EXPRESSION OF INSULIN-LIKE GROWTH FACTOR Ⅱ(IGF-Ⅱ)IN HUMAN HEPATOCELLULAR CARCINOMA AND LIVER CIRRHOSIS:ITS RELATIONSHIP WITH HEPATITIS B VIRUS X PROTEIN EXPRESSION

Sixty cases of hepatocellular carcinoma (HCC) and 47 cases of liver cirrhosis (LC) were examined with immunocytochemistry method using antibodies against IGF-II and HBxAg on formalin-fixed, paraffin-embedded tissue sections. 32 HCC and 37 LC were found to be positive to HBxAg, in which the positive rates of IGF-II were 100% (32/32) and 94.6% (35/37) respectively. 28 HCC and 10 LC were found to be HBxAg negative, IGF-II was positive in 23 HCC (83.1%) and 6 LC (60%). The positive expression rates of IGF-II in HBxAg positive tissues were significantly higher than those in HBxAg negative tissues (P<0.05). There were three types of distribution of IGF-II expression in HCC and LC: (1) perinucleus; (2) diffuse in cytoplasm; (3) inside nucleus. IGF-II was highly expressed in most of hyperplastic and neoplastic nodules hepatocytes and some of regeneration nodules. Small polygonal liver cells (SPLCs) were found in the liver tissues surrounding the tumor and cirrhosis and they were positive to both IGF-II and HBxAg. The positive rates of IGF-II in SPLC were 86.4% (38/44) in the HBxAg-positive tissues and 40.5%, (15/37) in the HBxAg-negative tissues. The above findings suggest that IGF-II plays an important role in abnormal proliferation of HCC and SPLC. The relation between IGF-II andHBxAg and the nature of SPLCs are also discussed.

Virus-related liver cirrhosis: Molecular basis and therapeutic options

Chronic infections with hepatitis B virus (HBV) and/or hepatitis C virus (HCV) are the major causes of cirrhosis globally. It takes 10-20 years to progress from viral hepatitis to cirrhosis. Intermediately active hepatic inflammation caused by the infections contributes to the inflammation-necrosis-regeneration process, ultimately cirrhosis. CD8+ T cells and NK cells cause liver damage via targeting the infected hepatocytes directly and releasing pro-inflammatory cytokine/chemokines. Hepatic stellate cells play an active role in fibrogenesis via secreting fibrosis-related factors. Under the inflammatory microenvironment, the viruses experience mutation-selection-adaptation to evade immune clearance. However, immune selection of some HBV mutations in the evolution towards cirrhosis seems different from that towards hepatocellular carcinoma. As viral replication is an important driving force of cirrhosis pathogenesis, antiviral treatment with nucleos(t)ide analogs is generally effective in halting the progression of cirrhosis, improving liver function and reducing the morbidity of decompensated cirrhosis caused by chronic HBV infection. Interferon-α plus ribavirin and/or the direct acting antivirals such as Vaniprevir are effective for compensated cirrhosis caused by chronic HCV infection. The standard of care for the treatment of HCV-related cirrhosis with interferon-α plus ribavirin should consider the genotypes of IL-28B. Understanding the mechanism of fibrogenesis and hepatocyte regeneration will facilitate the development of novel therapies for decompensated cirrhosis.

Distribution of HBV DNA and HBsAg in the liver of patients with liver cirrhosis and its significance

Hepatitis B virus(HBV)DNA and HBsAg were detected in 51 human paraf- fin-embedded sections of liver cirrhosis by the double labelling technique of in situ hybfidiza- tion and PAP method.The results showed that the positive sections were 21(41.2％)for HBV DNA,43(84.3％)for HBsAg and 19(37.3％)for both HBV DNA and HBsAg.HBV DNA-positive grains were localized predominantly in the cytoplasm of hepatic cells or in both nucleus and cytoplasm,a few only in the nucleus or the inner side of the cell membrane.In active cirrhosis and inactive cirrhosis,the positive rates of HBV DNA were 52.8％ and 13.3％,respectively,and for both HBV DNA and HBsAg,they were 47.2％ and 13.3％ restively.The positive rate is higher in active cirrhosis than in inactive cirrhosis(P<0.05).The results further indicated that the infection of HBV and the existence and persistent action of HBV DNA in the liver tissues are one of the important factors of the development of liver cirrhosis.

Antiviral Therapy of Liver Cirrhosis Related to Hepatitis B Virus Infection

Hepatitis B virus (HBV) infection is a leading cause of liver disease worldwide,with 75% of those affected distributed in the Asia-Pacific region.Approximately one million HBV-infected patients die of liver cirrhosis and hepatocellular carcinoma (HCC) each year.If left untreated,6-20% of chronic hepatitis B (CrHB) patients will develop cirrhosis over five years.The cumulative incidence of HBV-related cirrhosis,disease progression,and prognosis are closely associated with serum HBV DNA levels.Antiviral therapy in HBV-related cirrhosis has been documented by several long-term cohort studies to decrease disease progression to hepatic decompensation and HCC.The approval and availability of oral antiviral agents with better safety profiles has greatly improved the prognosis for HBV-related cirrhosis.Here,we discuss the significance of antiviral therapy for HBV-related cirrhosis and the management of HBV-related diseases in the future.

TT virus and hepatitis G virus infections in Korean blood donors and patients with chronic liver disease

AIM:To determine the prevalences of TTV and HGV infections among blood donors and patients with chronic liver disease in Korea,to investigate the association of TTV and HGV infections with blood transfusion,and to assess the correlation between TTV and HGV viremia and hepatic damage. METHODS:A total of 391 serum samples were examined in this study.Samples were obtained from healthy blood donors(n=110),hepatitis B surface antigen(HBsAg)-positive donors(n=112),anti-hepatitis C virus(anti-HCV)-positive donors(n=69),patients with type B chronic liver disease (n=81),and patients with type C chronic liver disease(n=19). Trv DNA was detected using the hemi-nested PCR.HGV RNA was tested using RT-PCR.A history of blood transfusion and serum levels of alanine aminotransferase(ALT)and aspartate aminotransferase(AST)were also determined. RESULTS:TTV DNA was detected in 8.2%of healthy blood donors,16.1%of HBsAg-positive donors,20.3%of anti- HCV-positive donors,21.0%of patients with type B chronic liver disease,and 21.1%of patients with type C chronic liver disease.HGV RNA was detected in 1.8%of healthy blood donors,1.8%of HBsAg-positive donors,17.4%of anti-HCV-positive donors,13.6%of patients with type B chronic liver disease,and 10.5%of patients with type C chronic liver disease.The prevalence of TTV and HGV infections in HBV- or HCV-positive donors and patients was significantly higher than in healthy blood donors(P<0.05), except for the detection rate of HGV in HBsAg-positive donors which was the same as for healthy donors.There was a history of transfusion in 66.7%of TTV DNA-positive patients and 76.9%of HGV RNA-positive patients(P<0.05).No significant increase in serum ALT and AST was detected in the TTV or HGV-positive donors and patients. CONCLUSION:TTV and HGV infections are more frequently found in donors and patients infected with HBV or HCV than in healthy blood donors.However,there is no significant association between TTV or HGV infections and liver injury.

Molecular interactions between hepatitis B virus and delta virus

As a deficient virus due to the lack of envelope proteins, hepatitis D virus(HDV) causes chronic or fulminant "delta hepatitis" only in people with simultaneous hepatitis B virus(HBV) infection. HBV encodes three types of surface proteins known as small(S), medium(M) and large(L) envelope proteins. All three types of HBV surface antigens(HBs Ags) are present on HDV virions. The envelopment process of HDV occurs through interactions between the HDV ribonucleoprotein(RNP) complex and HBV HBsA gs. While HBsA g is the only protein required by HDV, the exact interaction sites between the S protein and pre-mature HDV are not well defined yet. In fact, these sites are distributed along the S protein with some hot spots for the envelopment process. Moreover, in most clinically studied samples, HDV infection is associated with a dramatically reduced HBV viral load, temporarily or permanently, while HBsA g resources are available for HDV packaging. Thus, beyond interacting with HBV envelope proteins, controlling mechanisms exist by which HDV inhibits HBV-DNA replication while allowing a selective transcription of HBV proteins. Here we discuss the molecular interaction sites between HBs Ag and the HDV-RNP complex and address the proposed indirect mechanisms, which are employed by HBV and HDV to facilitate or inhibit each other's viral replication. Understanding molecular interactions between HBV and HDV may help to design novel therapeutic strategies for delta hepatitis.

Clinical features of HBs Ag seroclearance in hepatitis B virus carriers in South Korea: A retrospective longitudinal study

AIM To investigate the characteristic features of hepatitis B surface antigen(HBs Ag) seroclearance among Korean hepatitis B virus(HBV) carriers.METHODS Carriers with HBs Ag seroclearance were selected by analyzing longitudinal data collected from 2003 to 2015. The period of time from enrollment to the negative conversion of HBs Ag(HBs Ag-NC) was compared by stratifying various factors, including age, sex, hepatitis B e antigen(HBe Ag), HBV DNA, sequential changes in the signal-to-cutoff ratio of HBs Ag(HBs Ag-SCR), as measured by qualitative HBs Ag assay, and chronic liver disease on ultrasonography(US-CLD). Quantification of HBV DNA and HBs Ag(HBs Ag-QNT) in the serum was performed by commercial assay.RESULTS Among the 1919 carriers, 90(4.7%) exhibited HBs AgNC at 6.2 ± 3.6 years after registration, with no differences observed among the different age groups. Among these carriers, the percentages of those with asymptomatic liver cirrhosis(LC) and hepatocellular carcinoma(HCC) at registration were 31% and 7.8%, respectively. The frequency of HBs Ag-NC significantly differed according to the HBV DNA titer and US-CLD. HBe Ag influenced HBs Ag-NC in the 40-50 and 50-60 year age groups. HBs Ag-SCR < 1000 was correlated with an HBs Ag-QNT < 200 IU/m L. A gradual decrease in the HBs Ag-SCR to < 1000 predicted HBs Ag-NC. Six patients developed HCC after registration, including two before and four after HBs Ag-NC. The rate at which the patients developed new HCC after HBs Ag seroclearance was 4.8%. LC with excessive drinking and vertical infection were found to be risk factors for HCC in the HBs Ag-NC group.CONCLUSION HCC surveillance should be continued after HBs Ag seroclearance. An HBs Ag-SCR < 1000 and its decrease in sequential testing are worth noting as predictive markers of HBs Ag loss.

Direct antiviral agents in hepatitis C virus related liver disease:Don’t count the chickens before they’re hatched

Since molecules with direct-acting antiviral(DAA)became available,the landscape of the treatment of hepatitis C virus(HCV)infection has completely changed.The new drugs are extremely effective in eradicating infection,and treatment is very well tolerated with a duration of 8-12 wk.This review aims to report the outstanding clinical benefits of DAA and to highlight their critical disadvantages,identifying some clinically relevant hot topics.First,do the rates of virological response remain as high when patients with more advanced cirrhosis are considered?Large studies have shown slightly lower but still satisfactory rates of response in these patients.Nevertheless,modified schedules with an extended treatment duration and use of ribavirin may be necessary.Second,does the treatment of HCV infection affect the risk of occurrence and recurrence of liver cancer?Incidence is reduced after viral eradication but remains high enough to warrant periodic surveillance for an early diagnosis.In contrast,the risk of recurrence seems to be unaffected by viral clearance;however,DAA treatment improves survival because of the reduced risk of progression of liver disease.Third,can HCV treatment also have favorable effects on major comorbidities?HCV eradication is associated with a reduced incidence of diabetes,an improvement in glycemic control and a decreased risk of cardiovascular events;nevertheless,a risk of hypoglycemia during DAA treatment has been reported.Finally,is it safe to treat patients with HCV/hepatitis B virus(HBV)coinfection?In this setting,HCV is usually the main driver of viral activity,while HBV replication is suppressed.Because various studies have described HBV reactivation after HCV clearance,a baseline evaluation for HBV coinfection and a specific follow-up is mandatory.

Vitamin D deficiency and hepatitis viruses-associated liver diseases:a literature review

The secosteroid hormone vitamin D has, in addition to its effects in bone metabolism also functions in the modulation of immune responses against infectious agents and in inhibiting tumorigenesis. Thus, deficiency of vitamin D is associated with several malignancies, but also with a plethora of infectious diseases. Among other communicable diseases, vitamin D deficiency is involved in the pathogenesis of chronic liver diseases caused by hepatitis B and C viruses(HBV, HCV) and high prevalence of vitamin D deficiency with serum levels below 20 mg/mL in patients with HBV and HCV infection are found worldwide. Several studies have assessed the effects of vitamin D supplementation on the sustained virological response(SVR) to interferon(IFN) plus ribavirin(RBV) therapy in HBV and HCV infection. In these studies, inconsistent results were reported. This review addresses general aspects of vitamin D deficiency and, in particular, the significance of vitamin D hypovitaminosis in the outcome of HBVand HCV-related chronic liver diseases. Furthermore,current literature was reviewed in order to understand the effects of vitamin D supplementation in combination with IFN-based therapy on the virological response in HBV and HCV infected patients.

Coinfection of hepatitis B and hepatitis C virus in HIV-infectedpatients in south India

AIM: To screen for the co-infection of hepatitis B (HBV) and hepatitis C virus (HCV) in human immunodeficiency virus (HIV) infected patients in southern India. METHODS: Five hundred consecutive HIV infected patients were screened for Hepatitis B Virus (HBsAg and HBV-DNA) and Hepatitis C virus (anti-HCV and HCV-RNA) using commercially available ELISA kits; HBsAg, HBeAg/ anti-HBe (Biorad laboratories, USA) and anti-HCV (Murex Diagnostics, UK). The HBV-DNA PCR was performed to detect the surface antigen region (pre S-S). HCV-RNA was detected by RT-PCR for the detection of the constant 5' putative non-coding region of HCV. RESULTS: HBV co-infection was detected in 45/500 (9%) patients and HCV co-infection in 11/500 (2.2%) subjects. Among the 45 co-infected patients only 40 patients could be studied, where the detection rates of HBe was 55% (22/40), antiHBe was 45% (18/40) and HBV-DNA was 56% (23/40). Among 11 HCV co-infected subjects, 6 (54.5%) were anti-HCV and HCV RNA positive, while 3 (27.2%) were positive for anti-HCV alone and 2 (18%) were positive for HCV RNA alone. CONCLUSION: Since the principal routes for HIV transmission are similar to that followed by the hepatotropic viruses, as a consequence, infections with HBV and HCV are expected in HIV infected patients. Therefore, it would be advisable to screen for these viruses in all the HIV infected individuals and their sexual partners at the earliest.

Interleukin 28B polymorphisms as predictor of response in hepatitis C virus genotype 2 and 3 infected patients

Single nucleotide polymorphisms near the interleukin28B(IL-28B)gene have been identified as strong predictors of both spontaneous or Peg-interferon(Peg-IFN)and ribavirin(RBV)induced clearance of hepatitis C virus(HCV).Several studies have shown that,in patients with genotype 1(GT-1),rs12979860 C/C and rs8099917T/T substitutions are associated with a more than twofold increase in sustained virological response rate to Peg-IFN and RBV treatment.Although new treatment regimens based on combination of DAA with or without IFN are in the approval phase,until combination regimens with a backbone of Peg-IFN will be used,we can expect that IL28B holds its importance.The clinical relevance of IL28B genotyping in treatment of patients infected with HCV genotype 2(GT-2)and 3(GT-3)remains controversial.Therefore,after a careful examination of the available literature,we analyzed the impact of IL28B in GT-2 and-3.Simple size of the studies and GT-2 and GT-3 proportion were discussed.An algorithm for the practical use of IL28B in these patients was suggested at the aim of optimizing treatment.

Challenge of managing hepatitis B virus and hepatitis C virus infections in resource-limited settings

The global burden of hepatitis B virus(HBV)and hepatitis C virus(HCV)infections and coinfection represents a major public health concern,particularly in resource-limited settings.Elimination of HCV by 2030 has become foreseeable,with effective direct-acting antiviral oral therapies and the availability of affordable generics in low-and-middle-income countries(LMICs).However,access to oral nucleos(t)ide therapy for HBV remains critical and is limited outside the existing global HIV program platforms despite affordable prices.Prevention of mother-to-child transmission of HBV through scaling up of birth dose implementation in LMICs is essential to achieve the 2030 elimination goal.Most individuals living with HBV and/or HCV in resource-limited settings are unaware of their infection,and with improved access to medications,the most significant barrier remains access to affordable diagnostics and preventive strategies.The coronavirus disease 2019 pandemic interrupted hepatitis elimination programs,albeit offered opportunities for improved diagnostic capacities and raised political awareness of the critical need for strengthening health care services and universal health coverage.This review underpins the HBV and HCV management challenges in resource-limited settings,highlighting the current status and suggested future elimination strategies in some of these countries.Global efforts should continue to improve awareness and political commitment.Financial resources should be secured to access and implement comprehensive strategies for diagnosis and linkage to care in resource-constrained settings to fulfill the 2030 elimination goal.

Distribution and significance of HBV DNA and HBAg in human primary hepatocellular carcinoma and liver cirrhosis

In order to investigate the relationship between HBV and hepatocellular carcinoma(HCC),hepatitis B virus DNA(HBV DNA),HBxAg and HBcAg were detected in 44 paraffin-embedded samples of HCC tissue(17 cases with cancer-surrounding hepatic tissues) and 42 case

Molecular and clinical aspects of hepatitis D virus infections

Hepatitis D virus(HDV) is a defective virus with circular, single-stranded genomic RNA which needs hepatitis B virus(HBV) as a helper virus for virion assembly and infectivity. HDV virions are composed of a circular shape HDV RNA and two types of viral proteins, small and large HDAgs, surrounded by HBV surface antigen(HBs Ag). The RNA polymerase Ⅱ from infected hepatocytes is responsible for synthesizing RNAs with positive and negative polarities for HDV, as the virus does not code any enzyme to replicate its genome. HDV occurs as co-infection or super-infection in up to 5% of HBs Ag carriers. A recent multi-center study highlighted that pegylated interferon α-2a(PEG-IFN) is currently the only treatment option for delta hepatitis. Nucleotide/nucleoside analogues, which are effective against HBV, have no relevant effects on HDV. However, additional clinical trials combining PEG-IFN and tenofovir are currently ongoing. The molecular interactions between HDV and HBV are incompletely understood. Despite fluctuating patterns of HBV viral load in the presence of HDV in patients, several observations indicate that HDV has suppressive effects on HBV replication, and even in triple infections with HDV, HBV and HCV, replication of both concomitant viruses can be reduced. Additional molecular virology studies are warranted to clarify how HDV interacts with the helper virus and which key cellular pathways are used by both viruses. Further clinical trials are underway to optimize treatment strategies for delta hepatitis.

HBV genotype characterization and distribution in patients with HBV-related liver diseases in Zhejiang Province, P. R. China: possible association of co-infection with disease prevalence and severity

BACKGROUND: There are 8 well-documented genotypes of hepatitis B virus (HBV) at this time point. Genotyping can be accomplished based on a partial sequence of hepatitis B virus (HBV) genome such as the pre-S or S gene. Several methods have been developed and used for HBV genotyping including direct sequencing, restriction fragment length polymorphism, line probe assay and enzyme-linked immunoassay. Recently, a novel, rapid and cost-effective genotyping method based on PCR amplification assay using type-specific primers that can identify all six major genotypes has been developed. This study was undertaken to characterise HBV genotypes and investigate the association between the prevalence of different genotypes and the severity of HBV-induced liver diseases. METHODS: Serum samples from carriers of HBV and patients with HBV-related liver diseases from Zhejiang Province were screened for viral serological markers using commercially available radioimmunoassay (RIA) and enzyme linked immunosorbent assay (ELISA) kits. Serum HBV DNA load was determined by real-time detection PCR. A type-specific primer based the nested-PCR method was employed in the HBV genotyping. The genotype results obtained were confirmed by direct sequencing of nested PCR amplicons of the pre-S region. Ten samples of each genotype (B and C) were sequenced. RESULTS: The survey on a cohort of 125 HBV carriers in and around Hangzhou City, Zhejiang Province showed the existence of HBV genotypes A (0.8%), B (48%), C (40.8%), D (0.8%), mixed B and C (9.6%) and an absence of E and F genotypes. Distribution of HBV genotypes in patients with liver diseases revealed a statistically insignificant higher prevalence of genotype B in mild chronic hepatitis (CH). Among the three genotypes B, C and mixed B/C infections 11 (73.3%), 3 (20%) and 1 (6.7%), (P< 0.05), respectively in subjects with moderate CH, genotype B was significantly predominant. The infection patterns for genotypes B, C and B/C mixed in (i) liver cirrhosis (LC) 4 (23.5%), 10 (58.8%) and3 (17.7%) and (ii) hepatocellular carcinoma (HCC) 2 (28.6%), 5(71.4%) and 0 (0.0%) respectively revealed a marked association of C genotype with liver disease; however, the association was statistically insignificant (P >0.05). Differences in positive rate of HBeAg for the three genotypes B, 16(30.8%), C, 27(51.9%), and mixed B/C, 9(17.3%) were significant (P < 0. 05 ) , with genotype C showing predominance. CONCLUSIONS : These findings show an interesting distribution of HBV A-D genotypes in Zhejiang Province. Furthermore, our results indicate a novel and markedly high prevalence of mixed B/C genotype infections in subjects with severe CH and LC, and a possible association of mixed B/C infections with the severity of liver diseases in this region of China's Mainland.

Primary biliary cirrhosis in HBV and HCV patients:Clinical characteristics and outcome

AIM: To present the characteristics, management and outcome of patients with hepatitis B virus(HBV) or hepatitis C virus(HCV) infections concurrent with primary biliary cirrhosis(PBC).METHODS: Since January 2001 to September 2009,we retrospectively evaluated the medical records of all HBV(n = 1493) and HCV patients(n = 526) who are followed in our center for the presence of concurrent PBC. Seventeen patients identified with concurrent viral hepatitis and PBC(8 HCV and PBC; follow-up: 61 ± 37 mo and 9 HBV and PBC; follow-up: 57 ± 38 mo). PBC diagnosis was established if the patients met at least two of the following criteria: positivity for antimitochondrial antibody, elevated cholestatic enzymes and histological lesions of PBC.RESULTS: HCV or HBV diagnosis preceded that of PBC in most patients by many years. PBC diagnosis was based on the presence of antimitochondrial antibody and elevated cholestatic enzymes in all 17 patients,while one third(5/17; 29.4%) experienced severe pruritus many years before diagnosis. Patients with PBC and HBV were significantly younger at diagnosis of PBC compared to patients with PBC and HCV(56.1 ± 11.2vs 68.5 ± 10.3, respectively, P < 0.05). At initial clinical and histological assessment the majority of patients were cirrhotics(10/17; 58.8%) with the group of PBC and HCV carrying the highest frequency(87.5% vs33.3% in PBC and HBV; P < 0.05). The patients with HBV and concomitant PBC seem to have better outcome compared to those with HCV and PBC since none of the 6 non-cirrhotics with HBV and PBC developed cirrhosis during follow-up.CONCLUSION: PBC diagnosis in HBV or HCV patients is very difficult and usually delayed. Therefore, in any case, cholestasis should alert physicians to further search for PBC.

153名吸毒人员HIV、HBV、HCV、梅毒感染状况分析

目的了解怀化市吸毒人员HIV、HBV、HCV、梅毒感染状况。方法对吸毒人员采取统一调查表进行问卷调查,并采血检测HIV抗体、HBsAg、HCV抗体、快速血浆反应素试验(RPR)检测梅毒抗体。结果153名吸毒人员HIV、HBV、HCV、梅毒感染率分别为1.3%,21.57%,59.48%,3.92%。非静脉吸毒者未检出HIV、梅毒感染者,HBV在两种不同吸毒方式之间无显著差异,而HCV在两种不同吸毒方式之间有非常显著性差异(χ2=66.44,P<0.01)。结论在吸毒人群中开展爱滋病、丙型肝炎、梅毒知识的宣传与教育,采用有效的干预措施将是势在必行。

肝癌高发区不同人群HBV、HCV感染率及其与肝癌的关系

了解国内肝癌高发区ＨＢＶ、ＨＣＶ的流行情况及其与肝癌发病的关系。方法：在肝癌高发的江苏 省启东地区，对不同人群进行血清ＨＢｓＡｇ（固相放免法）、抗－ＨＣＶ（酶免法）、ＡＦＰ（固相放免法）测定，结果进行统计 学处理。结果：肝癌、肝炎、献血员三组人群中ＨＢｓＡｇ 及抗－ＨＣＶ阳性率分别为８６．０２％与７．５３％，５９．８１％与 ０．９３％，４．０４％与４．０４％。血清ＨＢｓＡｇ及ＡＦＰ含量与抗－ＨＣＶ间无明显关系。结论：国内肝癌高发区人群主要感 染ＨＢＶ并与肝癌发生有关，ＨＣＶ感染并不重要。

湛江市吸毒人群HIV、HBV、HCV、梅毒感染状况调查

[目的]了解湛江市吸毒人群HIV、HBV、HCV、梅毒感染状况及影响因素,为吸毒人群这几种疾病防治提供依据。[方法]对湛江市戒毒所350名吸毒人群进行匿名调查,采集静脉血进行HIV、HBV、HCV和梅毒血清学检测,并对结果进行统计学分析。[结果]350名吸毒人群中HIV抗体阳性15例,阳性率4.29%,HBsAg阳性103例,阳性率29.43%,HCV抗体阳性200例,阳性率57.14%,梅毒抗体阳性13例,阳性率3.71%,重叠感染HIV/HB-sAg共8人,占2.29%,重叠感染HBsAg/HCV共97人,占27.71%,重叠感染HBsAg/HCV/梅毒共9人,占2.57%,重叠感染梅毒/HCV共8人,占2.29%。[结论]吸毒人群中HIV、HBV、HCV感染率较高,与他们注射毒品行为有关,政府应开展针对性干预措施。

HCV、HBV与肝硬变及原发性肝癌关系的初步探讨

作者对８０例肝硬变（ＬＣ）、１１２例原发性肝癌（ＰＨＣ）的血清抗ＨＣＶ及ＨＢＶ检测发现：（１）ＰＨＣ、ＬＣ的抗ＨＣＶ阳性率分别为２８．６％和１８．８％，ＨＢＶ阳性率分别为６４．３％和６７．５％；（２）有无用血液及血液制品者间的抗ＨＣＶ及ＨＢＶ阳性率差异显著；（３）ＬＣ、ＰＨＣ患者的抗ＨＣＶ阳性率在ＨＢＶ阴性（１５．４％和２５％）与ＨＢＶ阳性（２０．４％和３０．６％）间无明显差异；（４）在抗ＨＣＶ阴、阳性ＰＨｃ中，抗ＨＢｅ、抗ＨＢｃ单阳性率，抗ＨＢｓ与抗ＨＢＣ及抗ＨＢｃ与抗ＨＢｅ双阳性率，差异非常显著。结果表明，ＨＢＶ感染仍为ＬＣ及ＰＨＣ的主要致病因素，但ＨＣＶ与ＨＢＶ存在着重叠感染，亦可能起着共同作用。