Occurrence of a novel DNA virus (TTV) infection in patients with liver diseases and its frequency in blood donors.

A novel DNA virus (TTV) was identified recently in Japanese patients with posttransfusion hepatitis non-A-E and has been implicated as a cause of acute and chronic liver diseases of unknown etiology in some patients. The frequency of TTV infections was investigated in 284 blood donors, 105 patients with different liver disorders before and after liver transplantation (OLT), as well as in 64 patients with chronic hepatitis C who received antiviral therapy. TTV infections were found more frequently by nested-PCR in patients with liver disorders (15%) as compared to blood donors (7%). TTV occurred independently of the aetiology of the liver disease (e.g., cryptogenic cirrhosis [12.5%], alcoholic cirrhosis [16%], fulminant hepatic failure non-A-E [35%], and chronic hepatitis C [12.5%]; p=n.s.). After OLT, a high rate of TTV de novo infections (44%) was observed. However, TTV viremia after OLT (in 56 out of the 105 patients) was not associated with graft hepatitis. Analysis of patients with chronic hepatitis C coinfected with TTV who have been treated with interferon alpha alone or in combination with ribavirin revealed that TTV is an interferon-sensitive virus. Phylogenetic analysis of TTV sequences suggest that at least four different genotypes and several subtypes exist in Germany. In conclusion, the high prevalence of TTV infections observed in patients with parenteral risk factors is an argument in favour of transmission of the virus via blood and blood products. A relevant hepatitis-inducing capacity of TTV, however, seems unlikely, considering the observation that in the majority of patients, TTV infection after OLT was not accompanied by graft hepatitis.     

SEN virus infection does not affect the progression of non-A to -E liver disease

SEN virus (SEN V) was discovered recently as a potential causative agent of non-A, non-B, non-C, and non-E (non-A to -E) hepatitis. The aim of this study was to obtain information about the prevalence of this virus in Japan and its association with non-A to -E liver disease. Sixty-seven patients hospitalized for non-A to -E liver disease, including hepatocellular carcinoma (19 patients), cirrhosis (7 patients), chronic hepatitis (18 patients), and acute hepatitis (23 patients), were tested, along with 49 blood donors. The patients were admitted to Nihon University Hospital between 1991 and 1998. SEN V DNA was detected by a nested polymerase chain reaction, targeting the 5' untranslated region. SEN V DNA was detected in 14 of 49 (28.6%) blood donors and in 33 of 67 (49.3%) patients with non-A to -E liver disease. The prevalence of SEN V DNA was similar among patients with various liver diseases, including hepatocellular carcinoma (42.1%), cirrhosis (57.1%), chronic hepatitis (55.6%) and acute hepatitis (47.8%) and among blood donors (28.6%). There were no significant differences in the clinical profiles of patients with SEN V DNA-positive or -negative chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Similarly, there were no significant differences in the clinical profiles between patients with SEN V DNA-positive and -negative acute hepatitis. In conclusion, SEN V infection is present among many blood donors and is common in patients with non-A to -E liver disease. There are insufficient data to prove a causal role for SEN virus infection in non-A to -E liver disease.     

Multiple hepatitis virus infections in chronic HBsAg carriers in Naples

Summary.  In order to determine the prevalence of multiple infections with hepatitis viruses in chronic HBsAg carriers in Naples, to assess the interaction between HBV, HDV and HCV infections and to evaluate the influence of multiple virus hepatitis infections on the clinical presentation, we studied 198 HBsAg chronic carriers observed consecutively from 1971 to 1988 at our Liver Unit. Of the 198 HBsAg chronic carriers, 171 had undergone percutaneous liver biopsy. The presence of HBcAg or HDAg in the liver biopsy was considered a marker of HBV or HDV replication, respectively; the presence of anti-HCV was considered a marker of HCV infection. Anti-HCV was observed in 13.6% of the 22 subjects with normal liver, in 27.7% of the 47 patients with minimal chronic hepatitis, in 40% of the 50 with mild chronic hepatitis, in 70.6% of the 17 with moderate hepatitis, in 66.7% of the 3 with severe chronic hepatitis and in 65.6% of the 32 with active cirrhosis. Anti-HCV positive cases were antiHD positive more frequently than the anti-HCV negative (59.2% vs. 43%, p=0.05). HDV infection exerted a clear inhibition on the HBV genome. Among the 171 HBsAg chronic carriers, the finding of an active chronic hepatitis (moderate chronic hepatitis+severe chronic hepatitis+active cirrhosis) is less frequent in subjects with HBV replication alone than in those with HDV replication or HCV infection. Patients with both HBV replication and HCV infection and those with both HDV replication and HCV infection showed a very high prevelance of active chronic hepatitis.     

Hepatitis B virus DNA in liver, serum, and peripheral blood mononuclear cells after the clearance of serum hepatitis B virus surface antigen

The integration of hepatitis B virus (HBV) DNA in the liver of chronic HBV carriers has been documented extensively. However, the status of the viral genome during acute infection has not been assessed conclusively. While HBV DNA sequences are detected often in serum, liver, and peripheral blood mononuclear cells (PBMCs) after the clearance of serum the hepatitis B virus surface antigen (HBsAg), the precise status of the viral genome, and in particular the possible persistence of integrated genomes in PBMCs, has not been established. A highly sensitive PCR-derived assay (Alu-PCR) was employed to re-examine liver and PBMC specimens obtained from patients with acute (n = 19) and chronic (n = 22) hepatitis in whom serum HBsAg was present (n = 12) (HBV-related chronic active hepatitis) or absent with anti-HCV (n = 10) (HCV-related chronic active hepatitis). Viral integration was demonstrated in 3 out of 19 liver specimens from patients with acute hepatitis and 12 out of 12 specimens from patients with chronic hepatitis. Viral integration was also observed in 4 out of 7 PBMC samples from HBV-related chronic active hepatitis patients and 2 out of 10 liver and PBMC samples from HCV-related chronic active hepatitis patients. In one liver specimen from an acute hepatitis patient, HBV DNA was found integrated in the intronic sequence of the tumour necrosis factor (TNF)-induced protein gene; viral integration into cellular sequences was also found in the PBMCs of four HBV-related chronic active hepatitis and two HCV-related chronic active hepatitis. The results demonstrate the early integration of HBV genome during acute viral infections and the persistence of the viral genome in an integrated form in PBMCs.     

Influence of hepatitis G virus infection on liver disease

The influence of hepatitis G virus (HGV) infection on disease activity in hepatitis C related and unrelated liver disease was investigated in 254 individuals using an EIA polymerase chain reaction assay for HGV. One hundred patients had chronic hepatitis C, 26 primary biliary cirrhosis, and 30 alcoholic liver cirrhosis. In addition, 51 hepatitis B surface antigen (HBsAg)-positive and 47 anti-hepatitis C virus (HCV)-positive blood donors were screened. Hepatitis G virus was detected in 18% of patients with chronic hepatitis C, 13% of patients with alcoholic liver cirrhosis, 11 % of patients with primary biliary cirrhosis, 10% of anti-HCV-positive blood donors, and 2% of HBsAg-positive blood donors. Virus load and alanine aminotransferase (ALT) levels did not differ significantly in patients with HCV alone versus patients coinfected with HCV and HGV. However, mild liver fibrosis correlated with HGV coinfection. Hepatitis G virus did not influence ALT levels or liver damage in liver disease unrelated to viral infection.     

Prognosis of chronic hepatitis C with regard to the aim of treatment

Epidemiology of hepatitis C virus(HCV) infection and clinical prognosis of chronic hepatitis C were presented here to reveal the object of treatment of Chronic Hepatitis C. Hepatitis C Virus is transmitted by blood and blood products. After acute HCV infection, about 70% developed persistent HCV infection, and the diagnosis is by finding viral RNA in the serum of patients with anti-HCV antibody. Persistent HCV infection causes chronic hepatitis, in which the natural clearance of HCV is almost impossible and there is almost no natural cure for chronic hepatitis caused by HCV. Chronic hepatitis C tends to develop gradually and to progress to liver cirrhosis, and is involved in the pathogenesis of hepatocellular carcinoma. In Japanese patients with chronic hepatitis C, 45% developed liver cirrhosis pass through a phase of chronic active hepatitis over a 15-year course after initial HCV infection, and 25% developed hepatocellular carcinoma over a 20-year course after the initial HCV infection. In addition the remaining patients may start to develop rapidly to chronic active hepatitis and to liver cirrhosis after 20 to 30 years duration of inactive phase. Thus, this type of chronic hepatitis reveals a poor long-term prognosis. For etiological treatment of chronic hepatitis C, eradication of persistent HCV infection is needed. If this is impossible, then preventing the development of liver cirrhosis and hepatocellular carcinoma is important.     

用~(125)IUdR标记K562细胞法检测乙型肝炎患者外周血中的NK细胞活性

本文用~(125)IUdR 标记的K 562细胞作为靶细胞,检测 29例病毒性乙型肝炎患者(急性期17例、慢迁肝7例、无症状 HBsAg 携带者3例和肝硬化2例)外周血中自然杀伤(NK)细胞的活性。结果发现40例正常对照组的NK活性平均值±SD 为35.24±12.24％;5例急性早期患者显著升高(P<0.001);7例慢迁肝患者明显降低(P<0.05);9例恢复期和 3例无症状 HBsAg携带者均在正常范围内。以上结果与中岛悦朗和Serdengerti的报道相符,但与另些作者的资料有差异。我们认为NK活性在病程初期升高和在慢性期降低与干扰素的生成和乙肝病人早期肝损害有关,与若干种其他病毒性疾病中所见的规律相仿。     

Low prevalence of antibody to hepatitis C virus in north east England

The prevalence of antibodies to hepatitis C virus (anti-HCV) was studied in North East England in blood donors, local multiply transfused patients, local high risk individuals, and chronic liver disease patients. Anti-HCV was detected by enzyme-linked immunosorbent assay (ELISA) in 2/1120 (0.18%) blood donors; 1/84 chronic renal failure patients on haemodialysis who had received 1,992 units of blood (seroconversion rate of 0.05% per unit transfused), 1/207 cardiac patients 6 months post cardiac surgery transfused with 1,403 units of blood (1 anti-HCV pre-operatively, seroconversion rate 0.07%), 40/50 haemophilia A patients treated with commercial factor VIII, and 38/100 intravenous drug users. In addition anti-HCV was detected by ELISA in 5/35 cryptogenic chronic liver disease patients, 5/5 confirmed by recombinant immunoblot assay (RIBA) (14%); 3/30 patients with autoimmune chronic active hepatitis, 2/3 by RIBA (7%); 2/50 primary biliary cirrhosis patients, 1/2 by RIBA (2%); 0/30 alcoholic cirrhosis patients; and 2/9 patients with hepatocellular carcinoma, 1/2 by RIBA (11%). HCV is uncommon in North East England; it may be implicated in the aetiology of a minority of cases of cryptogenic liver disease and less than 5% of autoimmune chronic active hepatitis and primary biliary cirrhosis.     

Anti-delta antibody in various HBsAg positive Argentine populations

One thousand five hundred and seventeen HBsAg carriers from different cities of Argentina were studied for the presence of anti-Delta antibody (anti-HDV) in their sera. One thousand one hundred and sixty-eight were volunteer blood donors and 349 were patients with liver disease. Different liver diseases were diagnosed by clinical, biochemical, and histological parameters. Among blood donors, 16 (1.4%) were positive for the antibody and none was Delta-antigen positive. In 130 patients with acute hepatitis, one (0.77%) was positive for anti-HDV, as well as three (2.22%) out of 135 patients with chronic active hepatitis (CAH), and three (5.77%) out of 52 patients with cirrhosis (C). No anti-HDV positive was found among seven fulminant hepatitis (FH) cases. The presence of HBeAg and anti-HBe was studied in anti-HDV positive sera; eleven (69%) volunteer blood donors were anti-HBe positive, and five (31%) were HBeAg positive. HBeAg was positive in the three CAH cases, and in one out of three C Cases with anti-HDV positive. Hepatitis Delta antigen was also positive in the hepatocytic nuclei in the three patients with C and two of the three CAH cases. The present results show that Delta infection is rare among blood donors in Argentina. A small variation without statistical significance could be found within different geographical areas. Among patients with HBsAg related liver disease, the presence of HDV markers was also low.     

乙型肝炎患者特异性细胞免疫功能检测的初步研究

目的 通过酶联免疫斑点法检测乙型肝炎（乙肝）患者特异性细胞免疫功能，初步研究各型乙肝患者特异性细胞免疫功能的差异。方法 选择急、慢性乙肝、肝炎肝硬化（乙型）、乙肝病毒（HBV）既往感染，接种乙肝疫苗后血清乙肝病毒学标志中仅表面抗体阳性及未接种过乙肝疫苗、未感染过HBV、血清HBV标志全部阴性者共6组研究对象，每组4例，采用酶联免疫斑点法（ELISPOT）检测其外周血单个核细胞中γ-干扰索分泌细胞的数量。结果 急性乙肝患者、慢性乙肝患者及急性乙肝患者、肝炎肝硬化患者外周血单个核细胞γ-干扰素分泌细胞数量明显不同（P=0．0209及P=0．0211）。结论 通过ELISPOT检测乙肝患者外周血单个核细胞γ-干扰索分泌细胞的数量可以了解乙肝患者特异性细胞免疫功能。急性乙肝患者特异性细胞免疫功能明显强于慢性乙肝患者及肝炎肝硬化患者。     

Clinical significance of TT virus infection in patients with chronic liver disease and volunteer blood donors in Egypt

Clinical significance of TT virus (TTV) infection was investigated in Egyptian patients with chronic liver disease and volunteer blood donors by a cross sectional analysis. TTV DNA in serum was assessed by a semi-nested polymerase chain reaction. The prevalence of TTV DNA did not differ among patients with chronic hepatitis B (11/24, 46%), chronic hepatitis C (22/72, 31%), or schistosomal liver disease (14/39, 36%). No difference in prevalence was found between blood donors (32/109, 29%) and each of the patient groups. Clinical background including mean age, sex distribution, history of blood transfusion, and mean level of alanine aminotransferase did not differ between TTV DNA-positive and -negative individuals in any of the study groups. Ultrasonographic evidence of liver cirrhosis was similar between TTV-positive and -negative patients in each of the chronic liver disease groups. TTV infection was not associated with hepatitis B or C virus infection in blood donors. The only significant difference observed was the lower concentration of serum HCV RNA in TTV DNA positive compared with negative patients with chronic hepatitis C (3.0 +/- 1.4 vs. 4.0 +/- 0.9 log copies/ml, P <. 001). In conclusion, TTV infection was not associated with either past history of blood exposure or infection with bloodborne hepatitis viruses in Egypt. No clinical significance of TTV was found in the present study. However, a reciprocal interaction was suggested between TTV and HCV replication.     

Seroprevalence of hepatitis C virus infection and its genotype in Lanzhou,Western China

The seroprevalence of hepatitis C virus (HCV) infection in Lanzhou, Western China was studied. HCV genotypes in 20 patients with HCV infection was determined by genotype-specific primer for polymerase chain reaction (PCR) based on HCV core region and compared with the genotype assigned by sequence comparison and molecular evolutionary analysis based on the same region. Antibody to HCV (anti-HCV) was present in 2.5% of volunteer blood donors and in 35.0% of paid blood donors (P < 0.01). HCV infection is uncommon in patients with liver disease who attended liver clinics in this locality; 4.0% with acute hepatitis and 4.0% with chronic hepatitis, 10.0% with liver cirrhosis, and none with hepatocellular carcinoma were seropositive for anti-HCV. Genotype 1b and 2a were both found to be prevalent. Together, they accounted for 19 of 20 (95%) patients with HCV infection. Sequencing of the HCV core region from two patients showed that the assignment of HCV genotype by genotype-specific primers for PCR matched well with the genotyping results based on sequence comparison and molecular evolutionary analysis. These data showed that HCV is present in Western China, HCV infection is more common in paid blood donors, and HCV genotypes 1b and 2a are both prevalent in Western China. © 1995 Wiley-Liss, Inc.     

急、慢性乙型肝炎及乙肝肝硬化患者 肝功能及血脂水平分析

目的 分析急、慢性乙型肝炎、乙肝肝硬化患者血脂水平及患者血脂水平的变化情况。方法 选择2015年1月~2018年12月我院收治的急性乙型肝炎患者40例作为急性乙型肝炎组,慢性乙型肝炎患者44例作为慢性乙型肝炎组、乙肝肝硬化患者35例作为乙肝肝硬化组,采用回顾性调查方法比较急、慢性乙型肝炎及乙肝肝硬化患者肝功能及血脂水平。结果 急性乙型肝炎组与慢性乙型肝炎组在ALT、AST、TBIL、DBIL比较,差异有统计学意义（P＜0.05）;急性乙型肝炎组与乙肝肝硬化组在ALT、AST、ALB、TBIL、DBIL、PT、PTA、INR比较,差异有统计学意义（P＜0.05）;慢性乙型肝炎组与乙肝肝硬化组在ALT、AST、ALB、PT、PTA、INR比较,差异有统计学意义（P＜0.05）。急性乙型肝炎组TG高于慢性乙型肝炎组与乙肝肝硬化组,差异有统计学意义（P＜0.05）;慢性乙型肝炎组CHO水平高于急性乙型肝炎组与乙肝肝硬化组,差异有统计学意义（P＜0.05）;急性乙型肝炎组、慢性乙型肝炎组、乙肝肝硬化组在HDL-C、LDL-C间比较,差异无统计学意义（P＞0.05）。结论 急、慢性乙型肝炎及乙肝肝硬化患者血脂水平逐渐降低,以TG下降为主,与肝功能损伤有关,是评估乙型肝炎病程进展的一个重要指标。     

Hepatitis C virus infection of mononuclear cells from peripheral blood and liver infiltrates in chronically infected patients

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. © 1995 Wiley-Liss, Inc.     

慢性乙型肝炎,肝硬化患者外周血LAK细胞活性和sIL—2R测定的意义

采用＾３Ｈ－ＴｄＲ释放法测定５１例慢性肝病患者（ＣＰＨ１０例、ＣＡＨ２３例、ＬＣ１８例）外周血ＬＡＫ细胞活性，并用酶联法测定患者血清中ｓＩＬ－２Ｒ含量；与２９例正常对照组比较，发现肝病患者ＬＡＫ活性降低，ＨＢＶＤＮＡ阳性组ＬＡＫ活性较阴性组低（Ｐ〈０．０５），ｓＩＬ－２Ｒ增高，且慢性肝病组ＬＡＫ活性与ｓＩＬ－２Ｒ水平呈负相关，说明ＬＡＫ活性与机体免疫功能状态有关，ＨＢＶ的复制和高浓度的ｓＩＬ－２Ｒ     

Serological studies and ultrasonographic diagnosis of chronic liver disease in Kenya

Blood samples were obtained from blood donors and patients with chronic hepatitis (CH), liver cirrhosis (LC) and hepatocellular carcinoma (HCC) from provincial hospitals and Kenyatta National Hospital (KNH). Patients with chronic liver disease (CH, LC and HCC) underwent abdominal ultrasound screening as well. The blood samples were screened for Hepatitis B surface antigen (HBsAg), anti hepatitis C virus (Hep CV) antibodies and alpha fetoprotein (AFP). A total of 44665 blood samples from blood donors were screened for HBsAg between July 1991 and January 1993. Of these 4.1% were found to be HBsAg positive. A total of 983 samples were taken from chronic liver disease patients out of which 22.2% were found to be HBsAg positive. Sixty-three patients were found to have liver cirrhosis and 53 patients had HCC on ultrasound screening. Anti Hep CV antibodies were found in 4.3% (5/116) of patients with LC and HCC. AFP levels were found to be significantly higher in HCC patients than in LC patients, levels of above 200 ng/ml being diagnostic of HCC. Follow up of high risk patients, i.e. those with HBsAg positive, chronic liver disease, by ultrasound screening and AFP detection may be useful in the early detection of HCC.     

庚型肝炎病毒致病性的初步研究

目的 探讨庚型肝炎病毒（ＨＧＶ）的致病性。方法 应用ＲＴ－ｎＰＣＲ检测３６８例肝炎患者血清ＨＧＶ ＲＮＡ和血清酶的变化,并对其中１例单独庚型肝炎肝硬化病例进行肝脏活组织是检测。结果 在７１例急性黄疸型肝炎中检出单纯性ＨＧＶ ＲＮＡ阳性７例,１５５例慢性肝炎中检出单纯性ＨＧＶ ＲＮＡ阳性２２例,５１例肝硬化中检出单纯ＨＧＶ ＲＮＡ阳性３例。其中１例肝穿组织免疫组化证实为ＨＧＶ ＮＳ ５Ａｇ阳性。结论 争性黄疸型肝炎及乙、丙型肝炎病毒携带者,其慢性肝炎、肝硬化和肝癌中均可检出ＨＧＶ ＲＮＡ,ＨＧＶ感染可为单独感中与乙／丙型肝炎病毒混合或重叠感染,肝脏病理和免疫组化检查证实庚型肝炎病毒是一种嗜肝病毒,其定位主要存在于细胞浆内,可引起慢性病毒性肝炎甚至肝硬化。庚型肝炎病毒很可能具有致病性。     

Infection with an unenveloped DNA Virus (TTV) associated with posttransfusion non-A to G hepatitis in hepatitis patients and healthy blood donors in Thailand

An unenveloped single-stranded DNA virus (TTV) has been reported in association with posttransfusion and acute and chronic hepatitis of unknown etiology. DNA of TTV was tested for by polymerase chain reaction with heminested primers in 127 patients with chronic liver disease and 105 healthy blood donors in Thailand. TTV DNA was detected in 23 (59%) of the 39 patients without hepatitis B surface antigen or RNA of hepatitis C virus, at a frequency significantly higher than the detection in 21 (36%) of the 59 patients with HBsAg (P < 0.05) or in 38 (36%) of the 105 blood donors (P < 0.05). Among patients with chronic liver disease, TTV DNA occurred in those with liver cirrhosis and hepatocellular carcinoma more frequently than in those with chronic hepatitis (35 of 65 or 54% vs. 20 of 62 or 32%, P < 0.05). There were no differences in age, sex, or markers of infection with hepatitis B, C and GBV-C/HGV viruses, indicating a mode of transmission of TTV different from those of the other hepatitis viruses. Phylogenetic analysis indicated three different genotypes of TTV with six distinct subtypes in Thailand. Based on these results, TTV would have a role in the development of chronic liver disease of unknown etiology in Thailand. J. Med. Virol. 56:234–238, 1998. © 1998 Wiley-Liss, Inc.     

Unusually rapid development of a HBsAG-positive liver cirrhosis after liver transplantation

Summary We report the case of a 44-year-old man who was transplanted in 1986 for hepatocellular carcinoma in a HBsAG-positive liver cirrhosis. The patient had no severe complications postoperatively. He received passive immunization for the prevention of hepatitis B reinfection during the first 6 months after liver grafting. Twelve months after the transplantation the new liver was reinfected with hepatitis B virus. Without any clinical or laboratory signs of severe hepatitis, the patient developed a histologically proven complete liver cirrhosis within 8 months after reinfection of the graft. The reasons for this might have been, first, a deleterious course of the infection under immunosuppressive therapy, and, second, the additional influence of a postoperatively acquired CMV infection or the combined toxic influence of cyclosporin A and its metabolites on the acute inflammation in the liver.Abbreviations ALT Alanine aminotransferase (EC No 2.6.1.2) - AST Aspartate aminotransferase (EC No 2.6.1.1) - CMV Cytomegalo virus - EBV Ebstein-Barr virus - ELISA Enzyme linked immunosorbentassay - HBV Hepatitis B virus - HLA Human leukocyte antigen - HSV Herpes simplex virus     

Prevalence of occult HBV infection in Western countries

Due to a lack of standardized tests, it is difficult to obtain prevalence data and define the real impact of occult HBV infection (OBI) in Western countries. The present review article addresses the prevalence of OBI, defined as presence of hepatitis B virus (HBV) DNA in liver tissue or plasma in HBsAg-negative subjects, in Western countries. This varies in different studies according to the different methodologies used (based on serology vs virology), to the sample analyzed for the diagnosis (liver tissue vs plasma), to the different populations studied, to the different geographical variations in the HBV spread, to the host characteristics (age, gender, risk factors for acquiring HBV infection) and to the presence of other parenteral infections (hepatitis C virus and/or human immunodeficiency virus [HIV] infections). Considering the different liver diseases analyzed, that is in patients with cryptogenic cirrhosis or advanced liver fibrosis, the prevalence of OBI ranges 4% to 38%. Considering the different populations studied, in the case of parenteral blood exposure it is about 45%, in patients with chronic hepatitis C it is estimated at about 52%, in HIV-infected patients it ranges from 0% to 45%, in blood donors from 0% to 22.7% and in hemodialysis patients it ranges from 0% to 54%. In conclusion, OBI is a virological entity to be considered when performing the patient's evaluation for immunosuppressive diseases, liver pathologies, or for blood transfusions. Knowing the prevalence and clinical impact of OBI will allow better patient management.