Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several of the common viral agents that can cause hepatitis have been detected in body fluids, including saliva and blood, which may both form important routes for transmission of disease. The viruses most commonly implicated include hepatitis A virus (HAV), hepatitis B virus (HBV), cytomegalovirus (CMV), and Epstein-Barr virus. Hepatitis delta virus (HDV) can be found in persons positive for hepatitis B surface antigen (HBsAg) and presumably follows the same routes of transmission as HBV. Herpes simplex and echo viruses can cause hepatitis on rare occasion. Other agents, not yet positively identified but collectively referred to as non-A, non-B are also believed to follow the same routes as HBV and/or HAV. The aim of this reviews is twofold. First, we will discuss hepatotropic viruses other than HBV that may be spread via saliva and blood and, therefore, should be considered along with HBV as a potential health hazard to dental personnel and also to dental patients. The second aim is to highlight the epidemiology and the risk of transmission of these viral infections. The potential hazards are discussed in relation to those associated with HBV and human immunodeficiency viruses (HIV), implicated in the acquired immunodeficiency syndrome (AIDS).
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PMID:Review of hepatitis non-A, non-B: the potential hazards in dental care. 296 86

We studied unselected, hepatitis B surface antigen (HBsAg)-positive parenteral drug abusers for antibody to hepatitis D virus (anti-HD) and antibody to human immunodeficiency virus (HIV). The prevalences of anti-HD and antibody to HIV were 67% and 58%, respectively, and there was no association between positivity for these two markers. In a logistic regression model, anti-HD was associated with older age (P = .001), longer duration of drug abuse (P = .045), and the presence of liver disease (P = .002). Antibody to HIV was associated with a younger age (P = .003) and increased serum globulin levels (P less than .001). In patients infected with HIV, the severity of hepatic dysfunction remained correlated with anti-HD. In anti-HD-positive patients, most indices of hepatic dysfunction were similar whether or not antibody to HIV was present, but serum aspartate aminotransferase levels were significantly higher in patients with both anti-HD and antibody to HIV. (124 +/- 16 vs. 74 +/- 11, P less than .05).
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PMID:Hepatitis D virus and human immunodeficiency virus antibodies in parenteral drug abusers who are hepatitis B surface antigen positive. 317 Dec 27

Orthotopic liver transplantation was done in 17 patients with fulminant hepatitis. The cause of the liver disease was infection with hepatitis B virus, or co-infection with hepatitis B virus and hepatitis D virus, or infection with hepatitis A virus in 6 patients; drug hepatotoxicity in 5; and indeterminate in 6. Grafts from incompatible blood groups, steatotic grafts, or reduced-size grafts were used in 5, 4, and 4 patients, respectively. Of the 17 patients, 5 died: 2 of early liver failure due to the poor quality of the graft, 1 presumably of accidentally transmitted acute infection with the human immunodeficiency virus, and 2 of decerebration occurring during or immediately after surgery. The 12 other patients were alive 2 to 15 months after transplantation.
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PMID:Emergency liver transplantation for fulminant hepatitis. 330 49

Serum samples from 56 patients with biopsy-proven chronic B viral hepatitis without superimposed delta hepatitis were analyzed for the various markers of viral replication, including serum hepatitis B e Ag (HBeAg), hepatitis B virus deoxyribonucleic acid (HBV-DNA), and hepatitis B core antigen (HBcAg) in the liver tissues. Twenty-seven patients had persistent viral hepatitis (PH) and 29 patients had chronic active hepatitis (CAH) with or without cirrhosis. HBV-DNA was identified in the sera of 81% of patients with PH and 60% of patients with CAH. Significantly higher levels of HBV-DNA were found in patients with PH than in those with CAH. Both HBeAg in serum and HBcAg in liver correlated positively with serum HBV-DNA. Nine patients had serum HBV-DNA in the absence of HBeAg (four had anti-HBe), and seven of these nine patients had stainable HBcAg in the liver (two did not have staining). None of these patients had hepatic HBcAg in the absence of serum HBV-DNA. When these patients were stratified according to their epidemiologic background, serum HBV-DNA was present in a significantly higher number of male homosexuals than in any other groups. This was unrelated to their status of human immunodeficiency viral serology.
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PMID:Markers of viral replication in patients with chronic hepatitis B virus infection. 334 Dec 83

Most hemophiliacs who are coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) have high serum levels of HCV RNA. To study the impact of multiple hepatitis virus infections, we evaluated all eight chronic carriers of hepatitis B surface antigen (HBsAg) from a previously studied cohort of 99 hemophiliacs with chronic HIV and HCV infections. Stored serum or plasma samples were tested for antibody to hepatitis D virus (anti-HDV) by ELISA; qualitatively for HCV RNA, HBV DNA, and HDV RNA by the polymerase chain reaction (PCR); and quantitively for HIV RNA, HCV RNA, and hepatitis B virus (HBV) DNA by a quantitative branched DNA signal amplification assay. HCV RNA was detected in only one of five patients with HDV infections on a cross-sectional study, and this individual had low levels (< 3.5 x 10(5) genome eq/ml) of HCV RNA. In contrast, all three without HDV infections had high levels (> 1.5 x 10(7) genome eq/ml) of HCV RNA. HIV RNA was present in all eight patients. There was no correlation between the level of HIV RNA and the presence of hepatitis viruses. Three of the eight patients (38%) died of liver failure and another has hypersplenism with hypoprothrombinemia. We conclude that HDV infection appears to suppress HCV replication and that liver failure is common in adult HIV-infected hemophiliacs with chronic HCV and HBV infections. These findings have implications for the therapy of HCV-infected hemophiliacs who are HBsAg positive.
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PMID:Suppression of hepatitis C virus (HCV) replication by hepatitis D virus (HDV) in HIV-infected hemophiliacs with chronic hepatitis B and C. 762 88

A group of 113 patients with chronic hepatitis D was investigated for the presence of anti-GOR and liver kidney microsomal antibodies. Eight patients were anti-GOR positive and also positive for hepatitis C virus-infection. In sera from 16 patients liver-kidney microsomal antibodies were detectable by immunofluorescence. They were classified as LKM-3 due to their fluorescence pattern. Two of the LKM-3-positive sera were also anti-hepatitis C virus and anti-human immunodeficiency virus positive. None of these patients were positive for anti-GOR. Fourteen sera from LKM-3-positive patients reacted in Western blot with a microsomal protein at 55 kDa that differs from the 50-kDa LKM-1 (cytochrome P450IID6) antigen. Our studies demonstrate that hepatitis D virus itself does not induce an autoimmune reaction against the GOR antigen and that autoimmunity to the LKM-3 antigen induced by hepatitis D virus infection does not correlated with anti-GOR. These studies support the specificity of the anti-GOR response for hepatitis C virus infection.
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PMID:Anti-GOR in hepatitis D: specific association with hepatitis C virus superinfection. 789 50

The prevalence of serum markers of delta hepatitis was determined prospectively in 82 intravenous drug abusers at various stages of human immunodeficiency virus (HIV) disease. Seventeen were HIV negative, 30 were HIV positive without acquired immunodeficiency syndrome (AIDS) and 35 had been diagnosed as having AIDS. Antihepatitis D virus (HDV) in serum was measured by a commercially available enzyme-linked immunosorbent assay (ELISA) and also by solid phase capture radioimmunoassays (RIAs) for immunoglobulin G (IgG) and immunoglobulin M (IgM) anti-HDV. HDV antigen and hepatitis B virus (HBV) DNA were also measured. Hepatitis B surface antigen (HBsAg) and anti-HBs were determined by using a commercially available RIA. Anti-HDV (RIA) was only detected in serum that contained HBsAg. These anti-HDV (RIA) positive samples also tested positive with the commercial anti-HDV electroimmunoassay. In addition, the commercial anti-HDV ELISA detected anti-HDV in some serum samples that were negative for HBsAg; these anti HDV-positive HBsAg-negative samples were frequently lipemic or contained rheumatoid factor. The prevalence of HBsAg and anti-HBs did not differ significantly with the stage of HIV disease. HBsAg was detected in 3 of 13 (23%) HIV-negative, 5 of 29 (17%) HIV-positive, and 4 of 18 (22%) patients with AIDS. IgG and IgM anti-HDV (RIA) was positive in 2 of 3 HIV-negative and 4 of 5 HIV-positive pre-AIDS HBsAg-positive subjects. However, none of 4 AIDS patients had anti-HDV. The difference between AIDS and non-AIDS patients was statistically significant (Fisher's exact test, p = 0.03). HDV antigen was detected in serum from one AIDS patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of HIV disease on serum markers of hepatitis delta infection in intravenous drug abusers. 793 Aug 80

To analyze the serological, clinical and histological significance of hepatitis B virus (HBV) replication among a group of patients with chronic delta hepatitis (CDH), we have studied the clinical and the histological activity in 49 patients with CDH. The HBV-DNA was analyzed by dot-blot and polymerase chain reaction (PCR). Concomitant infection with hepatitis C virus (HCV) was analyzed by reverse transcriptase (RT)-PCR, HDV replication by dot-blot, and human immunodeficiency virus (HIV) infection by enzyme-linked immunosorbent assay. The subjects were divided into three groups according to HBV-DNA status: group I: 14 patients HBV-DNA dot-blot positive; group II: 29 patients HBV-DNA positive only by PCR, and group III: 6 patients HBV-DNA negative by dot-blot and PCR. We have found HBV-DNA by dot-blot in 28.5% of patients, and by PCR in 87.7%. Also 22 patients were anti-HCV positive (86.3% had HCV-RNA by RT-PCR). The first group (HBV-DNA dot-blot positive) had significantly higher serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) than those in the second and third groups. Likewise, serum ALT and AST were significantly higher in the second group (HBV-DNA positive by PCR) than in those of the third group. Histological inflammatory activity was significantly higher in the group of patients with HBV-DNA detectable by dot-blot. The prevalence of serum HDV-RNA and IgM anti-HDV were similar in the three groups. These results were similar in the anti-HCV-positive and -negative patients. In conclusion, these data suggest that: (1) persistence of HBV replication is a major determinant of severe liver damage in chronic delta hepatitis, and (2) HCV and HIV infections do not influence the natural history of CDH.
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PMID:Correlation between hepatitis B viremia and the clinical and histological activity of chronic delta hepatitis. 799 89

Hepatitis A is usually a benign, self-limited infection. A chronic carrier state does not exist, and perinatal transmission does not occur. Hepatitis B may cause chronic infection, and infants delivered to infected mothers are at considerable risk of developing neonatal hepatitis. Passive and active immunization with HBIG and HBV is highly effective in preventing perinatal transmission. Hepatitis D typically occurs as a coinfection or superinfection with hepatitis B. Patients infected with both viruses are at high risk for chronic liver disease. Perinatal transmission of hepatitis D can be prevented by the immunoprophylaxis used for hepatitis B. Non-A, non-B hepatitis occurs in two distinct forms: parenterally transmitted hepatitis C and enterically transmitted hepatitis E. Perinatal transmission of hepatitis C can occur, particularly in women who are concurrently infected with the human immunodeficiency virus. Neonatal immunoprophylaxis is not yet available. Hepatitis E may be associated with high maternal mortality rates in developing nations. However, a chronic carrier state does not exist, and perinatal transmission does not occur. Table 2 summarizes the most important features of each form of viral hepatitis.
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PMID:Viral hepatitis in pregnancy. 816 22

Forty-one patients with hemophilia A were studied for the prevalence of serological markers for hepatitis A, hepatitis B, hepatitis C (non-A and non-B hepatitis), and delta hepatitis (hepatitis D). Ten of 41 (24.4%) patients demonstrated hepatitis A antibody and 31 of 41 (75.6%) patients had a serologic marker for previous hepatitis B infection; four of these 31 patients (13%) also demonstrated antibody to delta agent (hepatitis D). Thirty-seven of 41 (90.2%) patients demonstrated antibody for hepatitis C. Nine of 31 (29%) patients with a hepatitis B marker (no hepatitis B vaccinees) were negative for anti-HBc but positive for anti-HBs; all of these nine patients were HIV antibody positive, although they had no overt immunodeficiency. Twenty-six of 41 (63.5%) patients were HIV antibody positive. Of HIV antibody positive patients, 27%, 88%, and 100% demonstrated evidence of a previous hepatitis A, hepatitis B, or hepatitis C, respectively. Of HIV antibody negative patients; 20%, 53%, and 73% of the patients demonstrated evidence of a previous hepatitis A, hepatitis B, or hepatitis C infections, respectively. The difference between HIV antibody positive and HIV antibody negative groups was not significant for hepatitis A but was significant for hepatitis B (P < 0.001) and hepatitis C (P < .001). Of the 31 patients with a hepatitis B serologic marker, all had antibody to hepatitis C. Of 10 patients, without a hepatitis B serologic marker, only 6 (60%) had antibody to hepatitis C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serologic markers of viral hepatitis A, B, C, and D in patients with hemophilia. 826 2


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