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)

Surveillance of the staff and patients at the Cambridge Transplant and Dialysis Unit for hepatitis-B infection since 1968 has revealed the onset of antigenaemia in 6 patients in eight years. When the first serum of each patient admitted was examined for anti-HBc antibody, 23 of 380 (6-1%) patients were found positive. Since the presence of anti-HBc is taken to be evidence of previous infection, the occurence of antigenaemia in 3 of the positives when they were immunosuppressed after transplantation is believed to be due to reactivation of latent infection. This is a new factor to be considered in the control of hepatitis B after transplantation;
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PMID:Reactivation of hepatitis b after transplantation operations. 6 56

Liver dysfunction was observed in 33% of patients treated by hemodialysis and kidney transplantation. Fifty-eight percent of these cases of hepatitis occurred in patients with past or present HBs antigenemia, and 77% of HBsAg-positive patients showed evidence of LD. However, during the course of a program conducted from 1969 to 1976 and involving 267 patients, the decrease in the prevalence of HBs antigenemia observed during the last two years did not lead to any reduction in LD incidence. In a small number of patients, potentially hepatotoxic drugs could be incriminated, but in our experience azathioprine never appeared to be involved. In a few patients, LD was due to granulomatous disease of the liver, such as tuberculosis and schistosomiasis. Twenty-one (7%) of the 267 patients at risk developed chronic hepatitis, which contributed to death in nine patients. In 12 cases (three deaths), this form of hepatitis occurred in HBsAg-positive patients, and in nine cases (six deaths), in HBsAg-negative patients. In three of these latter individuals, cytomegalovirus could be incriminated. Routine monthly screening for CMV in kidney recipients confirmed the high incidence of this viral infection in such patients. Studies on murine CMV infection have demonstrated that this infection can be enhanced by histoincompatible graft or by cyclophosphamide in a model that is very close to the kidney recipient. As in mice, CMV infection in kidney recipients apparently results from reactivation of a latent infection. It seems to play a major role in the LD observed and could apparently lead to chronic hepatitis and even to cirrhosis of the liver. Finally, the occurrence of LD in HBsAg-, anti-HBs- and antiCMV-negative patients would suggest the responsibility of other viruses for the pathogenesis of liver disease in patients treated by hemodialysis and kidney transplantation. Besides Epstein-Barr virus, other viruses, such as hepatitis C virus, should be thoroughly scrutinized.
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PMID:Liver disease in patients undergoing hemodialysis and kidney transplantation. 11 44

Viral infections and clinical complications were studied during hemodialysis and after renal transplantation. Active cytomegalovirus infection developed in 96% of patients after renal transplantation; reactivation of herpes simplex, varicella-zoster, and Epstein-Barr viruses was found in 35%, 24%, and 0% of patients, respectively. Cytomegalovirus viremia developed in 42% of patients an average of two months after renal transplantation, lasted 1.75 (+/- 1.5) months (except in one patient with chronic viremia), and was followed by chronic viruria. Higher titers of infectious cytomegalovirus were found in the polymorphonuclear than in the mononuclear leukocyte fraction. Reactivation of a latent infection and, less likely, respiratory infection appear to be the most probable mechanisms of cytomegalovirus infection after renal transplantation. One to three months after transplant, cytomegalovirus infection may be related to fever, arthralgia, pneumonitis, and leukopenia; three to four months after transplant, the virus may be related to hepatitis; and 12-30 months after transplant, it may be related to retinitis in patients with chronic viremia. Although other causes of these complications are possible, herpes simplex virus, Epstein-Barr virus, varicella-zoster virus, measles virus, adenovirus, hepatitis B virus, and Toxoplasma gondii appear to be of lesser importance than cytomegalovirus in this respect.
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PMID:Epidemiology of cytomegalovirus infection after transplantation and immunosuppression. 17 15

Cytomegalovirus infections are common throughout the world. Certain populations, including pregnant women and their fetuses, immunosuppressed patients, and recipients of large amounts of transfused blood, are at increased risk. Although the majority of infections in all groups of patients are clinically inapparent, variable symptoms, including fever, rash, pneumonitis, and hepatitis, can occur. The infected host develops antibodies against CMF, but frequently, despite this appropriate immune response, infection becomes chronic with prolonged excretion of virus. In some instances, a latent infection, with disappearance of virus, develops and under a variety of circumstances, including immunosuppression, infection can later be reactivated with reappearance of viral excretion. The human consequences of latent infection with CMV are not yet fully appreciated, and future research on this virus with multifaceted potential will need to focus on this issue.
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PMID:Cytomegalovirus infections. 22 89

We studied the relations between HBV heterogeneity and different phases of HBV infection and disease in 145 HBsAg-positive carriers followed-up for 28 months (range 24-60 months). Viraemia was characterized for the relative prevalence of wild-type and HBeAg minus HBVs after HBV-DNA amplification by PCR using an oligonucleotide hybridization assay. HBeAg minus HBV was detected in 27% of immunotolerant HBV carriers, in 67% of patients with chronic hepatitis B (immunoelimination phase) and in 17% of HBsAg carriers with latent infection. Serum HBV-DNA and IgM anti-HBc became undetectable and ALT levels normalized, either spontaneously or after interferon therapy in 12 (36.3%) of 33 patients with an exclusive wild-type viraemia, but only in two (5.7%) of 35 patients with homogeneous HBeAg minus HBV (p = 0.005). An HBeAg minus viraemia higher than 20% was associated, in both HBeAg- and anti-HBe-positive patients, with HBV-induced liver disease and an unfavourable outcome of hepatitis. These findings suggest that surgence of HBeAg defective HBV is a virus strategy to survive under peculiar conditions dictated by the interplay between HBV and the host's immune system. The HBeAg/anti-HBe serological status is determined not only by the extent of virus replication and integration of HBV-DNA into cellular DNA but also by heterogeneity of HBV. The study of HBV heterogeneity in baseline sera of patients undergoing antiviral therapy appears to have a predictive value of the outcome of HBV infection in the single patient.
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PMID:'e' antigen defective hepatitis B virus and course of chronic infection. 182 19

To investigate the infectivity of hepatitis B virus (HBV) from mothers to their newborn offspring, HBV-DNA in plasma and peripheral mononuclear cells from 28 antihepatitis Be positive, hepatitis B surface antigen positive carrier mothers was examined by a highly sensitive polymerase chain reaction/Southern hybridisation technique. HBV specific DNA was detected in three maternal mononuclear cell samples, but was absent in plasma. Two of four infants born to the three mothers with HBV-DNA positive mononuclear cells developed acute or fulminant hepatitis within three months after birth. Two infants were effectively prevented from infection with HBV by combined hepatitis B immunoglobulin/HBV vaccine administration. The 25 infants born to the HBV-DNA negative mothers were free of HBV infection within the next seven months to 3.5 years. These results suggest that latent infection with HBV in maternal mononuclear cells is responsible for perinatal HBV infection.
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PMID:Perinatal hepatitis B virus infection caused by antihepatitis Be positive maternal mononuclear cells. 205 94

Epstein-Barr virus (EBV) is often associated with lethal lymphoproliferative diseases in immunologically compromised individuals. Recently, we have studied a 20-month-old boy with X-linked lymphoproliferative disease (XLP) who had succumbed to infectious mononucleosis (IM) complicated by fulminant hepatitis and virus-associated hemophagocytic syndrome following EBV infection. EBV genomes were detected in peripheral blood lymphocytes (PBL), cervical and mesenteric lymph nodes, liver, spleen, thymus, and bone marrow. According to restriction endonuclease analyses, the EBV-DNA pattern was similar in all samples except for the EBV-DNA from the bone marrow. Additionally, circular EBV-DNA (suggesting a latent infection) predominated in spontaneously established lymphoblastoid cell lines (LCLs) derived from both the lymph node and cord lymphocytes co-cultured with PBL. In contrast, both circular and linear EBV-DNA (suggesting a lytic infection) were noted in spontaneously established LCLs derived from his PBL. Furthermore, LCLs derived from both the lymph node and cord lymphocytes co-cultured with PBL expressed fewer reactive cells for early antigen (EA) and viral capsid antigen (VCA) than spontaneous LCLs from his PBL, thus providing evidence for different B cellular susceptibility to EBV infection in this patient with XLP. Finally, defective EBV-specific cytotoxic T cell activity was observed in this patient. Latent EBV infected cells may easily escape immunosurveillance by the host. These findings may explain the fatal course of EBV infection in this patient.
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PMID:Differential cellular susceptibility to Epstein-Barr virus infection in a patient with X-linked lymphoproliferative disease. 217 37

Herpes simplex virus (HSV, probably type 2) antigen has been detected in endometria and abortion tissue (companion paper) and in placentae, umbilical cords, and fetal and neonatal organs by avidin-biotin complex immunohistochemical studies. HSV cytologic abnormalities were not detected in any of the 12 normal and 64 abnormal cases analyzed, nor was HSV detected by culture or electron microscopy in selected cases. Antigen was present in single epithelial and, rarely, mesenchymal cells of various organs. Clinically unexplained fetal or neonatal problems associated with HSV antigen positivity included intrauterine death, fetal growth retardation, cystic brain degeneration, hydrops, interstitial pneumonitis, necrotizing enterocolitis, hepatitis, encephalitis, myocarditis, and renal failure. Maternal floor infarct of placenta and calcifying funisitis are the manifestations of intrauterine HSV infection in most cases. Maternal history of HSV infection was uncommon. It is concluded that intrauterine HSV infection may persist in the fetus and neonate in a latent fashion without cytologic abnormalities or detectable virus. This latent infection may be associated with intrauterine and neonatal death, organ damage, and neonatal disease.
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PMID:Intrauterine latent herpes simplex virus infection: II. Latent neonatal infection. 302 73

Evidence supporting the existence of two agents of human non-A, non-B hepatitis was obtained by the inoculation of chimpanzees sequentially with serum from a chronically infected human (Inoculum I) and with fibrinogen prepared from pooled plasma (Inoculum IV), each of which had transmitted non-A, non-B hepatitis to humans. Passage inoculations of serum samples obtained during the acute stages of chimpanzee infections transmitted by either the agent in Inoculum I or IV also transmitted non-A, non-B hepatitis to additional chimpanzees. Transmission and passage of the agent in Inoculum IV were conducted in chimpanzees which previously had recovered from infection by the agent in Inoculum I. Cytoplasmic tubules in hepatocytes, which have been described during non-A, non-B hepatitis, were observed by electron microscopy in liver biopsies obtained during all infections transmitted by the agent in Inoculum I. These cytoplasmic tubules were not detected in liver biopsies from chimpanzees infected by Inoculum IV, except in one chimpanzee inoculated by Inoculum IV without prior exposure to the agent in Inoculum I. The cytoplasmic tubules observed in this study were found to be composed of transverse bands arranged with a periodicity of approximately 17 nm. These studies suggest that two different agents or distinct serotypes of human non-A, non-B hepatitis may have been present in these inocula, although reactivation of latent infection or reinfection could not be ruled out completely.
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PMID:Additional evidence for more than one agent of human non-A, non-B hepatitis. Transmission and passage studies in chimpanzees. 642 90

The mechanisms underlying chronicity of hepatitis C virus (HCV) infection are poorly understood, but the importance of impaired viral clearance by the immune system has been suggested. The prevalence of HCV infection of peripheral blood mononuclear cells (PBMC) was in investigated in 34 persistently infected patients with anti-HCV (7 with liver cirrhosis, 10 with chronic active hepatitis, 5 with chronic persistent hepatitis, 4 with chronic lobular hepatitis, and 8 healthy carriers) by polymerase chain reaction (PCR). HCV infection of 116 T cell clones derived from liver infiltrating mononuclear cells obtained from 3 patients with chronic liver disease was examined using the same methods. HCV genomic sequences were found in fresh, unstimulated PBMC from 20 patients with cirrhosis, and chronic active and persistent hepatitis, but in none of the healthy carriers and only in mitogen-activated cells from 1 out of 4 patients with autoresolving chronic lobular hepatitis. Active PBMC infection was confirmed by identification of anti-genomic HCV sequences in the majority of HCV RNA-positive cells (fresh or mitogen-stimulated). A high percentage of T cell clones obtained from liver infiltrates were found to be infected by HCV. These findings suggest that HCV infection of lymphatic cells plays a role in the pathogenesis of chronically evolving liver damage. PBMC may represent a reservoir for latent infection and a site for viral multiplication.
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PMID:Hepatitis C virus infection of mononuclear cells from peripheral blood and liver infiltrates in chronically infected patients. 855 Dec 60


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