乙型肝炎病毒携带者的肝脏病理学特点

目的研究慢性HBV携带者和非活动性HBsAg携带者的肝脏组织病理改变。方法对219例HBsAg阳性且血清ALT持续正常6个月以上的HBV携带者进行了肝组织病理学和免疫组织化学检查,同时检测血清HBV DNA和HBV血清标记物,研究HBV携带者肝组织炎症和纤维化的发生率和程度,分析感染者组织学改变与血清病毒水平、HBeAg及年龄的关系。结果HBV携带者中95．0％（208／219）肝脏组织学有改变,其中轻度炎症和（或）纤维化（G0～1／S0～1）者占50．0％（104／208）,有8．7％（18／208）炎症活动度和（或）纤维化程度在3级（期）或以上。炎症活动度和纤维化程度的分布在慢性HBV携带者与非活动性HBsAg携带者两组间比较,差异无统计学意义;在慢性HBV携带组中,以HBeAg阳性和阴性分层分析,炎症活动度在两组间差异无统计学意义,但纤维化性程度在HBeAg阴性组严重于HBeAg阳性组（χ^2=9．551,P〈0．05）;不同年龄组炎症活动度和纤维化程度总体上差异无统计学意义,但40岁以上年龄组S3～4占21．1％,18岁以下年龄组S3～4仅占7．7％。免疫组织化学检查219例HBsAg全部阳性,HBcAg在慢性HBV携带者组均是阳性,在非活动性HBsAg携带者组中10例阳性（33．3％）。结论绝大部分HBV携带者存在不同程度肝脏炎症和纤维化,其中约50％为轻度改变,8．6%炎症和（或）纤维化程度在3级（期）或以上。炎症活动度和纤维化程度与血清病毒水平无显著相关。     

HBV carriers and HDV superinfection--studies on the cases of HBsAg clearance

We studied the annual clearance rates of hepatitis B surface antigen (HBsAg) and the annual seroconversion rates of HBsAg (HBs seroconversion rates), and the correlation between HBsAg clearance and hepatitis delta virus (HDV) superinfection in hepatitis B virus (HBV) carriers in Japan. Out of 1,029 HBV carriers followed for more than 36 months, 56 cases were cleared of HBsAg from the sera, and 24 of these cases developed hepatitis B surface antibody. The annual clearance rate of HBsAg was 0.94% and the annual HBs seroconversion rate was 0.27%. These rates increased with aging, especially above 30 years of age. Antibody to HDV was detected in three cases with increased serum alanine aminotransferase activity preceding HBsAg clearance. These data indicate that HDV superinfection may play a role in induction of the HBsAg clearance in HBV carriers in Japan.     

Serological and tissue markers of HBV infection in chronic active hepatitis patients and in healthy carriers of HBsAg

Summary We studied serological and tissue markers of Hepatitis B virus (HBV) infection in seven healthy carriers of HBsAg and in 58 patients with chronic active hepatitis (CAH), of whom 20 were HBsAg positive and 38 HBsAg negative. Surface antigen was found as the only marker of HBV infection in the liver tissue of all healthy carriers and HBsAg positive in 40% of the CAH patients. Core antigen was detected only in CAH patients: 7/20 HBsAg positive (in two alone and in five together with HBsAg) and 5/38 HBsAg negative (four with circulating anti-HBs and anti-HBc and one with only anti-HBc). All the healthy carriers of the surface antigen presented HBsAg in the liver as the only marker of HBV. Furthermore, all healthy carriers were found to be anti-HBe positive, whereas in the 16 HBsAg positive CAH patients examined for the e system, HBeAg and anti-HBe were found with the same frequency (43.7%). Of the 33 HBsAg negative CAH patients examined, anti-HBe was present in four who also had circulating anti-HBc and anti-HBs. In HBsAg positive CAH patients core antigen was found in the liver tissue of 4/7 HBeAg positive cases and in 2/7 anti-HBe positive, while surface antigen was detected in 3/7 HBeAg positive, 5/7 anti-HBe positive and in the two HBeAg/anti-HBe negative individuals. In HBsAg negative CAH patients, surface antigen was never found in the liver tissue; core antigen was detected, however, in five who had circulating anti-HBc (one in the presence and four in the absence of anti-HBe). In conclusion, from these data it would appear that the various serological patterns of HBV infection, particularly as concerns the presence of antibodies and presence or absence of HBsAg, are not invariably able to predict whether or not HBV antigens are present in liver tissue or, in other words, if active replication does occur.

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Serologische und Gewebe-Marker für die HBV-Infektion bei Patienten mit chronisch aktiver Hepatitis und gesunden Trägern von HBsAg

Zusammenfassung Wir haben serologische und Gewebe-Marker für die Hepatitis-B-Virus (HBV) Infektion bei sieben gesunden Trägern von HBsAg und 58 Patienten mit chronisch aktiver Hepatitis (CAH) geprüft, von denen 20 HBsAg positiv und 38 HBsAg negativ waren. Es zeigte sich, daß das Oberflächenantigen als einziger Marker der HBV-Infektion im Lebergewebe aller gesunden Träger positiv war und bei 40% der CAH-Patienten nachgewiesen werden konnte. Das Core Antigen wurde nur bei CAH-Patienten entdeckt: bei 7/20 HBsAg positiven Fällen (davon zweimal allein und fünfmal zusammen mit HBsAg) und bei 5/38 HBsAg negativen Kranken (viermal zusammen mit zirkulierendem anti-HBs und anti-HBc und einmal nur mit anti-HBc). Alle gesunden Oberflächenantigen-Träger wiesen in der Leber ausschließlich HBsAg als HBV-Marker auf. Es zeigte sich außerdem, daß alle gesunden Carrier anti-HBe positiv waren; dagegen konnten bei den 16 HBsAg positiven CAH-Patienten, die bezüglich des e Systems überprüft wurden, HBeAg und anti-HBe gleich häufig nachgewiesen werden (43,7%). Anti-HBe fand sich bei vier der 33 HBsAg negativen Patienten mit chronisch aktiver Hepatitis, sie wiesen gleichzeitig zirkulierendes anti-HBc und anti-HBs auf. Im Lebergewebe der HBsAg positiven CAH-Patienten wurde das Core Antigen bei 4/7 HBeAg positiven und bei 2/7 anti-HBe positiven Fällen gefunden; das Oberflächenantigen ließ sich bei 3/7 HBeAg positiven, bei 5/7 anti-HBe positiven und bei zwei HBeAg/anti-HBe negativen Kranken nachweisen. Bei HBsAg negativen Patienten mit chronisch aktiver Hepatitis wurde das Oberflächenantigen niemals im Lebergewebe gefunden. Hingegen entdeckten wir Core Antigen bei fünf Fällen, die zirkulierendes anti-HBc aufwiesen (in einem Fall gleichzeitig mit und viermal ohne den Nachweis von anti-HBe). Aus diesen Befunden könnte man schließen, daß die verschiedenen serologischen Muster der HBV-Infektion, insbesondere die Anwesenheit von Antikörpern und Vorhandensein oder Fehlen von HBsAg, nicht ausnahmslos geeignet sind, eine Voraussage zu treffen, ob sich HBV-Antigene im Lebergewebe befinden, das heißt, ob eine aktive Virusreplikation stattfindet.

     

Dilemma of HBsAg seroconversion in chronic hepatitis B infection: Dilemma of HBsAg in chronic HBV

Patients with chronic hepatitis B infection should be followed up to identify possible changes in disease status, such as HBsAg seronversion. There are little data on the outcome of such cases, and the response rate to HBV vaccine has not been discussed extensively.     

Correlation between HBsAg quantitative assay results and HBV DNA levels in chronic HBV

Background

Viral load has been used to diagnose and monitor patients who are being treated for chronic hepatitis B (CHB). The Diagnosis methods are molecular-based and expensive. Quantitation of hepatitis B surface antigen (HBsAg) by automated chemiluminescent micro-particle immunoassay has been proposed to be a surrogate marker. Quantitating HBV DNA levels molecularly is expensive; thus, a cheaper laboratory test as a surrogate diagnostic marker might simplify our management.

Objectives

We determined whether quantitative HBsAg levels correlate with HBV DNA levels in CHB.

Patients and Methods

In this cross-sectional study, all CHB patients who were referred by a gastroenterologist to undergo quantitative HBV DNA assay in a qualified laboratory in Mashhad, Iran in 2009 were enrolled, and blood samples was obtained. Patients who were positive for antibodies to HCV and HDV were excluded. HBV DNA was measured by real-time polymerase chain reaction, and serum HBsAg was quantified byelectrochemiluminescence assay (Roche Diagnostic).

Results

Of 97 patients, 70 were male (72%) and 27 were female (28%); the mean age was 39 ± 11 years. Eighty-seven percent wasHBeAg-negative. By Mann-Whitney test,HBSAg titer differed significantly between HBeAg-positive and -negative patients (P = 0.001), as did HBV DNA levels (P = 0.009). By Spearman test, there was no significant correlation between HBsAg and HBV DNA levels (P= 0.606 and r = 0.53).

Conclusions

HBeAg-negative patients have higher levels of HBsAg and lower levels of HBV DNA. By electrochemiluminescence assay,HBsAg has no significant correlation with HBV DNA levels in CHB with predominant genotype D and HBeAg negativity in Iran.     

慢性HBsAg携带者及非活动性HBV感染状态的病理学研究

目的观察临床诊断为慢性HBsAg携带者及病理诊断为非活动性HBV感染状态患者的临床病理特点。方法总结慢性HBsAg携带者41例、非活动性HBV感染状态患者65例的临床资料,通过HE、组织化学及免疫组织化学染色观察其肝穿刺组织切片的病理变化。结果慢性HBsAg携带者41例无明显异常的症状体征,各项肝功能检查基本正常;但肝穿组织病理检查仅有10例无明显病变,30例为轻度慢性乙型肝炎,1例为静止性肝硬化。非活动性HBV感染状态患者65例中,少数患者有较轻的肝功能异常改变;病理检查无明显炎症和纤维化。结论慢性HBsAg携带者主要是一组以轻度慢性乙型肝炎表现为主的患者,非活动性HBV感染状态患者也仅有轻度的肝功能异常;慢性HBsAg携带者及非活动性HBV感染状态是临床医师和病理医师对同一类病变的不同诊断用词,对其诊断应结合临床和病理资料综合判断。     

Interaction between HDV and HBV infection in HBsAg-chronic carriers

Summary We studied the interaction between HBV and HDV infection in 149 consecutive subjects with HBsAg positive chronic hepatitis and in 22 chronic HBsAg healthy carriers. Liver HBcAg was detected in 52 (30.4%) of the 171 subjects. Of these 52, 35 were HBV-DNA and HBeAg positive, 11 HBV-DNA positive only; two HBeAg positive only and four were negative for both HBeAg and HBV-DNA. None of the 119 HBcAg-negative subjects had detectable HBV-DNA in serum. HD-Ag in hepatocytes was detected in 31 of the 171 subjects (18%); it was detectable in none of the 22 HBsAg healthy carriers, in four of the 56 patients with chronic persistent hepatitis (7.2%), in six of the 24 patients with chronic lobular hepatitis (25%), in 16 of the 40 patients with chronic active hepatitis (40%) and in five of the 29 with cirrhosis (17%). A presence of anti-HD in serum in the absence of liver HD-Ag was found in 54 of the 171 subjects (32%). This condition was observed not only in patients with a progressive disease (37.7% of chronic active hepatitis or cirrhosis and 33% of chronic lobular hepatitis), but also in healthy carriers (36%) and in chronic persistent hepatitis patients (21.4%). Liver HBcAg was detected in 6.4% of the 31 HD-Ag-positive patients, in 12.9% of the 54 HD-Ag-negative/anti-HD positive, but in 50% of the 86 with no marker of HDV infection. HDV appears to inhibit HBV genome and such inhibition may persist even when anti-HD is the only HDV marker detectable.

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Interaktionen zwischen HDV und HBV bei chronischen HBsAg-Trägern

Zusammenfassung Bei 149 nacheinander eingewiesenen chronischen HBsAg-positiven Patienten mit chronischer Hepatitis und 22 gesunden HBsAg Trägern wurde die Interaktion zwischen der HBV- und HDV-Infektion untersucht. Bei 52 der insgesamt 171 Personen (30,4%) fand sich HBsAg in den Leberzellen. Bei 35 dieser 52 Fälle wurde HBV-DNA und HBeAg nachgewiesen, in 11 Fällen HBV-DNA allein. Bei den 119 HBcAg-negativen Personen waren HBV-DNA in keinem Fall im Serum nachweisbar. Bei 31 der 171 Personen wurden HD-Ag in Hepatozyten entdeckt (18%). Die 22 gesunden HBsAg-Träger waren alle HD-Ag negativ. Von den 56 Patienten mit chronisch persistierender Hepatitis waren vier positiv (7,2%); von den 24 Patienten mit chronischer lobulärer Hepatitis sechs (25%), von den 40 Patienten mit chronisch aktiver Hepatitis 16 (40%) und von den 29 Patienten mit Zirrhose fünf (17%). 54 der 171 Untersuchten (32%) wiesen im Serum anti-HD auf, ohne daß sich HD- Ag in der Leber nachweisen ließ. Dabei handelte es sich nicht nur um Patienten mit progressivem Krankheitsverlauf (37,7% der Patienten mit chronisch aktiver Hepatitis und 33% derer mit chronischer lobulärer Hepatitis) sondern auch um gesunde Träger (36%) und Patienten mit chronisch persistierender Hepatitis (21,4%). Bei 6,4% der 31 HD-Ag positiven Patienten ließ sich HBcAg in der Leber nachweisen; positiv waren auch 12,9% der 54 HD-Ag-Negativ/anti-HD-Positiven und 50% der Personen ohne Marker für eine HDV-Infektion. Offensichtlich hemmt HDV das HBV-Genom; diese Hemmwirkung kann bestehen bleiben, auch wenn anti-HD der einzige nachweisbare Marker für eine durchgemachte HDV-Infektion ist.

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This study was supported by MURST — Cirrhosis Project, Rome, Italy.     

HBV特异性抗原对HBV携带者T淋巴细胞免疫功能的影响

目的 通过分析不同类型HBV携带者外周血单个核细胞(PBMCs)的细胞免疫功能,分析HBV抗原对其的影响,探索HBV慢性感染的机制并寻求可能的免疫治疗方法.方法 用不同的抗原和(或)细胞因子刺激培养的无症状HBV携带者PBMCs,酶联免疫吸附法检测细胞培养上清液中不同细胞因子的水平;流式细胞术检测PBMCs的细胞表型.对数据进行t检验分析和相关性分析.结果 HBsAg刺激无症状HBV携带者PBMCs后产生的干扰素(IFN)γ为(48.3±19.8)Pg/ml,较健康对照人群低[(196.2±104.3)Pg/ml(t=3.023,P＜0.05)].HBsAg和HBcAg刺激HBeAg阳性患者PBMCs分泌的IFN y水平分别为(50.4±51.6)Pg/ml和(63.2±36.9)pg/ml,明显低于HBeAg阴性组[(86.2±42.3)Pg/ml和(101.4±32.5)pg/ml],t值分别为2.468和3.184,P值均＜0.05;HBeAg阳性患者组分泌白细胞介素(IL)-12 P70明显低于HBeAg阴性组(P＜0.05);补偿外源性IL-12可明显促进HBV携带者PBMCs分泌IFN γ(P＜0.01),IL-12协同HBV抗原可激活CD8+CD45RA+CCR7及CD8+CD45RA CD62L+细胞.结论 HBeAg阳性患者PBMCs分泌IL-12减少,这可能是HBV携带者持续感染的重要原因;外源性IL-12可促进HBV携带者PBMCs中的中枢记忆性T淋巴细胞的免疫功能.

Abstract：

Objective To investigate the effect of HBV antigens and pathological mechanism of chronic HBV infection by analyzing the cellular immune function of peripheral blood mononuclear cells (PBMCs) from HBsAg carriers. Methods PBMCs were prepared from individuals with chronic asymptomatic HBV infection and cultured in the presence of different antigens and/or cytokines. The levels of cytokines in culture supernatants were detected by ELISA method. The phenotype of the cells was detected by FACS.Results The levels of IFN γ secreted by PBMCs from HBsAg carriers were (48.3 ± 19.8) pg/ml, significantly lower than that from healthy controls (t = 3.023, P ＜ 0.05＝; The IFN γ produced by PBMCs from HBeAg positive patients due to HBsAg and HBcAg stimulation were (50.4±51.6) pg/ml and (63.2 ± 36.9)pg/ml, significantly lower than that of HBeAg negative patients (t = 2.468 and 3.184, P ＜ 0.05, respectively＝.The IL-12p70 secreted by PBMCs from HBeAg positive patients was also significantly lower than that of HBeAg negative patients (P ＜ 0.05＝; Exogenous IL-12 promoted significantly PBMCs to secrete IFN γ (P ＜0.01＝ and IL-12 combined with HBV antigens activated CD8+CD45RA+CCR7+ and CD8+CD45RA-CD62L+cells. Conclusion IL-12 secreted by PBMCs decreased in HBeAg positive patients, which may be the crucial reason of viral persistence in chronic HBV carriers. Exogenous IL-12 combined with specific HBV antigen could promote the central memory CD8+ T cells to produce IFN γ.     

Potential infectivity of blood from HBsAg asymptomatic carriers due to the presence of HBV-DNA and comparison with other markers of HBV infection

Serum samples from 356 HBsAg positive asymptomatic carriers, which were titrated by reverse passive hemagglutination, were analysed for the presence of HBV-DNA, HBsAg and IgM anti-HBc. The samples were divided in three classes, according to the titers of HBsAg and IgM anti-HBc and the distribution of HBV-DNA and HBsAg among these classes was studied. In the high titer class of HBsAg, 65% of samples have one or both markers against only 19% in the low titer class. From the total of 356 samples, 121 gave positive results for IgM anti-HBc (33.9%). From these, 38.9% of HBV-DNA and 47.9% of HBeAg were observed, whereas in samples with absence of IgM anti-HBc, 18.3% and 16.6% were respectively found. A higher frequency of agreement between all these markers was found in the class of high titers of HBsAg; however, HBV-DNA was detected in the low titer class of HBsAg and little or no IgM anti-HBc, showing potential blood infectivity even in HBsAg positive borderline samples.     

Assessment of noninvasive liver stiffness in inactive HBsAg carriers by transient elastography: Fibroscan in inactive HBsAg carriers

Background

Chronic viral hepatitis can be evaluated using invasive or noninvasive methods.

Objectives

The aim of this study was to evaluate liver stiffness in inactive HBsAg carriers compared with normal subjects and determine if it is influenced by viral load in these patients.

Patients and Methods

We prospectively evaluated 140 inactive HBsAg carriers and 152 normal subjects (without any signs or history of liver disease). In all subjects, liver stiffness was measured by 3 experienced physicians using a FibroScan® device (EchoSens, France) per standard procedures. We excluded patients for whom the SR of liver stiffness measurements was < 60% and those who had measurements with an IQR >30%.

Results

The mean liver stiffness in inactive HBsAg carriers was 5.6±2.1kPa, significantly higher than in normal subjects (4.8 ± 1.2 kPa, p = 0.0002). In 16.4% (23) of inactive carriers, liver stiffness exceeded 7 kPa (the cutoff for significant fibrosis F ≥ 2). In patients with undetectable viral loads, the mean liver stiffness was 4.9 ± 1.2 kPa, significantly lower than in those with detectable DNA (< 2000 IU/ml) (6.7 ± 2.7 kPa, p < 0.001).

Conclusions

Inactive HBsAg carriers have higher liver stiffness values compared with healthy individuals. Liver stiffness in inactive HBsAg carriers with detectable viral loads is higher than in those who are aviremic, suggesting that low viral loads promote fibrosis.     

Detection of HBsAg, HBcAg, and HBV DNA in ovarian tissues from patients with HBV infection

AIM: To investigate the presence of HBsAg, HBcAg, and HBV DNA in ovarian tissues from patients with HBV infection. METHODS: HBsAg and HBcAg were examined in ovarian biopsy tissues from 26 patients with HBV infection by immunocytochemistry, and HBV DNA was detected in ovarian tissues by PCR. RESULTS: HBsAg and HBcAg were present with the same positive rate of 34.6% (9/26). The total positive rate was 46.2% (12/26). HBsAg and HBcAg were positive in 6 (23.1%) of the 26 patients. Brown positive particles were diffusely distributed in ovarian cells. The positive rate of HBV DNA was 58.3% (7/12). CONCLUSION: HBsAg, HBcAg, and HBV DNA can be detected in ovarian tissues from patients with HBV infection. The presence of HBsAg and HBcAg in ovarian tissues does not correlate with the HBV markers in serum.     

Functional implications of hepatitis B surface antigen (HBsAg) in the T cells of chronic HBV carriers

This study was undertaken to investigate the role of T-lymphocyte-derived soluble factors in the maintenance of the hepatitis B virus (HBV) chronic carrier state. Cell-free supernatants from the peripheral blood T lymphocytes of chronic HBV carriers were produced by incubating them for 48h in tissue culture medium. These supernatants were added to in vitro hepatitis B s antibody (HBsAb)-producing cultures of peripheral blood mononuclear cells from hepatitis B surface antigen (HBsAg) vaccinees stimulated with HBsAg or pokeweed mitogen. T-cell supernatants from chronic carriers suppressed in vitro HBsAb antibody synthesis, whereas those from control subjects did not. This suppression was antigen specific as the supernatants did not suppress synthesis of total IgG or IgM. HBV viral sequences were demonstrable, by Southern and dot-blot hybridization, in the T cells secreting this factor. We also demonstrated the presence of HBsAg in T-cell supernatants derived from these cells. These results show that HBsAg of T-cell origin may have a role in suppressing HBsAb production. Our observations point to the role of HBsAg-specific cellular and humoral responses in favouring persistence of the chronic HBV carrier state.     

Frequency and clinical relevance of delta virus infection in HBsAg carriers in the Berlin area

The frequency of delta virus infection, immunoserological parameters and degree of liver inflammation were studied in 190 HBsAg carriers in the Berlin area from 1976 to 1986. Delta infection was detected in one of 50 HBsAg carriers (2%) in the period from 1976 to 1980. In contrast 19 of 140 HBsAg carriers (14%) with delta infection were found in the period from 1981 to 1986. This group included 12 Germans, 5 Turks and 2 Italians. Only 6 of these subjects belonged to a so-called risk group: 3 drug addicts, 2 homosexuals and 1 hemophiliac. Eighteen of the 20 patients with HDV infection showed progressive liver disease in the follow-up period. Nine cases developed complete liver cirrhosis over five years. Variable transaminase levels and elevation of immunoglobulin G were recorded. Humoral autoimmune phenomena were rarely observed. The increasing frequency of HDV infection in the Berlin area is presumably related to tourism, national origin and membership in specific risk groups. The data in our study underline the importance of effective prophylaxis by active immunization with HBsAg vaccines.     

Hepatitis C virus infection in anti-HBe-positive HBsAg carriers with chronic liver disease.

In the present study, sera from chronic hepatitis B surface antigen (HBsAg) carriers positive for antibody to hepatitis B 'e' antigen (anti-HBe) with evolutive liver disease as correlated with anti-HBe-positive healthy carriers, were examined for antibodies to hepatitis C virus (HCV). Anti-HCV antibodies were detected in 32/124 (25.8%) anti-HBe-positive carriers with chronic liver disease and in none of the 46 healthy carriers. When anti-HCV positivity was evaluated in relationship to the degree of severity of liver disease and possible confounding factors such as hepatitis B virus replication or other potential hepatolesive factors were eliminated by using logistic regression, the odds ratio of liver cirrhosis versus chronic persistent hepatitis was 18 (95%, CI 3.5-92.5). Therefore, our results indicate that HCV may be implicated in the determinism and severity of liver damage in a significant proportion of anti-HBe-positive chronic HBsAg carriers.     

The influence of HTLV-III infection on the natural history of hepatitis B virus infection in male homosexual HBsAg carriers

The presence of antibodies to HTLV-III and markers of active hepatitis B virus replication was examined in a longitudinal study of 33 consecutive male homosexual HBsAg carriers. The mean follow-up time was 37 months (range = 4 to 109 months). All patients were initially hepatitis B virus DNA-positive and HBeAg positive. Antibodies to HTLV-III were detectable in eight patients while they were positive for both of these markers. One of them cleared hepatitis B virus DNA and seroconverted from HBeAg to anti-HBe. This corresponds to an annual clearance/seroconversion rate of 4% (95% confidence limits = 0 to 15%). In two patients, antibodies to HTLV-III appeared after clearance of hepatitis B virus DNA and HBeAg, and in one of them, hepatitis B virus DNA reappeared. Among the 25 patients negative for HTLV-III antibodies, the annual hepatitis B virus DNA clearance rate was 20% and HBeAg to anti-HBe seroconversion rate was 11% (95% confidence limits = 11 to 31% and 4 to 20% respectively). The observed hepatitis B virus DNA clearance rates in the two groups were significantly different (p less than 0.05). Disease activity, as determined by transaminase levels, was significantly lower in HTLV-III-infected individuals as compared to individuals without HTLV-III infection (p less than 0.05). Infection with HTLV-III may extend the period of active viral replication or even reactivate hepatitis B virus replication and seems to diminish inflammatory disease activity in chronic HBsAg carriers.     

Geographic distribution of HBsAg carriers in China

We tested by radioimmunoassay the sera of 22,707 male Chinese government employees in Taiwan for HBsAg and found 15.2% to be positive. Almost all were confirmed as carriers by follow-up testing 1 year later. This paper presents HBsAg positivity rates of these men according to the province of China from which they originated, and compares the rates with published provincial mortality rates for primary hepatocellular carcinoma. Moderate variation in carrier rates between provinces was observed with high prevalence in men from provinces south of the Yangtze River. There was positive correlation between HBsAg prevalence and primary hepatocellular carcinoma incidence giving further support to the possibility of a causal relationship.     

HBV感染者HBsAg和抗-HBs双阳性发生机制

HBV感染后可产生一种保护性抗体抗-HBs,是病毒清除的典型特征。乙型肝炎表面抗原(HBsAg)和抗-HBs序贯表达,理论上在同一患者不可能同时检出。但是近年来,关于HBsAg和抗-HBs同时阳性的报道屡见不鲜。在临床中,HBsAg和抗-HBs同时阳性的现象多见于慢性乙型肝炎患者,及注射乙型肝炎疫苗或使用大剂量单克隆抗-HBs的患者。对于这种特殊现象的发生机制尚不清楚。总结了国内外相关研究结果,分析表明HBsAg和抗-HBs双阳性可能与HBV S基因变异和抗-HBs结合力下降等有关。     

Hepatitis delta virus RNA detection in chronic HBsAg carriers with and without HIV infection

Hepatitis delta virus (HDV) RNA detection was carried out, using a full-length HDV RNA probe, in serum of 43 patients with chronic HDV infection. Among them, 30 cases (70%) were HDV RNA-positive. With respect to other HDV markers, serum HDAg (detected by immunoblot) was found in 33 patients (77%) and IgM anti-HD in 29 (67%). A similar percentage of HDV RNA-positive patients with and without circulating hepatitis B virus (HBV) DNA (32.5 vs. 37%, respectively) was found. Antibodies against the human immunodeficiency virus (HIV) were detected in 15/43 subjects studied. The presence of HDV RNA was significantly higher (p less than 0.05) in anti-HIV-seropositive cases (93%) than in the HIV-seronegative ones (57%). Moreover, simultaneous HDV and HBV replication was found more frequently (60 vs. 18%, p less than 0.05) and at higher levels among the anti-HIV-positive patients than in the rest. In addition, in most of the anti-HIV-positive subjects, HDV RNA and HBV DNA were constantly positive during a whole year of follow-up.