining the prevalence of antibodies to selected pathogens, estimating survival rates, and identifying sources of mortality. We drew blood from 22 coyotes to evaluate the prevalence of heartworm (Dirofilaria immitis) antigens, and antibodies to canine distemper virus (CDV), infectious canine hepatitis (ICH), canine parvovirus (CPV), and seven serovars of Leptospira interrogans. We trapped and radiocollared 19 coyotes to determine survival rates. We performed necropsies on 19 coyotes to quantify their general health, the presence of internal and external parasites, and causes of mortality. No coyotes tested positive for heartworm antigens. The prevalence of antibody to CDV, ICH, and CPV was 27, 50, and 100%, respectively. Twenty-seven percent of coyotes tested positive for one of five serovars of L. interrogans. The diseases for which coyotes in Tucson possessed antibodies appear to be enzootic in the population. The annual survival rate of coyotes was 0.72. Eleven necropsied coyotes were killed by cars, five coyotes were hit by cars, two were killed by a trapper, and the cause of death for one coyote was unknown. Coyotes in Tucson appear to be exposed to the viral, bacterial, and parasitic infections common in many coyote populations, but humans are the major source of mortality.
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PMID:Morbidity-mortality factors and survival of an urban coyote population in Arizona. 1131 Aug 82

Parvovirus B19 has been associated by some investigators with cases of severe hepatitis. The aim of the present study was to determine the presence of active parvovirus B19 infection among 129 Brazilian patients with non-A-E hepatitis. The patients were assayed for antibodies against parvovirus B19, IgM class, by ELISA. In IgM-positive cases, parvovirus B19 DNA was assayed by PCR in serum and liver tissue and parvovirus VP1 antigen in liver tissue was assayed by immunohistochemistry. Antibodies against parvovirus B19, IgM class, were detected in 3 (2.3%) of 129 patients with non-A-E hepatitis. Previous surgery and blood transfusions were reported by these 3 patients. One patient was a 56-year-old female with severe hepatitis, with antimitochondrial antibody seropositivity and submassive necrosis at liver biopsy, who responded to corticosteroid therapy. Strong evidence for active parvovirus B19 infection was found in this patient, with parvovirus B19 DNA being detected by PCR in liver tissue. Furthermore, parvovirus VP1 antigen was also detected in liver tissue by immunohistochemistry. The other two IgM-positive patients were chronic hepatitis cases, but active infection was not proven, since neither viral DNA nor antigen were detected in their liver tissues. This and other reports suggest a possible relation between parvovirus B19 infection and some cases of hepatitis.
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PMID:Detection of human parvovirus B19 in a patient with hepatitis. 1151 36

Three-week-old cesarean-derived colostrum-deprived (CD/CD) pigs were inoculated with porcine circovirus type 2 (PCV2, n = 19), porcine reproductive and respiratory syndrome virus (PRRSV, n = 13), concurrent PCV2 and PRRSV (PCV2/PRRSV, n = 17), or a sham inoculum (n = 12) to compare the independent and combined effects of these agents. Necropsies were performed at 7, 10, 14, 21, 35, and 49 days postinoculation (dpi) or when pigs became moribund. By 10 dpi, PCV2/PRRSV-inoculated pigs had severe dyspnea, lethargy, and occasional icterus; after 10 dpi, mortality in this group was 10/11 (91%), and all PCV2/ PRRSV-inoculated pigs were dead by 20 dpi. PCV2-inoculated pigs developed lethargy and sporadic icterus, and 8/19 (42%) developed exudative epidermitis; mortality was 5/19 (26%). PRRSV-inoculated pigs developed dyspnea and mild lethargy that resolved by 28 dpi. Microscopic lesions consistent with postweaning multisystemic wasting syndrome (PMWS) were present in both PCV2- and PCV2/PRRSV-inoculated pigs and included lymphoid depletion, necrotizing hepatitis, mild necrotizing bronchiolitis, and infiltrates of macrophages that occasionally contained basophilic intracytoplasmic inclusion bodies in lymphoid and other tissues. PCV2/ PRRSV-inoculated pigs also had severe proliferative interstitial pneumonia and more consistent hepatic lesions. The most severe lesions contained the greatest number of PCV2 antigen-containing cells. PRRSV-inoculated pigs had moderate proliferative interstitial pneumonia but did not develop bronchiolar or hepatic lesions or lymphoid depletion. All groups remained seronegative to porcine parvovirus. The results indicate that 1) PCV2 coinfection increases the severity of PRRSV-induced interstitial pneumonia in CD/CD pigs and 2) PCV2 but not PRRSV induces the lymphoid depletion, granulomatous inflammation, and necrotizing hepatitis characteristic of PMWS.
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PMID:Experimental reproduction of severe disease in CD/CD pigs concurrently infected with type 2 porcine circovirus and porcine reproductive and respiratory syndrome virus. 1157 60


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