APOBEC has been reported to be a restriction issue for several

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An initial report using Huh7 hepatoma cells recommended that HBV DNA doesn't exhibit G-to-A hypermutation after CX-4945 web transfection of A3G, but that pregenomic RNA was inefficiently packaged (Seppen, 2004; Turelli et al., 2004). A3G levels appear to be low in primary hepatocytes, but can be induced by interferon (Bonvin et al., 2006). In addition, human A3B, A3C, A3G, A3H, and AID mRNAs are upregulated by inflammation, which often accompanies viral infection (Endo et al., 2007; Vartanian et al., 2010). HBV may replicate in non-hepatic cells, although replication in hematopoietic cells appears to be extremely low (Rosler et al., jir.2011.0103 2004; Untergasser et al., 2006). HBV DNA sequences in the livers of 4 individuals with high levels of viremia had been enriched by 3D-PCR (Susp e et al., 2005). Two of these patient samples gave PCR goods at a denaturation temperature of 90 , and sequencing of those merchandise revealed that a modest number had G-to-A mutations. The context of these mutations was consistent with the preference of A3G (Susp e et al., 2005).APOBEC has been reported to become a restriction factor for a number of DNA-containing viruses [reviewed by (Moris et al., 2014)]. Hepatitis B virus (HBV) is one of the most studied instances of APOBEC-mediated inhibition of a DNA virus. HBV is really a pararetrovirus which is a major reason for liver cirrhosis and cancer (Beggel et al., 2013; Bonvin and Greeve, 2008). Similar to foamy virus, HBV has a reverse transcriptase that copies packaged pregenomic RNA into DNA within scan/nsw074 the nascent capsid on the producer cells (Jones and Hu, 2013). In contrast to retroviruses, the reverse trascriptase is covalently attached to the 5 finish of the minus-strand DNA and doesn't fully complete plus strand synthesis inside producer cells. The remaining single-stranded DNA area represents a organic target for APOBEC household enzymes (Beggel et al., 2013). An initial report applying Huh7 hepatoma cells recommended that HBV DNA doesn't exhibit G-to-A hypermutation immediately after transfection of A3G, but that pregenomic RNA was inefficiently packaged (Seppen, 2004; Turelli et al., 2004). A3G appeared related with viral cores within the cytoplasm, and equivalent observations have been created for A3B, A3C, A3F, and A3G in a further hepatoma cell line (Susp e et al., 2005; Turelli et al., 2004). Additional investigation revealed that G-to-A hypermutations were observed at low frequencies (