scholarly journals Impact of hepatitis B virus (HBV) preS/S genomic variability on HBV surface antigen and HBV DNA serum levels

Hepatology ◽  
2012 ◽  
Vol 56 (2) ◽  
pp. 434-443 ◽  
Author(s):  
Teresa Pollicino ◽  
Giuliana Amaddeo ◽  
Agnese Restuccia ◽  
Giuseppina Raffa ◽  
Angela Alibrandi ◽  
...  
2009 ◽  
Vol 27 (4) ◽  
pp. 605-611 ◽  
Author(s):  
Winnie Yeo ◽  
Tung C. Chan ◽  
Nancy W.Y. Leung ◽  
Wai Y. Lam ◽  
Frankie K.F. Mo ◽  
...  

Purpose Reactivation of hepatitis B virus (HBV) infection is a well-recognized complication in cancer patients with chronic HBV (hepatitis B surface antigen [HBsAg] positive) undergoing cytotoxic chemotherapy. In patients who have resolved HBV (HBsAg negative and antibody to hepatitis B core antigen [anti-HBc] ± antibody to hepatitis B surface antigen [anti-HBs] positive), such incidence has been much less common until recent use of rituximab. In this study on HBsAg-negative/anti-HBc–positive lymphoma patients, the objectives were to determine the HBV reactivation rate in patients treated with rituximab-containing chemotherapy and to compare it with the rate in patients treated without rituximab. Patients and Methods Between January 2003 and December 2006, all patients diagnosed with CD20+ diffuse large B-cell lymphoma (DLBCL) had HBsAg determined before anticancer therapy. They were treated with either cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) alone or rituximab plus CHOP (R-CHOP). HBsAg-negative patients had anti-HBc determined; serum was stored for anti-HBs and HBV DNA. All patients were observed for HBV reactivation, which was defined as detectable HBV DNA with ALT elevation during and for 6 months after anticancer therapy. Results Among 104 CD20+ DLBCL patients, 80 were HBsAg negative. Of the latter, 46 patients (44.2%) were HBsAg negative/anti-HBc positive; 25 of these patients were treated with CHOP, and none had HBV reactivation. In contrast, among the 21 patients treated with R-CHOP, five developed HBV reactivation, including one patient who died of hepatic failure (P = .0148). Exploratory analysis identified male sex, absence of anti-HBs, and use of rituximab to be predictive of HBV reactivation. Conclusion Among HBsAg-negative/anti-HBc–positive DLBCL patients treated with R-CHOP, 25% developed HBV reactivation. Close monitoring until at least 6 months after anticancer therapy is required, with an alternative approach of prophylactic antiviral therapy to prevent this potentially fatal condition.


Vox Sanguinis ◽  
2008 ◽  
Vol 95 (3) ◽  
pp. 174-180 ◽  
Author(s):  
K. Satoh ◽  
A. Iwata-Takakura ◽  
A. Yoshikawa ◽  
Y. Gotanda ◽  
T. Tanaka ◽  
...  

2011 ◽  
Vol 38 (10) ◽  
pp. 2209-2214 ◽  
Author(s):  
MASARU KATO ◽  
TATSUYA ATSUMI ◽  
TAKASHI KURITA ◽  
TOSHIO ODANI ◽  
YUICHIRO FUJIEDA ◽  
...  

Objective.To evaluate the risk of reactivation of resolved hepatitis B virus (HBV) by immunosuppressive therapy in patients with autoimmune diseases.Methods.Thirty-five patients with autoimmune diseases were included in our study; all were hepatitis B surface antigen (HBsAg)-negative and antibody against hepatitis B core antigen-positive. They were followed for 8–124 weeks and clinical outcomes were analyzed, including serum levels of HBV-DNA and aminotransferase every 4 weeks during their immunosuppressive therapy for underlying autoimmune diseases. If HBV-DNA was detected during the immunosuppressive therapy, HBsAg, antibody against HBsAg (anti-HBs), hepatitis B e antigen (HBeAg), and antibody against HBeAg were also monitored every 4 weeks.Results.HBV-DNA was detected in 6 out of 35 patients. Anti-HBs titer was significantly lower in the patients in whom HBV-DNA was detected compared with the others at baseline: 2.83 (range 0.24–168.50) mIU/ml vs 99.94 (range 0.00–5342.98) mIU/ml, respectively (p = 0.036). Outcomes of the 6 patients with HBV reactivation were as follows: HBV-DNA turned negative in 2 patients without nucleic acid analog (NAA) and 1 with NAA; 2 died due to bacterial sepsis; and 1 died due to autoimmune hemolytic anemia. Significant elevation of aminotransferase was found in only 1 patient, but HBsAg converted to positive in 2 patients and HBeAg converted to positive in 1 patient.Conclusion.Reactivation of resolved HBV can occur during standard immunosuppressive therapy for autoimmune diseases. The low titer of baseline anti-HBs may carry its risk.


2007 ◽  
Vol 14 (02) ◽  
pp. 241-247
Author(s):  
JIANBO XIAO ◽  
Lei Zhang ◽  
XIAOQING CHEN ◽  
Ming Xu * ◽  
XINYU JIANG

Dried leaves of Marchantia convoluta are largely used to protect livers,and to treat tumefaction of skins in China. Flavonoids from Marchantia Convoluta (MCF) was one of the mostpotentially effective anti-inflammatory. MCF was studied here for its ability to inhibit the proliferation of 2,2,15 cells(clone cells derived from HepG2 cells that were transected with a plasmid containing HBV, DNA). All concentrations(5,10,20 and 40 :g/ml) of MCF inhibit hepatitis B surface antigen (HbsAg) and hepatitis B E antigen (HbeAg) in thecultured medium released from 2.2.15 cells. Analysis of morphological changes of MCF-treated phase- contrastmicroscope revealed a possible model of action for MCF to inhibit Proliferation of 2.2.15 cells by inducing apoptosis.


Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2053
Author(s):  
Mary C. Kuhns ◽  
Vera Holzmayer ◽  
Mark Anderson ◽  
Anne L. McNamara ◽  
Silvia Sauleda ◽  
...  

Background: Gaps remain in the detection of nucleic acid test (NAT) yield and occult hepatitis B virus (HBV) infection (OBI) by current HBV surface antigen (HBsAg) assays. The lack of detection may be due to HBsAg levels below current assay detection limits, mutations affecting HBsAg assays or HBsAg levels, or the masking of HBsAg by antibody to HBsAg (anti-HBs). In this study, we evaluate the incremental detection of NAT yield and OBI from five diverse geographic areas by an improved sensitivity HBsAg assay and characterize the samples relative to the viral load, anti-HBs status, and PreS1–S2–S mutations. Included is a comparison population with HBV DNA levels comparable to OBI, but with readily detectable HBsAg (High Surface–Low DNA, HSLD). Methods: A total of 347 samples collected from the USA, South Africa, Spain, Cameroon, Vietnam, and Cote D’Ivoire representing NAT yield (HBsAg(−), antibody to HBV core antigen (anti-HBc)(−), HBV DNA(+), N = 131), OBI (HBsAg(−), anti-HBc(+), HBV DNA(+), N = 188), and HSLD (HBsAg(+), anti-HBc(+), HBV DNA(+), N = 28) were tested with ARCHITECT HBsAg NEXT (HBsAgNx) (sensitivity 0.005 IU/mL). The sequencing of the PreS1–S2–S genes from a subset of 177 samples was performed to determine the genotype and assess amino acid variability, particularly in anti-HBs(+) samples. Results: HBsAgNx detected 44/131 (33.6%) NAT yield and 42/188 (22.3%) OBI samples. Mean HBV DNA levels for NAT yield and OBI samples were lower in HBsAgNx(−) (50.3 and 25.9 IU/mL) than in HBsAgNx(+) samples (384.1 and 139.5 IU/mL). Anti-HBs ≥ 10 mIU/mL was present in 28.6% HBsAgNx(+) and 45.2% HBsAgNx(−) OBI, and in 3.6% HSLD samples. The genotypes were A1, A2, B, C, D, E, F, and H. There was no significant difference between HBsAgNx(−) and HBsAgNx(+) in the proportion of samples harboring substitutions or in the mean number of substitutions per sample in PreS1, PreS2, or S for the NAT yield or OBI (p range: 0.1231 to >0.9999). A total of 21/27 (77.8%) of HBsAgNx(+) OBI carried S escape mutations, insertions, or stop codons. HSLD had more PreS1 and fewer S substitutions compared to both HBsAgNx(−) and HBsAgNx(+) OBI. Mutations/deletions associated with impaired HBsAg secretion were observed in the OBI group. Conclusions: HBsAgNx provides the improved detection of NAT yield and OBI samples. Samples that remain undetected by HBsAgNx have exceptionally low HBsAg levels below the assay detection limit, likely due to low viremia or the suppression of HBsAg expression by host and viral factors.


1997 ◽  
Vol 8 (9) ◽  
pp. 1443-1447
Author(s):  
M Cabrerizo ◽  
J Bartolomé ◽  
P De Sequera ◽  
C Caramelo ◽  
V Carreño

Patients undergoing chronic hemodialysis, as well as dialysis staff members, are at high risk of infection with hepatitis B virus (HBV). We have analyzed by PCR the presence of HBV DNA in serum and peripheral blood mononuclear cells (PBMC) from 33 hepatitis B surface antigen (HBsAg)-negative hemodialysis patients and 24 dialysis unit staff members; eight of the 24 staff members had an acute hepatitis B resolved 13 to 21 yr before. HBV DNA was detected in serum of 19 (58%) patients (12 of 17 with and 7 of 16 without anti-HBV antibodies). HBV DNA was found in PBMC of 18 (54%) patients (13 of 17 with and 5 of 16 without anti-HBV antibodies). In the staff members, serum HBV DNA was found only in the individuals who suffered a previous acute hepatitis (P < 0.005). HBV DNA was detected in PBMC of four of six staff members (all with previous acute hepatitis). In two HBV DNA-positive PBMC samples, viral RNA was detected by reverse transcription-PCR. To ascertain whether the HBV DNA detected in serum was encapsulated, seven HBV DNA-positive serum samples were digested with DNase before PCR. After treatment, HBV DNA remained detectable in four cases. In conclusion, HBV DNA in serum and PBMC is detectable in a high proportion of HBsAg-negative hemodialysis patients and may persist several years after a resolved acute hepatitis B. The viral DNA is encapsulated and remains transcriptionally active in PBMC. In the anti-HBs-negative patients, HBV DNA is, at the present time, the only means for diagnosing a past HBV hepatitis.


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