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    • br Introduction The rate of

    2018-10-25


    Introduction The rate of hepatitis B infection is very high in China, and hepatitis B can chronically induce cirrhosis and primary hepatocellular carcinoma. Hepatitis B has become a social problem compromising the health of civilians in China, and Chinese patients comprise about one third of all of the chronic hepatitis B patients in the world. Hepatitis B virus (HBV) is a DNA virus that affects the liver, and its genome is comprised of 3200 nucleotides and 4 open reading frames that encode 6 proteins. Three extracellular proteins encoded by the S NHS Biotin include small protein (HBsAg protein), middle protein (HBsAg and Pre-S2 proteins) and large protein (HBsAg, Pre-S1 and Pre-S2). Hepatitis B virus large envelope proteins (LHBs) play an important role in invasion, assembly and replication of HBV. Bruss et al. found that LHBs functioned as both the receptor protein for viral invasion and the matrix protein for viral assembly. Summers et al. found that LHBs could increase the copy number of cccDNA and initiate replication of cccDNA. The dual topological structure of the pre-S domain, instead of the Pre-S1 domain, determines the trans-activation function of LHBs. LHBs reside in Dane granules and subviral tubular granules, which are important markers of HBV with an intact capsule. These correlate well to HBV DNA, which can reflect the replication status of HBV in patients. Reports showed that LHBs were in good correlation with HBV DNA in patients with HBeAg-negative diseases, suggesting clinical potential for monitoring viral replication in HBeAg-negative patients.
    Materials and methods
    Results
    Discussion At present, detection of HBV replication mainly depends on tests for HBeAg and HBV DNA. It is thought that the seroconversion from HBeAg to HBeAb in HBV patients suggests cessation of HBV replication. However, many studies have shown that in some HBeAg-negative patients, the mutations of pre-C/CP domains inhibit the replication of HBeAg and lead to HBeAg-negative and HBV DNA-positive results, which are called HBeAg-negative chronic HBV. It also suggests that HBeAg cannot represent the termination or attenuation of HBV replication. The HBV DNA test is the common clinical assay for monitoring the effectiveness of the antiviral treatments. However, recent studies have shown that the seroconversion of HBV DNA in peripheral blood did not indicate the absence of HBV, as the subduction of cccDNA in the liver was much slower than that in the peripheral blood. Clinical cases showed that when cccDNA maintained in liver, even if HBV DNA in the peripheral blood was converted, the likelihood of recurrence was higher. LHBs with dual topological structures, residing in Dane granules and tubular subviral particles, are important components of the HBV envelope proteins. LHBs play important rolei s in trans-activating viral replication and i cccDNA copy increasing. Studies have shown that LHBs directly cause toxicity and carcinogenicity of liver cells, which lead to fibronic cholestatic hepatitis. LHBs are closely involved in cccDNA replication by their trans-activation function, and it is known that subviral particles can significantly enhance the viral replication and gene expression in the duck HBV model. The pre-S proteins, rather than the pre-S1 proteins, trans-activate signal transduction. Studies have also shown that HBV transmissibility depends not only on the quantity of infectious Dane granules, but also on the number of subviral particles, especially pre-S proteins on LHBs. This finding has important clinical significance for understanding the prognosis of HBV DNA-negative and LHB-positive patients, who are in the anaphase of clinical treatments. Meanwhile, Cheng Jun et al. has reported that different HBV pre-S fragments are able to self-activate. Therefore, LHB examination can help in clinically determining in vivo HBV replication and monitoring the effectiveness of the antiviral treatments. Wei Hongshan et al. showed that the LHB test was a helpful compensation for the HBeAg examination, especially in patients whose HBeAg expression was stopped due to selective pressure-induced HBV mutation.