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2015SupplementFULLTEXT

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970A AASLD ABSTRACTS HEPATOLOGY, October, 2015<br />

onymous (NS), genotype specific viral substitutions from wild<br />

type (WT) and entropy scores, were calculated across the<br />

whole genome (WG) and within specific structural (Envelope;<br />

Polymerase; precore-core, and; HBx) and regulatory regions<br />

(negative regulatory element- basal core promoter NRE-BCP)<br />

and correlated with baseline clinical and virological data and<br />

serological response at W192. Results 94 patients were successfully<br />

analysed (median age 32yrs; 75% male; genotype<br />

A/B/C/D 26%/23%/23%/28%; ALT 139 IU/mL; 24% cirrhosis;<br />

HBV DNA 8.43 log 10<br />

IU/mL; HBsAg 50,793 IU/mL;<br />

HBeAg 1,990 PEIU/mL; 77% TDF therapy W0-W48, 23%<br />

ADV therapy W0-W48). Median WG coverage, substitutions<br />

from WT and entropy scores are listed in Table 1. Entropy<br />

scores were similar across the genome, but three-fold greater<br />

in genotype B/C infection as compared to A/D (p< 0.0001).<br />

An increase in WG viral diversity was associated with lower<br />

baseline HBV DNA, HBeAg and HBsAg titres, independent<br />

of genotype (p< 0.0001 for all). Higher baseline viral diversity,<br />

specifically in BCP-NRE, was also associated with a lower<br />

likelihood of achieving HBeAg SC (p=0.04) and HBsAg loss<br />

(p

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