

Abstracts / Journal of Clinical Virology 82S (2016) S1–S142
S75
imens identified as subtype 1a; (iii) 11 specimens identified as
subtype 1b. All specimens were tested with the GT
Plus
assay on
the
m
2000 RealTi
m
e System. This assay targets the core region to
specifically identify subtypes 1a and 1b as well as genotype 6 and is
designed to be used as a reflex test if the GT II assay fails to subtype
genotype 1 (based on the 5 UTR and NS5B regions). The reference
method (RT-PCR and sequencing of the core and NS5B regions fol-
lowed by phylogenetic analysis) was performed in 49 specimens
either without assigned subtype by the GT II assay, with discrepant
subtype assignment between the two Abbott assays or with a “not
detected” result by the GT
Plus
assay.
Results:
Among those specimens without assigned subtype by
the GT II assay, the GT
Plus
assay was able to subtype 38 cases
(84.4%), while the other 7 cases (15.6%) were not detected. Among
those specimens identified as 1a by the GT II assay (
n
= 10), 9 (90%)
were concordantly identified by the GT
Plus
assay, while one spec-
imen was identified as having a mixed infection (1a + 1b). Among
those specimens identified as 1b by the GT II assay, 8 (72.7%) were
concordantly identified by the GT
Plus
assay, while three (27.3%)
were not detected. All viral loads were above the lower limit of
detection of the assay (range, 2.96–7.84 log(IU/mL)). Two speci-
mens corresponding to subtypes 1e (
n
= 1), and 1 g (
n
= 1) showed
“not detected” results in concordancewith the GT
Plus
assay design.
Another 8 “not detected” specimens (8/66, 12.1%) were classified
as 1b. Among the rest of specimens, all subtype assignments by
the GT
Plus
assay were in agreement with HCV classification by the
reference method (NS5B and core regions, confirming the absence
of recombination events) except for one specimen (97.4%) where a
mixed subtype infection was detected by the former assay (1a + 1b)
that could not be evidenced by Sanger sequencing.
Conclusions:
The GT
Plus
assay was able to subtype 84.4% of
the specimens not subtyped by the GT II assay and showed a good
agreement (97.4%) with the reference method for the identification
of 1a and 1b subtypes. Sequences generated in this study may help
to understand the reasons for not detected results among certain
1b isolates.
http://dx.doi.org/10.1016/j.jcv.2016.08.148Abstract no: 265
Presentation at ESCV 2016: Poster 109
Prevalence of hepatitis delta virus infection
among hepatitis b virus surface antigen positive
patients diagnosed in a Central Hospital in
Portugal, a 5 years retrospective study
F. Paramés
1 ,∗
, S. Paulo
2, P. Barbeiro
1,
J. Sampaio
1, H. Proenc¸ a
1, J. Melo-Cristino
11
Servic¸ o de Patologia Clínica – Hospital de Santa
Maria, Centro Hospitalar de Lisboa Norte, EPE,
Portugal
2
Servic¸ o de Patologia Clínica – Centro Hospitalar da
Cova da Beira, Portugal
Background and aims:
Hepatitis delta virus (HDV) is a single-
stranded, circular RNA virus that requires the hepatitis B surface
antigen (HBsAg) to infect. A dual HBV-HDV infection progresses
rapidly, and is associated with more complications: cirrhosis, end-
stage liver disease, and hepatocellular carcinoma when compared
with HBV monoinfection. HDV is transmitted by parenteral expo-
sure and the basis of the diagnosis is the presence of antibodies
against HDV (anti-HDV) and hepatitis B surface antigen (HBsAg) in
the serum of a patient with chronic liver disease. It is confirmed by
the presence of the HDV antigen.
The hepatitis D prevalence vary between geographic regions,
but it remains endemic in many regions of the globe. The Health
Care effective measures to control HBV infection have consistently
diminished the circulation of HDV in countries where they were
applied (vaccination + prevention). However, recent studies report
a rising prevalence of HDV infection attributed to immigration from
high prevalence areas and to local groups of intravenous drugs
users.
The aim of our study was to characterize hepatitis delta virus
infection prevalence among hepatitis B virus surface antigen posi-
tive patients diagnosed in a Central Hospital in Portugal in the last
5 years (2011–2015).
Results:
From 2011 to 2015, our Laboratory followed 1998
patients with detected HBsAg (1158 male, 840 female, mean age
44.9 [2–94 years old]). We were requested to study 2071 patients
for HDV infection (1140 male, 931 female, mean age 47.8 [1
month–98 years old]).
86 patients tested positive for acute or previous HDV infection
(AgHVD and/or AcHVD IgM and/or AcHVD IgG positive): 61 male,
25 female, mean age 42.4 [19–72 years old]. These patients were
followed mainly in Clinical Services of Gastroenterology (45) and
Infectious Diseases (28).
We found 41 patients with acute HVD infection (2 patients
AgHVD positive; 1 patient AgHVD/HVD IgG positive; 1 patient
AgHVD/HVD IgM/HVD IgG positive; 3 patients HVD IgM positive;
34 patients HVD IgM/IgG positive) and 45 patients with previous
HVD infection (HVD IgG positive).
Conclusions:
Precise rates of prevalence and risk factors must
be available to help clinicians decide who to screen. Because of the
more aggressive nature of HBV-HDV dual infection the diagnosis
and beginning of an adequate treatment regímen should not be
delayed.
http://dx.doi.org/10.1016/j.jcv.2016.08.149Abstract no: 270
Presentation at ESCV 2016: Poster 110
Clinical evaluation of the Veris HCV assay for
hepatitis C virus RNA quantification
Laure Izquierdo
∗
, Stéphanie Haim-Boukobza,
Corinne Prégermain, Anne-Marie Roque-Afonso
AP-HP Paul Brousse Hospital, Virology, Villejuif,
France
Background:
Accurate detection and quantification of hepatitis
C virus (HCV) RNA is essential for treatment monitoring but also
for viral safety of blood and organ donation. Molecular diagnostics
platforms are evolving towards reduced and simplified handling
procedures such as the fully automated, random access DxN VERIS
MDx System (Beckman Coulter). The clinical performance of the
Veris HCV assay was evaluated in comparison with the RealTime
HCV assay (Abbott Molecular).
Materials andmethods:
The panel comprised 286 plasma spec-
imens from146HCV-positive patients, including 142 serial samples
from 25 patients (3–11 time-points/patient) on treatment moni-
toring of whom 20 achieved sustained virological response (SVR)
and 5 experienced relapse. Quantitative results were compared by
Bland–Altman method.
Results:
Indeterminate Veris results (PCR inhibitors) were
obtained in 6 cases (2.1%). In the remaining 280 samples, all 54
Abbott undetectable results returned undetectable; from 46 sam-
ples with detectable HCV RNA below 12UI/ml, 42 (91.3%) returned
not detected and 4 returned viral loads ranging from 1.32 to
1.73 log UI/ml; among 180 samples with Abbott results within the