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HEPATOLOGY, VOLUME 62, NUMBER 1 (SUPPL) AASLD ABSTRACTS 1025A<br />

1674<br />

Long-term follow-up study of hepatitis delta virus quasispecies<br />

complexity<br />

Maria Homs 1,2 , Maria Buti 1,3 , Alicia Ruiz 4 , Pilar Reimundo 4 , Josep<br />

Gregori 5 , Maria Blasi 1,2 , Rosario Casillas 5 , David Tabernero 1,2 ,<br />

Marta Vila 5 , Leonardo Nieto 2 , Josep Quer 1,5 , Mar Riveiro-Barciela<br />

3 , Rafael Esteban 1,3 , Francisco Rodriguez-Frias 1,2 ; 1 Centro<br />

de Investigacion Biomedica en Red de Enfermedades Hepaticas y<br />

Digestivas, CIBERehd, Barcelona, Spain; 2 Microbiology, Hospital<br />

Vall d’Hebron, Barcelona, Spain; 3 Hepatology, Hospital Vall d’Hebron,<br />

Barcelona, Spain; 4 Biochemistry, Hospital Vall d’Hebron,<br />

Barcelona, Spain; 5 Liver Diseases, Research Institute of Vall d’Hebron,<br />

Barcelona, Spain<br />

Background The hepatitis delta virus (HDV) genome encodes<br />

two antigens essential for viral cycle, small and large (S- and<br />

L-HDAg). Genomes with a stop codon in position 196 encode<br />

S-HDAg, and with a tryptophan encode L-HDAg. Immune<br />

responses likely play a key role in controlling HDV infection;<br />

but changes occurring in the quasispecies (QS) complexity and<br />

in the percentage of genomes encoding S-HDAg and L-HDAg<br />

in the circulating HDV QS are unknown. Aim Evaluate changes<br />

in the complexity of HDV QS and in the percentage of genomes<br />

encoding S-HDAg and L-HDAg during long-term chronic HDV<br />

infection. Patient and methods Twelve consecutive serum samples<br />

from a patient with chronic HDV followed for 12 years<br />

were included. The patient was HDV genotype 1, HBeAg-negative,<br />

and HBV-DNA levels were

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