An epidemiological survey of HBV infection and low-level HBsAg in military camps in eastern China

Wang, Tong; Dai, Yuzhu; Lu, Wei; Zhou, Huajun; Chen, Yu; Xu, Xujian; Sun, Changgui; Cheng, Jun

doi:10.1097/md.0000000000012201

Cited by 8 publications

(6 citation statements)

References 19 publications

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“…In the present study, a routine method and an enrichment method were used to perform HBV DNA extraction and measurement in the low-level HBsAg group, yielding positive percentages of 24.74% (97/392) and 45.92% (180/392), respectively. These prevalences are higher than those reported in the literature for the routine method (10.3%) and the enrichment method (34.6%) (44). Therefore, the present re-assessment of the low-level HBsAg population contributes relevant clinical, epidemiological and molecular biological information.…”

Section: Discussioncontrasting

confidence: 66%

Clinical characteristics and association analysis of persistent low‑level HBsAg expression in a physical examination population with HBV infection

Dai¹,

Che²,

Jiang³

et al. 2019

Exp Ther Med

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Certain patients with hepatitis B virus (HBV) infection present with persistently low levels of serum hepatitis B surface antigen (HBsAg) and have been indicated to have low rates of HBV nucleic acid replication. To explore the serological and molecular epidemiological characteristics of HBV population with low-level HBsAg in the present study, associated serum markers and virologic genotype detection were performed accordingly. Determination of HBV markers was performed using a chemiluminescence immunoassay from which 2,544 out of 45,256 adults who underwent routine health examination were tested positive for HBsAg. HBV DNA was detected by real-time fluorescent quantitative PCR. The patients were divided into low-level and high-level groups, according to their HBsAg levels (cut-off value, 10 IU/ml). The prevalence and levels of HBsAg positivity and HBV DNA in patients with HBV infection were analyzed by age, sex, serological pattern and clinical type. The fibrosis status of patients with low-level HBsAg was assessed by determining the aspartate aminotransferase-to-platelet ratio (APRI), and sequencing was employed to determine serotypes and genotypes. HBV-infected patients with low-level HBsAg (<10 IU/ml) accounted for 15.41% of the 2,544 HBsAg-positive patients, and the prevalence of HBsAg positivity exhibited a tendency to increase with age. The male-to-female ratio was ~1.9:1, and the average age was 54.98±16.28 years among HBV-infected patients with low-level HBsAg. The major serological pattern and clinical types were HBsAg/antibody against hepatitis Be antigen (anti-HBe)/antibody against hepatitis B core antigen (anti-HBc)-positive (94.90%) and chronic asymptomatic (ASC) (97.95%), respectively. HBV DNA exhibited a low-level of replication and the prevalence of HBV DNA positivity assessed by the routine method and by the enrichment method was 27.74% (97/392) and 45.92% (180/392), respectively. No significant differences among the age groups were identified in the different HBsAg level groups (P>0.05). The prevalence of HBV DNA positivity was associated with HBsAg only in patients with serological pattern HBV-M2 (HBsAg/anti-HBe/anti-HBc-positive) in the low-level HBsAg group (odds ratio: 1.30; 95% CI: 1.15–1.47; P<0.05). The APRI had no association with age, HBsAg, HBV DNA level or liver function index in ASC patients in the low-level HBsAg group (P>0.05). The prevalence of the serotype adw and genotype B was 85.53 and 89.47%, respectively. Further improvement in the systematic study of populations with low-level HBsAg has important clinical and epidemiological significance for improving the detection of HBV serological markers, elucidating the mechanisms leading to low-level HBsAg, overcoming immune tolerance to eliminate HBV infection and preventing HBV transmission.

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Section: Discussioncontrasting

confidence: 66%

Clinical characteristics and association analysis of persistent low‑level HBsAg expression in a physical examination population with HBV infection

Dai¹,

Che²,

Jiang³

et al. 2019

Exp Ther Med

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“…Every year, about 5 million people worldwide die due to hepatitis [1]. Literature data indicate that viral infections are the major causative factor of hepatitis, where there are no early markers available to detect the infection [2].…”

Section: Introductionmentioning

confidence: 99%

Eugenol attenuates concanavalin A-induced hepatitis through modulation of cytokine levels and inhibition of mitochondrial oxidative stress

Liu

Mao

2019

Arch biol sci (Beogr)

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Therapeutic management of hepatitis with conventional drugs alone worsens hepatic functioning in the long term because of sustained oxidative stress. Active compounds from several plant sources have been investigated to counteract this. Eugenol, a phytochemical abundant in various plants, is known for its wide range of pharmacological effects. There is a lacuna in the deeper understanding of its hepatoprotective activity at the molecular level. Our present study aimed to determine the effects of eugenol on the changes in antioxidant components, inflammatory cytokines and modulation of mitochondrial oxidative stress in immune-mediated hepatitis. We employed a model that mimics viral hepatitis using concanavalin A (ConA) to induce T-cell-mediated acute hepatitis. Eugenol increased (P<0.01) antioxidant enzyme activities, including reduced glutathione (GSH)-regenerating enzyme, glutathione reductase, and glucose-6-phosphate dehydrogenase. Its antiinflammatory and antifibrogenic effects were evident from the reduction (P<0.01) in interleukin and tumor necrosis factor levels. Eugenol was found to decrease mitochondrial oxidative stress, which was elevated in hepatitis. The hepatoprotective effects of eugenol were confirmed by histological findings. The current investigation shows that eugenol exerts a hepatoprotective effect through the modulation of different pathways which include restoration of mitochondrial oxidative stress. Eugenol could be a promising candidate for human hepatitis management, warranting preclinical studies.

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“…Generally, hepatitis B remains a major health concern worldwide, infecting ~350 million patients ( 29 ). HBV also ranks first among the causes of liver fibrosis in China, infecting ~7% of the entire population ( 30 ). At present, although anti-HBV treatment has limited success, chronic HBV infection gradually leads to the development of liver fibrosis and even liver cancer ( 31 , 32 ).…”

Section: Discussionmentioning

confidence: 99%

HBV induces liver fibrosis via the TGF‑β1/miR‑21‑5p pathway

Chen

et al. 2020

Exp Ther Med

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MicroRNA (miR)-21-5p is a newly discovered factor that mediates TGF-β1 signaling. The present study was designed to investigate the role of TGF-β1/miR-21-5p in hepatitis B virus (HBV)-induced liver fibrosis. HBV-infected sodium taurocholate co -t ra nspor ting polypeptide (NTCP)-transfected Huh7.5.1 cells were co-cultured with LX2 cells to simulate HBV infection in the present study. A total of 29 patients with chronic HBV infection were enrolled. Cells were transfected with miR-21-5p mimic or inhibitor with or without TGF-β1 stimulation. The demographic, biochemical and virological data from the 29 patients were analyzed and liver tissues were collected. miR-21-5p levels and the mRNA and protein expression of α-smooth muscle actin (SMA), collagen type 1 α 1 (CoL1A1), tissue inhibitor of metalloproteinase (TIMP)-1 and Smad from liver cells or tissues were detected by quantitative PCR analysis and western blotting, respectively. Cell viability was observed, and the liver fibrosis score was evaluated. The association between miR-21-5p and liver fibrosis was evaluated by correlation analysis. HBV infection upregulated TGF-β1/miR-21-5p mRNA expression in NTCP-Huh7.5.1 cells compared with mock infection (P<0.05). TGF-β1 incubation significantly increased miR-21-5p levels, as well as the mRNA and protein expression of α-SMA, CoL1A1 and TIMP-1, and reduced Smad7 expression in LX2 cells compared with the normal group, and these effects were counteracted by miR-21-5p inhibitor (P<0.05). miR-21-5p overexpression also contributed to TGF-β1-induced α-SMA, CoL1A1 and TIMP-1 expression in LX2 cells (P<0.05). Co-culture with HBV-infected NTCP-Huh7.5.1 cells upregulated TGF-β1/miR-21-5p activity and CoL1A1 expression in LX2 cells compared with normal control, which were significantly reduced by miR-21-5p inhibitor (P<0.05). miR-21-5p levels were significantly correlated with the liver fibrosis score (r=0.888; P<0.05). These data demonstrated that HBV induced liver fibrosis via the TGF-β1/miR-21-5p pathway and suggested that miR-21-5p may be an effective anti-fibrosis target.

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An epidemiological survey of HBV infection and low-level HBsAg in military camps in eastern China

Cited by 8 publications

References 19 publications

Clinical characteristics and association analysis of persistent low‑level HBsAg expression in a physical examination population with HBV infection

Clinical characteristics and association analysis of persistent low‑level HBsAg expression in a physical examination population with HBV infection

Eugenol attenuates concanavalin A-induced hepatitis through modulation of cytokine levels and inhibition of mitochondrial oxidative stress

HBV induces liver fibrosis via the TGF‑β1/miR‑21‑5p pathway

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