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Biomedical subjects

Z S Liang

Publications and source records attributed to Z S Liang.

9 recordsLinked to original sources
PubMed1994

[Correlation between HBV pre-C/C gene mutations and advanced pathologic activity in chronic hepatitis B].

To investigate the relationship of the HBV preC/C gene mutations with the disease persistence and exacerbation, the sequence of this region was analysed with direct sequencing by using the polymerase chain reaction product of the DNAs extracted from 24 such cases. A mutant with preC stop codon at the site 28 was detected in all the 11 anti-HBe-positive patients with different severity. This stop 28 mutant also coexisted with wild virus in seven of 18 HBeAg-positive patients. C gene mutations clustered in a small segment of codon 84-101, of those especially codon 97 was substituted in 11 of 15 mutants. There were 2, 6 and 20 codon mutations in 8 mild, 6 moderate and 10 severe cases respectively. In addition, the deletion of 144bp was also found in this region in a moderate case and that of 96bp in a severe case. Follow up of six patients revealed a close correlation between increase of genetic variation and advance of pathology.

Adult↗
PubMed1993

Etiological investigation of acute post-transfusion non-A, non-B hepatitis in China.

The etiology of acute post-transfusion hepatitis (PTH) non-A, non-B (NANB) in China was investigated with the combination of advanced techniques, including a second generation of enzyme immunoassay for detection of the antibodies to hepatitis C virus (anti-HCV), a reverse transcription and nested polymerase chain reaction (RT-nPCR) for HCV RNA, and a PCR for hepatitis B virus DNA. Of the 57 patients who were diagnosed as acute PTH-NANB, 46 (80.7%) were positive for anti-HCV and 41 (71.9%) had HCV RNA. Combining together, 53 (93.0%) were seropositive for anti-HCV and/or HCV RNA. Surprisingly, 18 of these with HCV markers were also positive for HBV DNA, although they were negative for HBsAg, suggesting that a portion of the patients with acute PTH NANB were coinfected by both HCV and HBV. In addition, 4 (7%) of the patients with acute PTH-NANB had no detectable HCV and HBV markers with the use of the above-mentioned techniques. These results indicate that etiologic agents(s) other than HCV and HBV may also cause acute PTH-NANB or that the current techniques may still not be sensitive enough to detect trace levels of HCV and HBV markers.

Adolescent↗
PubMed1992

Correlation between the prevalence of serum HBV DNA and immunoserologic HBV markers in the subjects with or without hepatitis.

The prevalence of serum HBV DNA, detected by polymerase chain reaction, and that of immunoserologic HBV markers (HBsAg, HBeAg, anti-HBs, and anti-HBc), determined by immunoassays, were compared among three groups of subjects: (A) chronic active hepatitis B patients, (B) chronic asymptomatic HBV carriers, and (C) normal individuals. Except five of the normal individuals, all of the subjects are positive for anti-HBc while some of them were also positive for other immunoserologic HBV markers, such as anti-HBs, HBsAg, and HBeAg. Serum HBV DNA were detected in 81% in group A, 52% in group B, and 20% in group C. In both group A and B, serum HBV DNA were detected in all the subjects with anti-HBc+/HBsAg+/HBeAg+. However, the percentage of seropositive HBV DNA in the subjects with anti-HBc+/HBsAg+ in Group A was much higher than that in Group B. Interestingly, the percent of serum HBV DNA+ in the individuals with anti-HBc+ only was markedly higher than that in the subjects with anti-HBc+/anti-HBs+ in both Group A and C, suggesting that anti-HBs may play a role in the inhibition of HBV replication and clearance of HBV virion from blood. Above serological profiles will provide important information concerning the significance of serum HBV DNA detection in judgement of HBV replication in the individuals with or without HBV infection. Cautions should be taken to clarify those so called normal individuals who have no symptoms of hepatitis B, no HBsAg in the sera and normal transaminase, but have HBV replication in their bodies.

China↗
PubMed1991

Hepatitis B virus DNA in sera of virus carriers positive exclusively for antibodies to the hepatitis B core antigen.

The prevalence of serum HBV DNA in individuals positive for anti-HBc alone was determined by the polymerase chain reaction in two groups with endemic HBV infection from Canton (group A) and Hainan (group B), provinces of China. Twenty-one out of 294 individuals in group A (7.2%) and 193 out of 1995 in group B (9.7%) were positive for anti-HBc but negative for other markers of ongoing or past HBV infection (HBsAg and anti-HBs). HBV DNA was detected in 6/21 sera in group A (28.6%) and 68/193 in group B (35.2%) in their initial serum specimen. One of the six HBV-DNA-positive individuals in group A became negative after 6 months and four of the 58 positive in group B became negative at 4 years of follow-up. All of the individuals remained positive for anti-HBc and negative for anti-HBs, but one of them became positive for HBsAg on follow-up. None of the anti-HBc- and HBV-DNA-positive subjects had symptoms of liver diseases. They were, therefore, defined as chronic asymptomatic HBV carriers with undetectable HBsAg. This type of carrier should be added to the typical HBsAg-positive carrier, who constitutes about 10-15% of the general Chinese population, to give a more complete estimate of asymptomatic HBV carriers in China.

Adolescent↗
PubMed1991

[Identification of HBV infection in HBsAg-negative chronic active hepatitis with polymerase chain reaction].

To explore the etiological agent(s) of HBsAg negative chronic active hepatitis, serum HBV DNA was tested in thirty-six of such cases with polymerase chain reaction. In total, viral DNA was detected in 24 cases (67%), including 11 of the 12 cases with positive anti-HBc alone, four of the nine cases with positive anti-HBs and nine of the 15 cases without any HBV markers. The results suggest that in cases of HBsAg-negative chronic active hepatitis, the etiology may still be hepatitis B virus, especially in cases with positive anti-HBc. Furthermore, the cause of activated histology might be due to viral replication.

Adolescent↗