急性血吸虫病患者HBsAg(RPHA)假阳性反应的观察

采用RPHA法对41例急性血吸虫病患者检测HBsAg,阳性率高达70.73％(29/41)。对RPHA法阳性的29例患者血清用ELISA法检测HBsAg、抗HBs、抗HBc、HBeAg、抗HBe等5项HBV感染血清标志物,HBsAg(ELISA)阳性率12.20％(5/41)。ELISA法HBsAg阳性的5例中有4例同时伴有抗HBe、抗HBc阳性,另1例仅抗HBc阳性:而HBsAg在ELISA法阴性,RPHA法阳性患者的血清无1例查出HBV感染的其它4项标志物。     

急性乙型肝炎病毒感染小鼠模型的建立

目的采用尾静脉液压法建立小鼠急性HBV感染的动物模型。方法以液压法将具有复制能力的HBV质粒pAAV-HBV1.2通过尾静脉注射到免疫功能正常的BALB/c小鼠体内,注射后第1、2、4、6、8d,分别采用改良赖氏法、时间分辨免疫荧光法、实时荧光定量PCR检测小鼠血清中谷丙转氨酶(ALT)、HBsAg、HBeAg、抗HBs、抗HBe、HBV DNA的水平,免疫组化检测肝组织HBsAg、HBcAg的表达。结果16只小鼠注射pAAV-HBV1.2后,有14只(85.7%)小鼠在注射后第1d血清中可检测到HBsAg,小鼠血清中HBsAg和HBeAg水平在第1d达高峰,之后逐渐下降,第8d均未能检测到。小鼠血清中HBV DNA在第2d达高峰,之后仍维持在较高水平,至第8d时为1.9×104copies/mL。至第8d肝组织中可见约5%的HBcAg阳性肝细胞和2%的HBsAg阳性肝细胞。结论采用尾静脉液压法成功的建立了小鼠急性HBV感染的动物模型。     

慢性乙型肝炎血清标志物少见模式分析

HBV感染后血清标志物的模式表现呈多样化。本科血清免疫室2004年共检测到42例少见模式，占阳性总例数的0．6％（42／6744）。其中HBsAg（-）、抗HBs（-）、HBeAg（＋）、抗HBe（-）、抗HBc（＋）者33例，HBsAg（＋）、抗HBs（-）、HBeAg（＋）、抗HBe（＋）、抗HBc（＋）者9例。更换不同厂家试剂检得相同结果。HBVDNA．PCR检测42例均呈阳性。笔者分别对上述2种少见模式的HBsAg（-）（P／N0．1～2．0）和抗HBe（＋）（抑制率0．6～0．8））作进一步检测分析。     

抗—HBs阳性不同血清学模式病毒学及临床意义分析

目的：通过对抗－HBs阳性不同血清学模式病毒学和临床意义的分析,了解抗－HBs阳性不同血清学模式特点,探讨其形成机理及抗－HBs的作用。方法：采用Abbott和PCR定量、PCR定性方法分别检测抗－HBs阳性不同血清学模式病人的HBV血清标志物和HBV DNA。结果：抗－HBs、抗－HBe、抗－HBc阳性组与其它模式组比较,其抗－HBs值显著升高（P＜0．05）;HBsAg、抗－HBs、HBeAg阳性组与其它模式组比较,其HBV DNA含量显著增高（P＜0．01）;定性检测HBV DNA阳性组与HBV DNA阴性组比较抗－HBs值,前者抗－HBs值显著降低（P＜0．05）;抗－HBs阳性不同血清学模式病人生化指标比较无显著性差异（P＞0．05）;抗－HBs阳性不同血清学模式病人比较其肝炎临床类型的构成有非常显著性差异（P＜0．005）：即抗－HBs、抗－HBe、抗－HBc阳性组主要表现为急性肝炎,HBsAg、抗－HBS、HBeAg阳性组与HBsAg、抗－HBs阳性组主要表现为慢性肝炎。结论：抗－HBs阳性时HBV处于复制水平,但并不标志HBV复制的停止,仅预示病人感染相和恢复相的动态消长过程。如抗－HBs水平不断提高,则感染相向稳定的恢复相发展。同时从肝功能损伤的程度及肝炎临床类型分析,提示抗－HBs引发的免疫效应最终使部分病人由感染相进入恢复相。     

132例HBeAg阳性HBsAg阴性的乙型肝炎患者HBV-M演变结果分析

目的:了解某些乙型肝炎患者HBsAg阴性,HBeAg阳性特殊感染模式的不稳定性,分析其产生的可能原因。方法:对符合主题的132例乙型肝炎患者,用ELISA法检测、复查血清乙肝病毒标志物(HBV-M)。结果:132例HBsAg阴性、HBeAg阳性患者入院时抗-HBc阳性123例、HBV DNA阳性65例(49.2％)。第1次复查有75例HBsAg转为阳性,16例抗HBs阳性、60例HBeAg阳性、65例抗HBe阳性、131例抗HBc阳性。第2次复查HBsAg阳性83例、抗-HBs阳性15例,HBeAg阳性78例、抗-Hbe阳性53例、抗-HBc阳性131例,HBV DNA阳性69例(52.27％)。结论:这种乙肝病毒感染的特殊模式很不稳定,大部分可以转变为HBsAg阳性,一小部分确也可以转变成抗-HBs阳性。     

乙型肝炎患者胃粘膜中HBcAg和HBVDNA表达分析

目的 探讨乙型肝炎患者胃粘膜中是否有HBcAg和HBVDN的存在。方法 随机选择120例乙型肝炎患者并对其行胃粘膜活检。采用ELISA法检测其静脉血HBVM，采用免疫组织化学SP法检测其胃粘膜中的HBcAg，采用原位分子杂交法检测其胃粘膜中的HBVDNA。结果 乙型肝炎患者胃粘膜中有HBcAg和HBVDNA的存在，主要呈胞浆型分布，少数在胃粘膜腺细胞胞核上表达。胃粘膜腺腔、胃小凹及间质中也可见HBcAg和HBVDNA颗粒。血清HSsAg合并HBeAg和抗HBc阳性、HBsAg和抗—NBe及抗—HBc均阳性与抗—HBc阳性或HBsAg阳性或抗HBe阳性，但HBeAg阴性者的乙型肝炎患者胃粘膜中HBcAg、HBVDNA阳性率比较，差异无显著性(P＞0．05)。结论 乙型肝炎患者胃粘膜中有HBcAg和HBVDNA的存在，与其血清中HBV复制状态不相关。     

慢性乙型肝炎患者血清HBV复制标志物与肝组织HBsAg和HBcAg抗原表达的相关性研究

目的探讨血清HBV复制标志物与肝组织HBsAg和HBcAg抗原表达的相关性。方法用免疫组化法检测肝组织HBsAg、HBcAg,与血清HBeAg和/或HBV DNA进行相关性比较。结果血清HBeAg阳性与阴性组中肝组织HBsAg阳性率无显著性差异,而血清HBeAg阳性者肝组织HBcAg阳性率显著高于HBeAg阴性者;血清HBV DNA阳性与阴性组中肝组织HBsAg阳性率无显著性差异,但血清HBV DNA阳性者肝组织HBcAg阳性率显著高于HBV DNA阴性者。结论血清HBeAg和HBV DNA水平与肝组织HBcAg阳性率呈正相关。     

乙型肝炎病毒核酸定量检测与临床的关系

目的：探讨血清HBV DNA水平与HBV标志（HBV M）表现模式，肝功能状态，肝内炎症的关系。方法：对219例排除甲，丙，丁和戊型肝炎病毒的混合与重叠感染患者中的HBsAg阳性的慢性乙型肝炎患者进行肝穿刺病理检查。HBV DNA定量采用荧光定量PCR分析系统，HBV M采用ELISA法。结果：血清HBV DNA水平与HBVM表现模式有关，HBsAg与HBeAg的存在影响HBV DNA水平变化。在HBsAg阳性患者中，HBV DNA水平与Scheuer分级无明显相关。血清谷丙转氨酶水平与HBV DNA水平无明显相关。结论HBeAg和HBV DNA有明显的相关，抗－HBe阳性者病毒未完全停止复制，只是复制水平降低。单抗HBe阳性，单抗HBc阳性，抗HBs阳性和抗HBc阳性未检出HBV DNA，肝内炎症活动程度与血清HBV DNA水平无明显关系。     

HBV前S1抗原在乙型肝炎临床诊断中的意义

目的探讨乙型肝炎(乙肝)病毒前S1抗原在乙肝病毒感染中的临床意义。方法分析1088例HBV前S1抗原阳性结果与乙肝5项病毒学指标和HBV DNA结果的关系。结果前S1抗原阳性的乙肝5项病毒学指标结果出现6种模式,其中HBsAg、HBeAg、抗HBc阳性患者的前S1抗原阳性率为88.74%;HBsAg、抗HBe、抗HBc阳性患者前S1抗原阳性率为41.32%,2组间有显著差异(P<0.05),而HBsAg及抗HBc阳性组前S1抗原阳性率介于HBsAg、HBeAg、抗HBc阳性组与HBsAg、抗HBe、抗HBc阳性组之间。HBsAg、HBeAg、抗HBc阳性患者前S1抗原阳性率随着HBV DNA载量的升高而增加(各组间P<0.05)。HBeAg、前S1抗原与HBV DNA三者间有很好的一致性。结论检测前S1抗原是对HBsAg、HBeAg及HBV DNA检测的重要补充。在防止乙肝漏诊、误诊及了解疾病的转归等方面都具有重要的临床意义。     

隐匿性乙型肝炎

随着分子生物学技术在病毒检测技术中的应用 ,近年来发现部分复制水平较低的乙型肝炎病毒携带者血清中检测不到HBV表面抗原 (HBsAg) ,这种感染状态可发生于抗HBs或抗HBc阳性的患者 ,也可见于HBV标志物全阴性的患者 ;部分HBsAg阴转的急性或慢性乙肝患者 ,其血清中仍可检测出低水平HBV -DNA或肝组织中检测出HBsAg或HBcAg,这种患者被称为HBV隐匿感染[1] 。HBsAg阴性的HBV感染与许多临床情况有关 ,由于HBsAg阴性HBV感染难以用常规方法检出 ,成为较复杂的流行病学和临床问题。1　隐匿性HBV感染的发生机制隐匿性HBV感染的发生…     

Low rate of occult hepatitis B virus infection among anti-HBc positive blood donors living in a low prevalence region in Brazil

OBJECTIVE: The aim of this study was to determine the rate of occult hepatitis B virus (HBV) infection among blood donors living in a geographic region of low (5.6%) anti-HBc prevalence. SUBJECTS AND METHODS: Sera from 150 candidate blood donors whose blood was rejected due to total anti-HBc reactivity (despite absence of HBsAg) were tested for anti-HBs and IgM anti-HBc antibodies, as well as for HBeAg/anti-HBe. Serum HBV DNA was sought by using a PCR assay able to amplify part of the surface gene. Viral load was measured in the PCR positive samples. RESULTS: The pattern 'anti-HBc alone' (without HBsAg and anti-HBs antibodies) was found in 64 (42.7%) subjects. IgM anti-HBc and anti-HBe antibodies were detected in 2 (1.3%) and 80 (53.3%) samples, respectively. No sample was HBeAg-reactive. HBV DNA was repeatedly found in five (3.3%) samples, three of which were anti-HBs positive and two anti-HBs negative. All five HBV DNA positive samples showed a low viral load (<1000copies/ml). CONCLUSIONS: The data indicated a low rate of occult infection among anti-HBc positive, HBsAg negative blood donors living in a region of low prevalence of infection. Viral load was very low in all HBV infected subjects.     

Changes in levels of hepatitis B virus markers in patients positive for low-titer hepatitis B surface antigen

Aim: Recently, patients positive for the low-titer hepatitis B surface antigen (HBsAg) have been found occasionally owing to the increase in the accuracy of detection methods. The aim of this study is to clarify the clinical status of acute hepatitis B virus (HBV) infection in patients positive for low-titer HBsAg. Method: Eight patients, who were positive for HBsAg at low titers and diagnosed as having acute HBV infection, were enrolled in this study. Assays of HBsAg, hepatitis B core antibody (anti-HBc), hepatitis B e-antigen (HBeAg), hepatitis B e-antibody (anti-HBe), hepatitis B surface antibody (anti-HBs) and HBV DNA, and biochemical tests were basically conducted every 4 weeks for at least 24 weeks. Result: The average cut-off index of HBsAg was 8.7 ± 9.6 (range, 1.0–25.7). All the patients were negative for anti-HBc, HBeAg, anti-HBe and HBV DNA on their initial visit. The genotype of HBV could be determined in four patients: two were infected with genotype B/HBV, one was infected with genotype A/HBV, and the remaining patient was infected with genotype C/HBV. Although HBsAg clearance was observed within 4 months in all the patients, none of the other HBV markers seroconverted during the observation period. Conclusion: HBV infection terminating with seronegativity for HBV markers may occur in transient HBV infection.     

乙型肝炎病毒转基因小鼠免疫耐受状态及血液生物化学指标的研究

目的 了解HBV转基因鼠HBV基因的复制表达和免疫耐受状态,为探讨乙型肝炎发病机制和抗HBV新药评价提供可靠的参考依据.方法 选取遗传背景相同的SPE级HBsAg阴性非转基因鼠和转基因鼠.化学发光法检测HBsAg、HBeAg、HBV DNA,ELISA检测前S1、HBcAg,肝组织行病理学检查,免疫组织化学染色检测不同时期转基因鼠肝HBsAg表达,流式细胞仪检测小鼠淋巴细胞增殖情况,酶联免疫斑点检测(ELISPOT)分泌IFNγ的T淋巴细胞斑点数,双色免疫荧光法检测脾细胞悬液和脾树突状细胞(DC)中Toll样受体(TLR)2和TLR9的表达.数据行t检验和F检验.结果 HBV转基因鼠可复制表达HBsAg、前S1、HBeAg、HBcAg和HBVDNA,而抗-HBs、抗-HBc、抗-HBe均阴性;肝组织无明显病理改变,肝细胞中HBsAg在胞质表达,HBcAg在胞核表达.HBsAg刺激后,HBV转基因鼠T淋巴细胞增殖能力为(697.6±67.3)cpm,显著低于非转基因鼠的(1315.5±191.6)cpm.经HBsAg刺激后,HBV转基因鼠脾细胞分泌IFNγ的T淋巴细胞斑点数为8.25±1.10,低于非转基因鼠的28.50±4.21(F=155.967,P=0.000).HBV转基因DC表达CD11c+、TLR2和TLR9与非转基因鼠比较,差异无统计学意义(均P＞0.05).在18日龄胎鼠和1日龄仔鼠肝组织观察到HBsAg表达.结论 HBV转基因鼠有HBV相关抗原表达,并对HBV相关抗原存在免疫耐受,其先天和获得性免疫功能均正常,类似于人类慢性HBV无症状携带者.HBV转基因鼠是比较理想的动物模型.     

重庆地区无偿献血人群隐匿性乙型肝炎病毒感染的特征

目的了解重庆地区无偿献血人群中隐匿性乙型肝炎病毒感染(occult hepatitis B virus infection,OBI)情况,分析其血清学和病毒学特征。方法应用酶联免疫法(筛查HBs Ag、抗-HCV、抗-HIV)及核酸检测(nucleic acid testing,NAT)法(筛查HBV、HCV、HIV)筛查重庆地区93 625份初筛合格的无偿献血者血液标本。对其中HBs Ag(-)但HBV DNA(﹢)的标本进行抗-HBs、抗-HBc、HBe Ag、抗-HBe 4项血清学标志物测定,进一步对抗-HBc(﹢)标本做病毒载量测定以及基因分型。结果 93 625份标本中HBs Ag(-)但HBV DNA(﹢)的检出率为0.097%(91/93 625)。91份阳性标本中79份为抗-HBc(﹢),检出率为0.084%(79/93 625)。该部分标本阳性者被视为OBI献血者。OBI献血者的血清学特征可以分为4种模式:单抗-HBc(﹢)、抗-HBc(﹢)/抗-HBs(﹢)、抗-HBc(﹢)/抗-HBe(﹢)以及抗-HBc(﹢)/抗-HBs(﹢)/抗-HBe(﹢)。病毒载量为0~1056.8IU/ml(中位数为108.6 IU/ml),基因型以B型为主。结论重庆地区无偿献血者中OBI检出率较高,其血清学和病毒学特征具有地区性。NAT能提高OBI检出的灵敏度,但也存在一定的假阳性,对血液安全具有重要影响。     

Serologic and Molecular Profile of Anti-HBc-Positive Blood Bank Donors in an Area of Low Endemicity for HBV

Hepatitis B virus (HBV) infection leaves serological markers that indicate prior contact with the virus or an occult infection. The aim of this study was to determine the profile of HBV markers of individuals from a region of low HBV endemicity excluded from blood donation due to the presence of total anti-HBc antibodies but who tested negative for HBV surface antigen (HBsAg). The profile of 244 subjects exclusively anti-total hepatitis B core (anti-total HBc) reactive was determined. Markers such as anti-HBsAg, HBeAg (HBV core antigen) and anti-HBe (antibody to hepatitis Be antigen) were determined, and HB viral DNA (HBV-DNA) was identified by PCR analysis. Overall, 85.7% of the subjects had an anti-HBs (hepatitis B surface antigen antibody) titer higher than 10 IU/L; 154 samples were negative for HBeAg and 66.5% were reactive for anti-HBe. All samples were negative for HBV-DNA (n = 241). We found a significant association between the anti-HBe and anti-HBs titers (P = 0.026). Most individuals from a low endemic area for HBV have shown anti-HBs titers that confer immunity against HBV, even though they were negative for HBV-DNA. In the light of a shortage of donated blood worldwide, we suggest that special measures should be considered that would facilitate the possible use of these rejected blood units in areas of low endemicity for HBV.     

Differential distribution of hepatitis B core and E antigens in hepatocytes: analysis by monoclonal antibodies

Current knowledge on the expression of HBeAg in hepatocytes is incomplete because of difficulties in obtaining monospecific antisera devoid of anti-HBc reactivity. In this study, we have examined by immunofluorescence the expression of HBcAg and HBeAg in cryostat liver sections from 25 chronic carriers of HBsAg using monoclonal antibodies. Although virtually all liver biopsies displayed concordance for HBeAg and HBcAg expression, the pattern of fluorescence differed markedly. Thus, monoclonal anti-HBc gave nuclear staining in all 13 reactive biopsies, while cytoplasmic staining was observed in only two of these. In contrast, monoclonal anti-HBe showed cytoplasmic reactivity coexisting with nuclear reactivity in 10 of 13 reactive biopsies. Hepatitis B virus DNA polymerase activity in the serum appeared to correlate better with the presence of HBcAg in hepatocytes rather than HBeAg. These results provide further evidence that HBeAg is expressed both in the nuclei and in the cytoplasm of infected hepatocytes. The observation that the number of cells expressing HBeAg exceeds those expressing HBcAg in carriers with active virus replication would suggest that assembly of core particles occurs in only a proportion of infected hepatocytes expressing HBeAg.     

Latent hepatitis B virus infection with full-length viral genome in a patient serologically immune to hepatitis B virus infection

The presence, state, physical structure and cellular localization of hepatitis B virus (HBV) DNA were investigated in a patient with hepatitis B surface antigen (HBsAg)-negative chronic liver disease. HBV serology was positive for antibodies to hepatitis B core antigen (anti-HBc), to hepatitis B e antigen (anti-HBe) and to HBsAg (anti-HBs); no HBV DNA was detectable in serum. Southern blot analyses of DNA extracted from the liver demonstrated free monomeric HBV DNA as two distinct species: a predominant species of fully double-stranded relaxed circular molecules and a minor species of linear molecules of 3.2 kilobase pairs (kbp) length. Restriction enzyme analyses identified the HBV genome as HBsAg subtype adw2. Cell fractionation studies further revealed that the free viral DNA species were localized exclusively in liver cell nuclei. These findings in a patient serologically immune to HBV infection demonstrate that in hepatocytes HBV can establish a latent infection, characterized by the extrachromosomal presence of a full-length viral genome without production of infectious virus or synthesis of viral antigens.     

Histopathological analysis of chronic hepatitis B virus (HBV) infection in relation to HBV replication

The interrelationship among expression patterns of hepatitis B surface and core antigens (HBsAg and HBcAg) in the liver, hepatitis B virus (HBV) DNA in sera, HBeAg/anti-HBe status and histological features was examined in 189 liver specimens and 106 sera from Japanese patients with chronic HBV infection, utilizing immunoperoxidase methods and a spot hybridization technique. HBsAg and HBcAg were distributed uniformly among the lobules in 8 viral carriers with "normal" liver (NVC) and 30 patients with persistent hepatitis (PB) seropositive for HBcAg. This uniform staining pattern was quite distinct from the non-uniform and irregular patterns in 137 patients with chronic active hepatitis (CAH) associated with or not associated with cirrhosis. HBcAg was often found to be stained strongly in the cytoplasm as well as in the nucleus of hepatocytes in HBeAg-positive CAH, in contrast to NVC/PH, in which cytoplasmic HBcAg was very weak. Serum HBV DNA was detected in all 22 cases with HBeAg-positive NVC/PH, 41 of 46 (89.1%) cases with HBeAg-positive CAH, 6 of 23 (26.1%) casew with anti-HBe-positive CAH and none of 3 cases with anti-HBe-positive NVC/PH. The level of serum HBV DNA and staining of HBcAg were in decreasing order in these groups. While the presence of serum HBV DNA and HBcAg staining was always associated with HBeAg seropositivity in NVC/PH, this was not always found in CAH. Moreover, necroinflammatory activity in the liver did not always parallel viral replication in CAH. These findings seem to confirm that NVC/PH and CAH have different biologic processes; viral replication is always concordant in the former, but is sometimes discordant in the latter with HBeAg/anti-HBe status. The immunologic response of the host seems to suppress and distort replication of the virus to a varying degree among patients and areas of the same liver in CAH differently to that in NVC/PH. The different life cycle of the virus, including integration of viral DNA into the cellular genome, may subsequently result in discordant states of various virus markers in CAH.     

A novel stop codon mutation in HBsAg gene identified in a hepatitis B virus strain associated with cryptogenic cirrhosis

AIM: HBsAg is the most important serological marker for acute or chronic hepatitis B. Nevertheless, there were reports of HBsAg-negative infection caused by hepatitis B virus in recent years. We had a patient with crytogenic cirrhosis who was negative for HBsAg, positive for anti-HBs and HBeAg.This paper was to explore the pathogenic and molecular basis of the unusual serological pattern.METHODS: HBV serologic markers were qualitatively and quantitatively determined. HBV DNA in serum was qualitatively tested using routine Polymerase chain reaction (PCR), and the viral level was determined with real-time fluorescence quantitative PCR. HBsAg gene was amplified and cloned. Four clones were sequenced. The new genomic sequences were compared with GenBank on the DNA level as well as the protein level.RESULTS: The qualitative results of serological markers were HBsAg(-), anti-HBs(+), HBeAg(+), anti-HBe(-) and anti-HBc(+). The quantitative results of serological marker were HBsAg (S/N): 0.77 (cut off of S/N: ≥2.00), HBeAg (S/N): 56.43 (cut off S/N: ≥2.10), anti-HBc (S/Co): 2.03 (cut off of S/Co: ≤ 1.00). The viral level was as high as 1.54×109copies/ml. Sequencing of the HBsAg gene clones revealed a unique point mutation at nucleotide 336 (C to A), which resulted in a novel stop codon at aa 61. The novel HBsAg gene stop mutation had not been described.CONCLUSION: The lack of detection of HBsAg in the presence of high viral levels of replication may be caused by the existence of viral genomes harboring point mutations which resulted in stop codon upstream of the″a″ determinant in HBsAg gene.     

Hepatitis B virus markers in peripheral blood mononuclear cells]

Recent studies have shown tropism of the hepatitis B virus (HBV) by peripheral blood mononuclear cells (PBMC). The consequences of this phenomenon and their clinical use are not yet clear, however. Seventy-nine patients were studied between March 1989 and October 1990. Sixty-nine patients had chronic liver disease with histological evaluations, and 10 were vaccinated for HBV. The following markers were determined: serum: HBsAg, HBeAg, anti-HBe, antitotal-HBc, anti-HBs, anti-HCV, HBV-DNA; lysated PMBC cells: HBsAg, HBeAg. Hepatic tissue: HBsAg, HBcAg. Four groups were formed according to serology. Group I--positive HBsAg patients (n = 25) HBsAg was observed in the lysated of PBMC in 19 (76%) of the patients. HBeAg in PBMC was detected in 8 (32%), all of them showed evidence of viral replication (presence of HBcAg and/or HBV-DNA in the serum HBcAg in the tissue). Group II--antitotal HBc/anti-HBs positive (n = 14), HBsAg in PBMC was found in 5 (36%) and HBeAg in 1 (7.0%). In this patient replication markers in the serum and in the tissue (HBV-DNA, HBcAg) was also present. Three patients out of 9 anti-HBs positive had HBsAg in PBMC. Group III--seronegative patients for HBV. HBsAg was present in PBMC in 2 (6.6%) of the patients, but was absent in all of them. There was concomitant presence of HBsAg in MN and the hepatic tissue in 1 patient. Replication markers were not observed in the group. Group IV--10 asymptomatic individuals vaccinated for HBV. Except anti-HBs in serum, no other HBV marker could be identified in serum or in PBMC.(ABSTRACT TRUNCATED AT 250 WORDS)