Absence of hepatitis B virus DNA detected by polymerase chain reaction in blood donors who are hepatitis B surface antigen negative and antibody to hepatitis B core antigen positive from a United States population with a low prevalence of hepatitis B serologic markers

A recent study in hepatitis B surface antigen (HBsAg)-negative, antibody to hepatitis B core antigen (anti-HBc)-positive blood donors from a population with a high prevalence of hepatitis B serologic markers showed the presence of hepatitis B virus DNA (HBV DNA) as detected by polymerase chain reaction (PCR) in 4 percent of these donors. A sensitive, nested PCR assay was used to assess the prevalence of HBV DNA in a population of HBsAg-negative, anti-HBc-positive blood donors from a United States population with a low prevalence of hepatitis B serologic markers. The lower limit for detection by the PCR assay was 10(-5) pg per mL of HBV DNA. There was a review of 26,492 consecutive blood donations in a 12-month period. During this time, only 1 unit (0.004%) was HBsAg positive. An additional 158 units (0.6%) were repeatably reactive for anti-HBc. These 158 HBsAg-negative, anti- HBc-positive units were given by 119 donors of blood for allogeneic and autologous use. HBV DNA was not detected by PCR in blood from 83 allogeneic blood donors (93 samples) or 36 autologous blood donors (65 samples). Anti-HBc testing is an inefficient means of screening for potential hepatitis B infectivity and is associated with low test specificity in populations with a low prevalence of hepatitis B serologic markers.     

Donor screening for antibody to hepatitis B core antigen and hepatitis B virus infection in transfusion recipients

BACKGROUND: Testing for antibody to hepatitis B core antigen (anti-HBc) as a surrogate for hepatitis C viremia is no longer needed for blood donor screening. Currently, the important question is how much its use supplements hepatitis B surface antigen (HBsAg) donor screening in preventing transfusion-transmitted hepatitis B virus (HBV) infection. STUDY DESIGN AND METHODS: In a study conducted in the 1970s, 64 blood donors were associated with 15 cases of HBV (1.0%) in 1533 transfusion recipients. Sera from 61 donors at donation and 29 follow-up visits were available for present-day assays for HBsAg, HBV DNA, anti-HBc, and antibody to HBsAg (anti-HBs). RESULTS: HBsAg was found in four previously negative blood donors; HBV DNA was limited to three of these four. Anti-HBc was detected in six HBsAg-negative donors. Two other donors were negative in all assays at donation, but positive for anti- HBc and anti-HBs 2 to 4 months later. The remaining donors were negative for all HBV markers, which left five recipient cases unexplained. No HBV transmission was observed when anti-HBs sample-to- negative control values were > or = 10. CONCLUSION: Some 33 to 50 percent of cases of hepatitis B that could be transmitted by transfusion of blood from HBsAg-negative donors are prevented by anti- HBc screening. Anti-HBc-positive donors unequivocally positive for anti- HBs should be considered noninfectious for HBV and should be allowed to donate. Anti-HBc screening of paid plasmapheresis donors, supplemented by anti-HBs testing, would reduce the amount of HBV to be processed by virus inactivation and increase the content of anti-HBs in plasma pools.     

Evaluation of a multiplex human immunodeficiency virus-1, hepatitis C virus, and hepatitis B virus nucleic acid testing assay to detect viremic blood donors in northern Thailand

BACKGROUND: Screening of blood donors with nucleic acid testing (NAT) for human immunodeficiency virus (HIV) and hepatitis C virus (HCV) has been implemented recently in the United States. There are limited data, however, on the additional NAT yield of donors in developing countries in Asia where the prevalence of infection is higher. In addition, data on hepatitis B virus (HBV) NAT in high prevalence areas are minimal. STUDY DESIGN AND METHODS: A total of 5083 whole-blood donors at the Chiang Mai University Hospital, Thailand, blood bank were evaluated with a commercially available NAT assay (Procleix Ultrio, Gen-Probe, Inc.) to screen individual donations. RESULTS: No NAT yield cases were found for HIV-1 or HCV. There were 17 samples with discrepant HBV DNA NAT and hepatitis B surface antigen (HBsAg) tests, however. Seven of these were HBV DNA NAT-positive, HBsAg-negative; of these 7, 1 was NAT-positive at baseline, but negative on follow-up, and considered a false-positive, 1 had an acute infection, and 5 had chronic prevalent HBV infections, for a NAT yield of 6 in 4798 HBsAg negative donors (1:800). In addition there were 10 NAT-negative, HBsAg-positive serum samples. All were anti-hepatitis B core antigen immunoglobulin G-positive; on testing with a more sensitive NAT target capture assay, 5 were positive (1.8-20.6 IU/mL) and 5 were negative. CONCLUSION: Multiplex NAT screening of individual-donor serum samples in Northern Thailand detected approximately 1 per 800 HBV NAT-positive, HBsAg-negative donors. The especially high prevalence of HBV infection in Thailand and other Asian countries suggests that HBV NAT screening of donors will be more cost-effective than in other areas.     

Anti-hepatits B core antigen testing, viral markers, and occult hepatitis B virus infection in Pakistani blood donors: implications for transfusion practice

BACKGROUND: The purpose of this study was to determine the seroprevalence of anti-hepatitis B core antigen (HBc) and the impact of its testing along with other markers of hepatitis B, hepatitis B virus (HBV) DNA, hepatitis C virus antibody (anti-HCV), and syphilis in Pakistani blood donors. STUDY DESIGN AND METHODS: The study design was cross-sectional. A total of 966 donors were selected randomly for testing of anti-HBc and HBV markers, including HBV DNA, of 94,177 blood donors who were routinely screened for hepatitis B surface antigen (HBsAg), anti-HCV, human immunodeficiency virus antibody (anti-HIV), Treponema pallidum hemagglutination assay (TPHA), and malarial parasites from 2003 to October 2005. RESULTS: The seroprevalence of various infectious markers was as follows: HBsAg, 2.16 percent; anti-HCV, 4.16 percent; anti-HIV, 0.004 percent; TPHA, 0.75 percent; and malaria, 0.002 percent. Anti-HBc prevalence in HBsAg-negative, HBV DNA-negative blood donors was 167 of 966 (17.28%), with 76 percent demonstrating anti-HBs positivity. Younger donors with mean age of 25 years were exposed to HBV to a lesser extent compared to those with a mean age of 29 years. Anti-HBc positivity was significantly higher in anti-HCV-reactive individuals. HBV DNA was detectable in 5 blood donors who were HBsAg-, anti-HBc-positive and were categorized as having occult HBV infection. CONCLUSIONS: The study shows that more than 17 percent of healthy, young blood donors in Pakistan are already exposed to HBV, with two-thirds showing anti-HBs levels of greater than 100 mIU per mL. One in 200 blood donors who are HBsAg-, anti-HBc-positive, however, have occult HBV infection, with likelihood of transmission of hepatitis B in recipients of blood components derived from them. HBsAg-negative individuals who are anti-HBc-negative and those who are anti-HBc-positive, anti-HBs-positive, and HBV DNA-negative should be selected as regular blood donors to minimize transmission due to occult hepatitis B infection.     

Frequent presence of HBV in the sera of HBsAg-negative, anti-HBc-positive blood donors

BACKGROUND: Recent studies have revealed that HBV may not be cleared even after the disappearance of serum HBsAg. The purpose of this study was to investigate whether the replication of HBV persists in HBsAg-negative blood donors who lack apparent liver disease. STUDY DESIGN AND METHODS: Serum HBV was examined by using PCR coupled with Southern blotting in 50 blood donors who were identified to be HBsAg negative but anti-HBc positive. RESULTS: HBV DNA was detected in the sera from 19 (38%) of 50 donors. In 11 of the 19, HBV existed exclusively as immune complexes, while HBV presumably did not exist as immune complexes in the remaining eight. The levels of HBV DNA were similar to those in patients who had recovered from acute HBV. Some nucleotide substitutions, which did not confer amino acid changes in the major epitope of HBsAg, were found in the preS-S regions. CONCLUSION: The replication of HBV is ongoing in a substantial proportion of healthy blood donors who have anti-HBc. Blood from such donors may contain very low levels of HBV free of immune complex formation and should be excluded for transfusion. The fact that such blood donors apparently lacked liver disease suggests no pathogenicity of such "occult" HBV.     

Serum HBV-DNA (hepatitis B virus DNA) in acute and chronic hepatitis B infection

HBV DNA was measured in the sera of 69 patients with hepatitis B virus infections. Sixteen patients had acute hepatitis B, 24 had chronic active hepatitis (CAH), 6 had chronic persistent hepatitis (CPH), 5 had cirrhosis without CAH and 18 were asymptomatic HBsAg carriers. In patients with acute hepatitis B who recovered, HBV DNA was present in the serum transiently early in the illness. HBV DNA persisted in the serum in the two patients who developed chronic hepatitis. Sera of 23 of 24 patients with CAH were persistently positive for HBV DNA. There was no relationship between the quantity of HBV DNA in the serum and the histological intensity of activity. Thirteen of the 24 patients with CAH had histological evidence of cirrhosis in addition to CAH and HBV DNA was detected in the sera of all 13. The sera of 2 of 6 patients with CPH were positive for HBV DNA. In one it was positive only where there was clinical evidence of reactivation of HBV infection. The other patient subsequently developed CAH. Sera of 5 patients with established HBsAg positive cirrhosis but without evidence of CAH were negative for HBV DNA. Two of these patients had hepatocellular carcinoma. Sera of 18 asymptomatic anti-HBe positive carriers with normal ALT were negative for HBV DNA. HBeAg and HBV DNA were not always found in the serum together. In acute hepatitis 5 patients with HBV DNA in the serum were HBeAg positive, but in 6 patients the sera were HBeAg positive inthe absenceof HBV DNA.     

Posttransfusion hepatitis B transmitted by blood from a hepatitis B surface antigen-negative hepatitis B virus carrier

A female blood donor at our institution was implicated in three cases of clinical posttransfusion hepatitis B. She had given blood 25 times in 8 years. Twenty-seven recipients were followed up, and about one-half of those who were still living had serologic markers of hepatitis B virus (HBV) infection. The donor was repeatedly negative for hepatitis B surface antigen (HBsAg) and antibody, but she had high titers of antibody to hepatitis B core antigen. We conclude that blood from this HBsAg-negative blood donor was capable of transmitting hepatitis B.     

Occult hepatitis B virus infection in Thai blood donors

BACKGROUND: An evaluation by the National Blood Center, the Thai Red Cross Society, of two commercial multiplex nucleic acid tests (NATs; the Chiron PROCLEIX ULTRIO test and the Roche Cobas TaqScreen MPX test) for screening Thai blood donors for hepatitis B virus (HBV), hepatitis C virus, and human immunodeficiency virus Type 1 identified 175 HBV NAT–reactive/hepatitis B surface antigen (HBsAg)‐negative donors. The classification of the HBV infection of these donors was confirmed by follow‐up testing. STUDY DESIGN AND METHODS: Index samples were tested for HBV serologic markers and HBV viral loads were determined. Donors were followed for up to 13 months and samples were tested with both NAT assays and for all HBV serological markers. RESULTS: Of 175 HBV NAT–yield donors, 72 (41%) were followed. Based on the follow‐up results, the majority of donors who were followed had an occult HBV infection (66.7%), followed by donors with a primary, acute infection (26.4%). The majority of donors in this latter group (20.8%) were in the window period. Three donors (4.2%), who were anti‐HBs positive, had a reinfection or breakthrough infection. CONCLUSION: The majority of donors detected during routine screening, who were HBsAg negative and NAT reactive, had an occult HBV infection, thus validating the decision to introduce NAT for blood donations in Thailand.     

不同核酸检测方法对献血者隐匿性乙肝病毒感染的研究

目的了解无偿献血者中隐匿性乙肝病毒感染情况,并比较不同核酸检测方法对隐匿性乙肝病毒感染检测能力的差异。方法分别采用nested-PCR和Procleix Ultrio全自动核酸检测系统对无偿献血者血浆标本进行HBV核酸检测,对核酸阳性标本进行HBV DNA序列分析。结果在总计9 209例次标本的检测中,共有9 159例为HBsAg(-);HBsAg(-)标本中nested-PCR方法检出18例HBV DNA阳性(0.19%,18/9 159),而Procleix Ultrio检出7例(0.076%,7/9 159),两者间差异有统计学意义(P<0.05);测序结果显示隐匿性HBV感染者中C基因型所占的比例(64.7%,11/17)明显高于HBsAg阳性的HBV感染者(23.1%,6/23,P<0.01)。结论闽南地区无偿献血者中存在较高比例的隐匿性乙肝病毒感染;不同核酸检测方法对献血者隐匿性乙肝病毒感染的检测能力存在差异。     

Infectivity of blood from PCR-positive, HBsAg-negative, anti-HBs-positive cases of resolved hepatitis B infection

BACKGROUND: Numerous reports have noted the existence of sera, particularly from resolving cases of HBV infection, that are positive for HBV DNA by PCR, despite being negative for HBsAg and IgM anti-HBc. If such blood is infective and detectable by HBV NAT screening, it seems desirable to introduce such screening for transfused blood. STUDY DESIGN AND METHODS: Three chimpanzees were inoculated with serum and lymphocytes from three patients who were HBV DNA PCR positive, but HBsAg negative. The animals were tested over a period of 15 months for HBsAg, anti-HBs, anti-HBc, and HBV DNA by PCR. RESULTS: All animals remained uninfected. CONCLUSION: Small amounts of plasma and MNCs from HBV DNA-positive HBsAg-negative blood do not appear to be infectious; however, further studies with larger volumes of inoculum should be conducted.     

Monoclonal anti-HBs antibodies radioimmunoassay and serum HBV-DNA hybridization as diagnostic tools of HBV infection: relative prevalence among HBsAgnegative alcoholics, patients with chronic hepatitis or hepatocellular carcinomas and blood donors

Anti-HBs monoclonal antibodies radioimmunoassay (m-RIA) and HBV-DNA hybridization techniques were used to detect HBs antigen (HBsAg)--associated determinants (evidence of HBV on-going infection) and HBV-DNA sequences (evidence of viral multiplication) in the serum samples of 479 patients who were HBsAg negative by standard solid-phase radioimmunoassay. They included 128 alcoholics, 104 patients with chronic hepatitis, fifty-four with an hepatocellular carcinoma, 100 with coagulation disorders and ninety-three blood donors. The aim of this study was the comparison in these populations of the prevalence of the various HBV markers. m-RIA detected HBsAg-associated determinants in 1% of blood donors, 3% of coagulation disorders, 3.1% of the alcoholics, 21.1% of chronic hepatitis and 16.6% of hepatocellular carcinoma; hybridization identified HBV-DNA sequences in 0.9%, 2.2%, 10.9%, 9.6% and 5.5% of these cases, respectively. The combined prevalence of both markers of an on-going HBV infection (with or without viral multiplication) was 14.16%, 26.9% and 22.2% in the latter groups, respectively, as compared with only 3% in patients with coagulation disorders and 2.1% of blood donors. These results confirm the frequency of HBV or HBV-related virus infection in alcoholics, in chronic hepatitis and hepatocellular carcinomas, despite the absence of HBsAg by standard RIA (or even of any other usual marker); this gives further evidence for variations in the expression of HBV infection. A high and quite similar prevalence of usual serum markers and hybridization results was observed in the alcoholics and in the patients with chronic hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)     

闽南地区无偿献血者隐匿性乙型肝炎病毒感染研究

目的研究闽南地区无偿献血者中隐匿性乙型肝炎病毒感染(OBI)情况,探讨现有输血传播乙肝病毒(HBV)的检测方法的有效性。方法依据多种与HBV相关血清学指标的检测情况对献血者标本进行HBV携带风险评价分级,对较高携带风险的标本做单份多区段巢式-PCR检测其HBV DNA,对低携带风险的标本做10份混合的巢式-PCR检测。采用这一方案,对闽南地区19 360例HBsAg阴性的无偿献血者标本做检测分析。结果闽南地区HBsAg阴性献血者中的HBV DNA阳性检出率为0.21%(40/19 360,95%CI:0.15%—0.28%),属于OBI;其中抗-HBc阳性检出率85%(34/40),但阳性预测值仅为3.4%(34/995,95%CI:2.4%—4.7%);HBV NRAg阳性预测值30%(6/20),但灵敏度为15%(6/40)。结论现有筛查体系下无偿献血者中仍存在一定比例的OBI,需要寻求更为有效的检测方法。     

Hepatitis B virus DNA in blood donors with anti-HBc as a possible indicator of active hepatitis B virus infection in Yucatan, Mexico

Hepatitis B virus (HBV) may be present in serum even when negative for HBV surface antigen (HBsAg). If routine screening of sera for anti-HBV core antigen (anti-HBc) is not done, low-level HBV viraemia may not be identified. A study was done on the presence of HBV DNA in serum samples from Mexican blood donors negative for HBsAg. Sera from 158 volunteer blood donors, negative for HBsAg and anti-HBs, but positive for anti-HBc, were analysed using nested polymerase chain reaction (PCR). HBV DNA was detected in sera from 13 (8.23%) of the 158. Specificity of the PCR-amplified products was corroborated using Southern blot. Single strand conformation polymorphism (SSCP) analysis showed identical SSCP-banding patterns for all 13 PCR products, suggesting similar cDNA sequences. Occult HBV infection was observed in approximately 8% of anti-HBc only donors. The absence of HBsAg in the blood of apparently healthy individuals may not be sufficient to ensure lack of circulating HBV, and blood containing anti-HBc only may be infectious until proven otherwise.     

Efficacy of hepatitis B virus (HBV) DNA screening and characterization of acute and occult HBV infections among blood donors from Madrid, Spain

BACKGROUND: Screening of blood units for hepatitis B virus (HBV) DNA identifies donations collected during the window period (WP) of the acute infection and may improve viral safety of the blood supply. It also leads to the detection of occult hepatitis B infection (OBI).
STUDY DESIGN AND METHODS: From January 2005 to December 2006, a total of 383,267 blood units were screened for hepatitis B surface antigen (HBsAg) and HBV DNA in two transfusion centers in Madrid, using either individual-donation nucleic acid testing (ID-NAT) or minipool (MP-NAT) of eight donations (MP8). Samples positive for HBV DNA and negative for HBsAg were confirmed by a second molecular test, the viral DNA was quantified, and a genome fragment including the region encoding the major hydrophilic region (MHR) of HBsAg was sequenced.
RESULTS: The overall yield of HBV DNA–positive, HBsAg-negative units was 1 in 21,282 (18 cases), higher when using ID-NAT than MP8-NAT (1:9862 vs. 1:51,011; p < 0.01). Four donations (1/95,817) were collected during the infectious pre-HBsAg WP, one during an early recovery stage, and the remaining 13 (1/29,482) were OBIs, six of whom had no detectable antibody to HBsAg. Low-level Genotype D HBV DNA was detected in all OBI cases; the frequencies of this genotype and MHR amino acid substitutions were significantly higher than reported from unselected Spanish HBsAg carriers. Donors with OBI had normal aminotransferase levels and were significantly older than donors carrying HBsAg.
CONCLUSIONS: Blood donors in the WP and with OBI are not uncommon in Madrid and are detected at a higher frequency with ID-NAT than MP-NAT.     

乙型肝炎病毒标志物及其DNA相关性及联合检测临床价值

目的探讨乙型肝炎病毒（HBV）血清免疫标志物（HBV M）和HBV DNA含量的相关性及两种指标联合检测的临床应用。方法酶联免疫吸附试验检测HBV M;荧光定量聚合酶链反应（FQ-PCR）检测HBV DNA含量。结果乙型肝炎表面抗原（HBsAg）、乙型肝炎e抗原（HBeAg）阳性的标本HBV DNA阳性率高,分别为：Ⅰ组[HBsAg、HBeAg和乙型肝炎核心抗体（抗-HBc）阳性],HBV DNA阳性率98.9%（181/183）;Ⅳ组（HBsAg和HBeAg阳性）,HBV DNA阳性率96.3%（26/27）;Ⅶ组[HBsAg、HBeAg、乙型肝炎e抗体（抗-HBe）和抗-HBc阳性],HBV DNA阳性率100.0%（2/2）;HBsAg阳性、HBeAg阴性,HBV DNA阳性率也较高,为Ⅱ组（HBsAg、抗-HBe、抗-HBc阳性）60.4%（58/96）;Ⅲ组（HBsAg、抗-HBc阳性）50%（10/20）;HBeAg、HBsAg阴性有一定的HBVDNA阳性率,但阳性率低,分别为：Ⅴ组（抗-HBs、抗-HBe、抗-HBc阳性）13.3%（2/15）;Ⅵ组（抗-HBs、抗-HBc阳性）8.3%（1/12）;Ⅷ组（抗-HBs阳性）0（0/26）;Ⅸ组（HBV M全阴性）6.7%（1/15）。结论血清HBV DNA水平与HBV M表现模式有关,与HBsAg,HBeAg有良好的相关性,而HBV M阴性的患者也可能有HBV DNA阳性,因此HBV M和HBV DNA联合检测,可有效提高乙型肝炎的检出率,为临床提供HBV感染、复制及传染性判断以及指导治疗的实验室依据。     

Low-level viraemia of hepatitis B virus in an anti-HBc- and anti-HBs-positive blood donor

summary In many countries, screening of hepatitis B virus (HBV) in blood donors is limited to HBsAg testing. However, if anti-HBc testing and sensitive HBV nucleic acid amplification testing (NAT) for routine screening are not prescribed, HBV viraemia might remain unrecognized. A clinically inconspicuous HBsAg-negative 35-year-old female blood donor was detected with anti-HBc antibodies following the introduction of anti-HBc screening of donors. Based on her history, she had seroconverted to anti-HBs positive (titre >7000 IU/L) after vaccination. Blood donations were routinely tested HBV-DNA negative by minipool NAT. The individual donor samples were reinvestigated by an ultrasensitive NAT with a lower detection limit of 3.8 IU/mL. Intermittent HBV viraemia was detected over a 7-year period from this donor, with a concentration ranging from 8 to 260 IU/mL. In the subsequent donor-directed lookback study, no post-transfusion hepatitis was detected. Low-level HBV viraemia in simultaneous anti-HBc- and anti-HBs-positive blood donors could only be identified with enhanced sensitivity individual polymerase chain reaction assays and is not detectable by pool HBV NAT.     

New hepatitis B virus mutant form in a blood donor that is undetectable in several hepatitis B surface antigen screening assays

BACKGROUND: Envelope mutant forms of hepatitis B virus (HBV), impairing HBV antibody recognition, have been reported with mutations in single or multiple sites of the hepatitis B surface antigen (HBsAg) group- specific "a" determinant. Blood donors infected with such an HBsAg mutant form of HBV may escape detection by HBsAg screening assays and therefore may affect the safety of the blood supply. CASE REPORT: A repeat blood donor became HBsAg-reactive in an enzyme immunoassay. Confirmatory testing yielded negative results for HBsAg in a radioimmunoassay and in four enzyme immunoassays used in blood donor screening. The specificity of the HBsAg reactivity in the first enzyme immunoassay was confirmed by HBsAg neutralization with antibody to HBsAg. Additional HBV confirmatory test results were positive for antibody to hepatitis B core antigen and antibody to hepatitis B e antigen; negative for antibody to HBsAg and for hepatitis B e antigen; and positive for HBV DNA. DNA sequence analysis of the "a" determinant region of HBsAg revealed amino acid substitutions from Q (Gln) to R (Arg) at codon 129 and from M (Met) to T (Thr) at codon 133. CONCLUSION: This case illustrates the presence of HBsAg mutant forms of HBV in a West European blood donor population that were undetected by several HBsAg screening assays. Adaptation of HBsAg screening is indicated to overcome deficiencies in sensitivity in detecting HBsAg mutant forms of HBV. Screening for antibody to hepatitis B core antigen or HBV DNA may also detect blood donors infected with HBsAg mutant forms of HBV     

Transfusion-transmitted HBV infection in an endemic area: the necessity of more sensitive screening for HBV carriers

BACKGROUND: By NAT, HBV DNA is occasionally detectable in blood donors with past HBV infection but negative for HBsAg. Whether or not these donors can cause transfusion-transmitted HBV infections is uncertain. STUDY DESIGN AND METHODS: To determine whether or not donors with past HBV infection but negative for HbsAg can cause HBV transfusion-transmitted infections, recipients followed for blood transfusion in a university medical center in Taiwan were studied. HBV DNA and serologic markers were tested in donors and recipients. RESULTS: Of 1,038 enrolled recipients, 910 completed the 6-month post-transfusion follow-up visit. Of these, only 39 patients (4.3%) tested negative on the pretransfusion sample for HBsAg, anti-HBs, anti-HBc, and HBV DNA by PCR. These 39 HBV-naive recipients had been transfused with blood from 147 donations for which stored samples were available for HBV DNA testing by PCR; 11 of these HBsAg-negative samples tested positive for HBV DNA and anti-HBc. Two of the 11 patients who received the HBV-DNA-positive donations (18%) became positive for HBV DNA, and one seroconverted to anti-HBc and finally to anti-HBs, with a mild transient elevation of serum ALT activities. Based on the one confirmed case of HBV transmission, a projection was made that approximately 200 post-transfusion HBV infections could occur in one million units of transfused blood in Taiwan. CONCLUSIONS: In HBV-endemic areas like Taiwan, where blood donors are screened for HBsAg only, the risk of transfusion-transmitted HBV appears to be substantial. Implementation of NAT for blood screening in these settings warrants consideration.     

HBV-LP检测在慢性乙型肝炎患者抗病毒治疗中的应用

目的 探讨乙型肝炎病毒外膜大蛋白(HBV-LP)检测在慢性乙型肝炎患者抗病毒治疗中的应用价值.方法 对抗病毒治疗有效并-70 ℃冻存的56例慢性乙型肝炎患者系列血清做HBV-LP、雅培(ABBOTT)乙型肝炎两对半和HBV DNA定量检测.结果 在56例抗病毒治疗有效病例中,HBeAg阳性组的HBV-LP的A值为1.11±0.40,阴性组的A值0.561 6±0.21,差异有统计学意义.56例干扰素治疗有效病例的HBV-LP和HBV DNA随用药时间的同时下降,两者有很好的相关性,P=0.023 2,r2=0.860 3.结论 HBV-LP可作为判断慢性乙型肝炎抗病毒较为可靠的指标,尤其在HBeAg阴性的乙型肝炎患者进行抗病毒治疗时更具有重大意义.     

Transmission of serologically silent hepatitis B virus along with hepatitis C virus in two cases of posttransfusion hepatitis

The polymerase chain reaction (PCR) was used to investigate the presence of hepatitis B virus (HBV)-related DNA sequences in blood from three blood donors and two transfusion recipients who developed posttransfusion non-A, non-B hepatitis (NANBH). In the first case, the sole donor was positive for antibody to hepatitis B surface (HBs) and core (HBc) antigens and had elevated alanine aminotransferase (ALT) levels, while the recipient had no HBV serologic markers. Both the donor and the recipient had serologic markers of hepatitis C virus (HCV) and were found positive for HBV DNA and HCV RNA sequences by PCR. The second case involved two donors and one recipient. Serologic tests for conventional HBV markers were negative in all three individuals, but one of the donors had elevated ALT. HBV DNA sequences were detected by PCR in the serum of the recipient and of the donor with high ALT, but not in the serum of the donor with normal ALT. Anti-HCV was detected in the serum of the recipient and of the suspect donor but not in that of the donor with normal ALT. The sequences amplified in the S region and determined after cloning of PCR products for both donor-recipient pairs were indistinguishable from each other and identical to the sequence of the major HBV subtype of adw in the first case and ayw in the second case. Furthermore, for the second case, an identical single-point mutation was found in both the donor and the recipient. These data confirm the transmission of conserved HBV sequences together with HCV in posttransfusion NANBH.(ABSTRACT TRUNCATED AT 250 WORDS)