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Inhibition of Hepatitis B Virus Replication by the Apobec3 Proteins (Paperback) Loot Price: R1,544 Discovery Miles 15 440
Inhibition of Hepatitis B Virus Replication by the Apobec3 Proteins (Paperback): David H Nguyen
Inhibition of Hepatitis B Virus Replication by the Apobec3 Proteins (Paperback): David H Nguyen

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Inhibition of Hepatitis B Virus Replication by the Apobec3 Proteins (Paperback)

David H Nguyen

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Loot Price R1,544 Discovery Miles 15 440

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Hepatitis B virus (HBV) is a major cause of acute and chronic viral hepatitis. In the United States, there are approximately 250,000 to 300,000 new cases of HBV infections annually, and roughly 1.25 million chronic carriers of HBV. Globally, it is estimated that 350 million individuals are chronically infected with HBV and that one million people die annually from chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma induced by HBV. HBV belongs to the family of Hepadnaviridae, which are small enveloped viruses, with a partially double-stranded, relaxed-circular (RC) DNA genome. The hepadnaviruses are classified as para-retroviruses because they replicate this DNA genome through reverse transcription of an RNA intermediate, the pregenomic RNA (pgRNA). In the cytoplasm of the hepatocyte, pgRNA is selectively packaged along with the virally encoded reverse transcriptase (RT) into HBV nucleocapsids. The encapsidation of pgRNA requires the recognition and binding of RT to a stem-loop structure located at the 5' end of the pgRNA called epsilon (epsilon). The formation of the RT-epsilon ribonucleoprotein complex triggers viral assembly and leads to the specific incorporation of both the pgRNA and RT into replication-competent nucleocapsids where reverse transcription takes to form the mature RC DNA genome. For a long time, it was thought that the adaptive and innate immune responses were primarily responsible for providing protection against viral pathogens. However, during mammalian evolution, a variety of mechanisms have arisen to rid the host of viral infectious agents. It is becoming increasingly clear that dominant inhibitory cellular factors can also have an important role in controlling host susceptibility. Recent studies have established that the APOBEC3 cytidine deaminases represent a major defense barrier against a wide range of viruses. APOBEC3 is a member of the APOBEC family of cytidine deaminases that also includes APOBEC1, -2, and the activation induced deaminase. In humans, the APOBEC3 subfamily has been expanded to include seven members, APOBEC3A to H, which lies in tandem on chromosome 22. Recently, the cellular protein APOBEC3G (A3G) was shown to inhibit the infectivity of Vif-deficient HIV-1. A3G packaged into the viral particle mediated deamination of dC residues in the nascent minus-strand DNA during reverse transcription of the HIV-1 genome. As a result of this deamination, G-to-A hypermutation of the plus-strand DNA could occur, resulting in an increased proportion of non-infectious virus. Alternatively, the uracil-containing DNA may prevent accumulation of reverse transcripts, either by triggering degradation by cellular DNA enzymes or by impairing viral protein synthesis. The known specificity of A3G on single-stranded DNA suggested that it might inhibit any virus with a single-stranded DNA intermediate, such as the para-retrovirus HBV. We showed that A3G, as well as several of the other APOBEC3 proteins, could inhibit HBV DNA replication by acting mainly at the DNA level, with only a minor effect on viral RNA packaging. However, inhibition of HBV DNA synthesis was not by editing of the viral genome, but rather, the main mode of inhibition was via a deaminase-independent mechanism. Although it is still poorly understood, the editing-independent mechanism of A3G seemed to target a very early stage during viral reverse transcription to block HBV DNA synthesis. Furthermore, by using a native agarose gel electrophoresis assay that can specifically measure the levels of A3G incorporation into HBV nucleocapsids, we found that A3G was specifically packaged into replication-competent HBV nucleocapsids in a...

General

Imprint: Proquest, Umi Dissertation Publishing
Country of origin: United States
Release date: September 2011
First published: September 2011
Authors: David H Nguyen
Dimensions: 254 x 203 x 17mm (L x W x T)
Format: Paperback - Trade
Pages: 260
ISBN-13: 978-1-243-56592-1
Barcode: 9781243565921
Categories: Promotions
Books > Science & Mathematics > Biology, life sciences
Books > Science & Mathematics > Biology, life sciences > General
LSN: 1-243-56592-6

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