Get your own Free Home PageHBV AND HCV GENOME IN PERIPHERAL BLOOD MONONUCLEAR CELLS IN PATIENTS UNDERGOING CHRONIC HEMODIALYSIS.
Oesterreicher C; Hammer J; Koch U; Pfeffel F; Sunder-Plassmann G; Petermann D; Müller C Universitätsklinik für Innere Medizin IV, Klinische Abteilung Gastroenterologie and Hepatologie, Universität Wien, Austria. Kidney Int, 1995 Dec, 48:6, 1967-71
Patients undergoing chronic hemodialysis are at risk for infection with hepatitis B virus (HBV) and hepatitis C virus (HCV). As peripheral blood mononuclear cells (PMNC) are known to be susceptible to infection of both HBV and HCV, assessment of viral genomes in those cells could uncover occult infections not detected by serologic methods or virus determination in serum. We investigated all 67 patients undergoing chronic hemodialysis at a single dialysis unit by PCR for the presence of HBV or HCV genomes in serum as well as in PMNC. None of the 67 patients was HBsAg positive or showed HBV-DNA in serum, but in 5 patients HBV-DNA in PMNC was detected as the only marker of HBV-infection; those patients were also anti-HBc negative. In 9 patients HCV-RNA was positive in serum; in 5 of those patients it was also found in PMNC. Three of these infected patients were negative for anti-HCV. One other patient had no anti-HCV or HCV-RNA in serum, but was positive for HCV-RNA in PMNC. Thus, in 6 patients (8.9%) undergoing chronic hemodialysis we found evidence of infection with HBV or HCV by detecting viral genomes in PMNC without the presence of viremia, antigenemia or specific viral antibodies in serum. The detection of viral genomes in PMNC could be useful in the positive identification of additional potentially infectious patients.
DETECTION OF HEPATITIS C VIRUS RNA IN PERIPHERAL BLOOD MONONUCLEAR CELLS and in saliva
C. Young, T. T. Chang, T. C. Liou & H. L. Wu; Department of Medical Technology, National Cheng Kung University, Tainan,Taiwan, Republic of China. J Med Virol 41: 55-60 (1993)
The nested polymerase chain reaction (PCR) technique was applied to investigate hepatitis C virus (HCV) RNA in the peripheral blood mononuclear cells (PBMCs), saliva, and serum of patients with chronic type C hepatitis. The specificity of the amplified products was analyzed and confirmed by agarose gel electrophoresis, Southern blot hybridization, and restriction endonuclease pattern analysis. HCV RNA was detectable in the PBMCs of 24% (12/50) of the patients. The HCV RNA detected in PBMCs was not due to the contamination from plasma, since no viral sequences could be detected in the third washing of PBMCs. Of the 12 patients with HCV RNA in PBMCs, five were negative for HCV RNA sequences in the serum. Thus the presence of HCV RNA in PBMCs was not strictly correlated to the results for sera. Among 25 patients with HCV RNA in their saliva, 18 were negative for PBMCs. Among 25 patients without HCV RNA in their saliva, five had HCV RNA in PBMCs. In conclusion, PBMCs are an extrahepatic target for chronic HCV infection.
SURREPTITIOUS HEPATITIS C VIRUS (HCV) INFECTION DETECTED IN THE MAJORITY OF PATIENTS WITH CRYPTOGENIC CHRONIC HEPATITIS AND NEGATIVE HCV ANTIBODY TESTS.
Schmidt WN; Wu P; Cederna J; Mitros FA; LaBrecque DR; Stapleton JT; Department of Internal Medicine and Pathology, University of Iowa, College of Medicine, and VA Medical Center, Iowa City, USA. J Infect Dis, 1997 Jul, 176:1, 27-33
Reverse transcription-polymerase chain reaction was used to identify hepatitis C virus (HCV) RNA in peripheral whole blood (WB) and plasma samples from 15 patients with chronic, unexplained hepatitis. These patients were serologically negative for hepatitis A, B, and C and were classified as having chronic non-A, non-B, non-C hepatitis (NANBNC). HCV RNA was repeatedly detected in WB samples from 10 (67%). In contrast, plasma samples from only 5 were intermittently positive. Statistically, HCV RNA detection in WB was significantly more sensitive than in plasma. Nucleic acid hybridization and HCV genotypic analysis confirmed the specificity of the HCV RNA assay. Liver biopsies from these patients suggested histopathologic differences between HCV RNA-positive and -negative groups. These data demonstrate that HCV infection is present in patients with unexplained chronic hepatitis more frequently than previously believed. Additionally, WB HCV RNA detection is more sensitive than plasma assays in identifying antibody-negative HCV infection.
DETECTION OF HEPATITIS B VIRUS DNA IN PERIPHERAL BLOOD MONONUCLEAR CELLS FROM PATIENTS WITH VARIOUS HEPATOPATHIES USING IN SITU HYBRIDIZATION
Suñén E; Fernández de Aranguiz A; De Las
Heras B; Gorriño MT; Sarriá L; Malavé C;
Campelo C; Cisterna R; Departamento de Microbiología e
Inmunología, Universidad del País Vasco UPV/EHU,
Hospital Civil de Bilbao, Lejona, Vizcaya. An Med Interna,
1991 Aug, 8:8, 372-6
We have investigated, by "in situ" hibridisation, the presence of hepatitis B virus (HBV) DNA in peripheral blood mononuclear cells (PBMC) from 45 patients with acute and chronic hepatic disorders directly related with HBV or with some seric HBV marker. Results has been related with serological markers and the different types of hepatopaties. The HBV-DNA was detected in PBMC more frequently in patients with hepatic alterations more prolongated (chronic active hepatitis, chronic persistent hepatitis and cirrhosis) than in acute hepatitis patients. It was not detected in any asymptomatic patient with HBV serological markers. As regards HBV serological markers, HBV-DNA was detected in PBMC in 8/11 HBsAg positive patients and in 11/34 HBsAg negative patients: 3 antiHBc positive, 5 antiHBc and antiHBs positive and without conventional seric markers. The detection of HBV-DNA in antiHBc and/or antiHBs positive subjects means the virus may persist after recovery of infection and suggests PMBC could serve as additional reservoirs for reinfection of hepatocytes leading to a reactivation of the liver disease. Our results suggest that HBV infection of PBMC is a frequent event during HBV infection and can have important consequences fundamentally with respect to pathogenic mechanisms of HBV induced liver disease and to the transmission of the virus.
HEPATITIS B VIRUS OCCULT INFECTION IN SUBJECTS WITH PERSISTENT ISOLATED ANTI-HBc REACTIVITY.
Sánchez-Quijano A; Jauregui JI; Leal M; Pineda JA; Castilla A; Abad MA; Civeira MP; García de Pesquera F; Prieto J; Lissen E; Viral Hepatitis and AIDS Study Group, Virgen del Rocio University Hospital, Seville, Spain. J Hepatol, 1993 Mar, 17:3, 288-93
The aim of this study was to investigate the presence of hepatitis B virus occult infection in asymptomatic subjects with persistent anti-HBc reactivity but no other hepatitis B virus serological markers, including HBsAg, anti-HBs, IgM anti-HBc and HBV-DNA. For this purpose we used both polymerase chain reaction assays in sera and immunohistochemistry for HBsAg and HBcAg in liver biopsy specimens. Twenty-four cases were studied: 15 were drug abusers or homosexuals (eight with normal alanine aminotransferase levels) and nine were heterosexuals with raised alanine aminotransferase levels (> 45 U/l) but with no history of blood transfusion or ethanol intake (< 80 g daily). In all but five cases, liver biopsy was performed in subjects with persistent elevated alanine aminotransferase levels. In 10 out of 24 cases (41.66%) hepatitis B virus infection was demonstrated by polymerase chain reaction or immunohistochemistry, and when results from both procedures were available (n = 11) hepatitis B virus infection was detected in 63.63% of the subjects. The only clinical feature associated with HBV infection was the presence of persistent elevated alanine aminotransferase levels (p < 0.05). In conclusion, persistent isolated anti-HBc reactivity may be a relatively common serologic pattern for hepatitis B virus occult infection, at least in patients with chronic liver disease.
HEPATITIS B VIRUS AND APPARENT FULMINANT NON-A, NON-B HEPATITIS
Wright TL; Mamish D; Combs C; Kim M; Donegan E; Ferrell L; Lake J; Roberts J; Ascher NL Department of Veterans Affairs Medical Center, San Francisco, California 94121. Lancet, 1992 Apr 18, 339:8799, 952-5
While there is evidence that hepatitis C virus (HCV) does not cause fulminant non-A, non-B hepatitis, the causal agent remains unknown. To evaluate the role of hepatitis B virus (HBV) in this disease, we used a two-step polymerase chain reaction (PCR) to amplify the surface and core regions of HBV DNA in serum and liver samples taken prospectively from twenty-six patients (mean age 36 years, range 1 to 64) with acute hepatic failure undergoing liver transplantation. HBV DNA was absent from the serum of all patients before transplantation. Seventeen patients were diagnosed as having non-A, non-B hepatitis because they lacked serological evidence of HAV or HBV infection. Liver samples were taken from twelve of these patients, and six samples( 50% ) were positive for HBV DNA. By contrast HBV DNA was not detected in liver from three patients with acute liver failure caused by hepatitis A or toxins. HCV RNA was not found in pretransplant samples by PCR. Four of the six patients with detectable HBV DNA in liver and presumptive non-A, non-B hepatitis had detectable HBV DNA in serum after transplantation. One additional patient who did not donate pretransplant liver had HBV DNA in a post-transplant serum sample. Thus, HBV DNA was present before or after transplantation in seven of seventeen patients with apparent non-A, non-B hepatitis. Three of five patients with detectable post-transplant serum HBV DNA were serologically positive for HBV surface antigen. These findings indicate that HBV may be a common cause of fulminant hepatic failure in patients lacking serological evidence of HBV infection.
DETECTION OF HEPATITIS B AND HEPATITIS C VIRAL SEQUENCES IN FULMINANT HEPATIC FAILURE OF UNKNOWN ETIOLOGY
Hytiroglou P; Dash S; Haruna Y; Fernandez M; Theise ND; Schwartz M; Miller C; Bodenheimer HC Jr; Thung SN; Gerber MA; Lillian and Henry M. Stratton-Hans Popper Department of Pathology, Mount Sinai Medical Center of the City University of New York, NY, USA. Am J Clin Pathol, 1995 Nov, 104:5, 588-93
Summary: Hepatitis B virus, either alone or in conjunction with hepatitis D virus or hepatitis A virus, appears to be a frequent cause of fulminant hepatic failure in seronegative patients
Abstract: In a significant number of patients, the etiology of fulminant hepatic failure(FHF) is unknown. To determine whether hepatitis B virus (HBV) and hepatitis C virus (HCV) play a role in patients without serologic markers of HBV and HCV infection, the authors examined tissue samples from 15 liver explants with massive hepatic necrosis for the presence of viral sequences by the polymerase chain reaction (PCR). The specimens were derived from nine patients with FHF of unknown etiology; two with serum hepatitis B surface antigen (HBsAg); two with antibodies to HCV; one with antibodies to hepatitis A virus (HAV) and anti-HBc of the IgM class; and one with isoniazid toxicity. Nucleic acids were extracted from frozen liver samples. RNA was used as a template for reverse transcription, followed by double PCR with nested primers for the 5'-untranslated region of HCV. DNA was tested by single PCR for S gene sequences of HBV. Hepatitis B virus sequences were detected in the specimens of the two HBsAg positive patients, the anti-HAV/anti-HBc positive patient, and three of nine patients with FHF of unknown etiology. Hepatitis C virus sequences were present in the explant of one patient with FHF of unknown etiology, but not in the two patients with antibodies to HCV. In two specimens with molecular findings of HBV infection (1 from a patient with serum HBsAg and 1 without), there was immunohistochemical evidence of coinfection or superinfection with hepatitis delta virus (HDV). In conclusion, in this patient population, HBV, alone or with HDV or HAV, causes fulminant hepatic failure more often than HCV infection. However, in the majority of patients, the etiology of fulminant hepatic failure remains unknown.
ETIOLOGY AND PROGNOSIS OF CRYPTOGENIC LIVER CIRRHOSIS: POSSIBLE CONTRIBUTION OF HEPATITIS B VIRUS.
Watanabe A; Aiba N; Harada R; Miyabayashi C; Entani A; Wakabayashi H; Nishimori H; Kuwabara Y; Third Department of Internal Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan. J Med, 1997, 28:1-2, 31-44
Three female patients without type B or type C viral hepatitis, alcoholic, metabolic or autoimmune liver disease, were selected from 250 cases with histologically proven liver cirrhosis (M:F = 183:67). All three cases showed at least one positive aspect among three parameters of serum anti-HBc (RPHA, x1), HBV-DNA (gene S, nested PCR) and liver HBs and/or pre-S2 antigen (immunoperoxidase methods). Two cases may suggest a spontaneous disappearance of HBV from sera. Another case may suggest a contribution of mutant HBV which can not be detected by the routine tests. These HBV-related cirrhotic patients have done well clinically and have not been associated with hepatocellular carcinoma during the period from 6 to 12 years of follow-up when compared with 59.6% and 65.4% prevalence of hepatocarcinogenesis in type B and type C hepatitis-associated cirrhosis during the observation period of six and seven years on average, respectively.
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