

S76
Abstracts / Journal of Clinical Virology 82S (2016) S1–S142
1.08–8 log UI/ml range, 10 (5.5%) with viral loads ranging from 1.18
to 1.87 log UI/ml were missed by the Veris assay and 1 with a
7.97 log UI/ml returned >8 log UI/ml. Quantification bias was calcu-
lated for the remaining 169 samples (67 gt1, 17 gt2, 33 gt3, 46 gt4,
2 gt5, and 4 gt6), the mean bias (Abbott–Veris) was 0.087 log UI/ml
(CI
−
0.894 to 1.068), with <0.5 log = “0” = “5-1” and =>1 log UI/ml
difference in 69.9%, 26.6% and 3.5% of cases, respectively. The max-
imal bias was observed for genotype 4 samples (0.572; CI
−
0.287 to
1.430), where an underestimation of viral load of 0.5–1.5 log UI/ml
was observed in 56.5% of cases. Regarding treatment monitoring,
HCV RNA remained detectable at low levels by the Abbott assay
1 to 3 time-points after Veris negativation in 17/20 patients who
achieved SVR; relapse was detected earlier by the Abbott assay in
2/5 cases.
Conclusions:
Discordances in HCV RNA detection between the
Veris assay and the Abbott assay were observed for low viral loads,
with little or no impact on patient monitoring in the present study.
However, significant underestimation of genotype 4 samples raises
concerns and requires optimisation of assay design for this highly
variable genotype.
http://dx.doi.org/10.1016/j.jcv.2016.08.150Abstract no: 271
Presentation at ESCV 2016: Poster 111
Reconstruction of the regional transmission of
HCV in Southern Sweden by phylodynamics
Malik Salam
1 ,∗
, Birgitta Holmgren
2,
Anna Söderlund Strand
2 , Gülsen Özkaya Sahin
2 ,Mattias Waldeck
3, Anders Widell
1,
Patrik Medstrand
11
Lund University, Faculty of Medicine, Department
of Translational Medicine, Malmö, Sweden
2
Department of Clinical Microbiology, Laboratory
Medicine, Lund, Sweden
3
Infection Control Unit, Region Skåne, Malmö,
Sweden
Background:
The molecular epidemiology studies of HCV are
useful to gain in-depth knowledge of timing and patterns of
viral spread. Analysis of laboratory testing sequence data can
give insights for prevention of virus spread. The objectives of the
current project were to characterize the genetic diversity and
transmission dynamics of HCV in Southern Sweden, as well as
identifying socio-demographic variables that are associated with
onward transmissions.
Methods:
Partial HCV
NS5B
gene sequences (339 bp) were
available from routine clinical testing for genotyping of clinical
isolates. The sequences were collected between 2004 and 2015.
Sub-genotyping was based on similarity search using Los Alamos
HCV sequence database BLAST tool. Phylogenetic analysis using
maximum likelihoodmethod (ML) was done based on Swedish and
reference sequences retrieved from GenBank using BLAST tool. ML
trees were reconstructed for determination of transmission clus-
ters representing domestic spread of HCV in Sweden. Analysis of
the transmission clusters was done using Cluster Picker software
withmonophyletic Swedish clades defined as those having approx-
imate Likelihood Ratio Test SH like (aLRT-SH) support value of 0.90
and containing more than 70% Swedish sequences. Transmission
clusters with two sequences were defined as dyads, those contain-
ing between three and 14 sequences were defined as networks and
those having more than 14 sequences were defined as large clus-
ters. Estimation of the evolutionary rate and time to most recent
common ancestors (tMRCAs) of the large Swedish clusters were
determined using Bayesian approach in BEAST.
Results:
A total of 3912 sequences with Open Reading Frames
(ORFs) were available for analysis. Genotyping revealed the fol-
lowing distribution: 1a (39%,
n
= 1513), 3a (38%,
n
= 1481), 2b (10%,
n
= 390) and 1b (10%,
n
= 374). For sub-genotype 1a, 550 sequences
were part of 138 transmission clusters (36%). Those clusters were
classified as 83 dyads, 50 networks and five large clusters. Possi-
ble geographic origins of some clades that resulted in domestic
spread of sub-genotype 1a included: Cyprus, Greece, Ireland, Iran,
Netherlands and USA. For sub-genotype 3a, 698 sequences were
part of 142 transmission clusters (47%). Those clusters were clas-
sified as 73 dyads, 60 networks and nine large clusters. Possible
geographic origins of some clades that resulted in domestic spread
of sub-genotype 3a included: Canada, Spain, Brazil, Malaysia,
Switzerland, China, Uzbekistan, Iran and Netherlands. For sub-
genotype 2b, 178 sequences were part of transmission clusters
(46%). Those clusters were divided into 36 dyads, 21 networks and
one large cluster. For sub-genotype 1b, 43 sequences were part
of transmission clusters (11%) and were classified into 17 dyads
and two networks. The time to Most Recent Common Ancestor
(tMRCA) of the oldest sub-genotype 1a cluster dated back to 1967
(95% HPD: 1959–1975). The tMRCA of the oldest sub-genotype 3a
cluster dated back to 1969 (95% HPD: 1962–1976).
Conclusions:
Four HCV sub-genotypes were prevalent in South-
ern Sweden between 2004 and 2015, with sub-genotypes 1a and
3a dominating the infections in terms of prevalence. The phylody-
namic approach unravelled patterns of viral spread and possible
geographic origins of HCV in Southern Sweden. Further studies
including association of socio-demographic variables to members
of clusters are underway and might be helpful in implementing
strategies for infection control.
http://dx.doi.org/10.1016/j.jcv.2016.08.151Abstract no: 287
Presentation at ESCV 2016: Poster 112
Occupational exposure to hepatitis E virus
(HEV) in Portuguese swine workers
J. Teixeira
1 ,∗
, S. Pereira
1 , R.M.S. Oliveira
1 ,J. Abreu-Silva
1, J.R. Mesquita
2, A. Rodrigues
3,
M.S.J. Nascimento
11
Laboratório de Microbiologia, Departamento de
Ciências Biológicas, Faculdade de Farmácia da
Universidade do Porto, Porto, Portugal
2
Escola Superior Agrária de Viseu, Instituto
Politécnico de Viseu, Viseu, Portugal
3
Escola Superior de Saúde de Leiria, Instituto
Politécnico de Leiria, Leiria, Portugal
Introduction:
The concept of zoonotic hepatitis E has emerged
with the discovery of animal strains of hepatitis E virus (HEV)
closely related to human HEV. Today, pigs are recognized as major
reservoirs and sources of HEV infection in humans. Different routes
of zoonotic HEV transmission have been recognized such as the
consumption of undercooked or raw meat from infected swine as
well as the contact with infected pigs. Many studies have reported
a high seroprevalence of anti-HEV in swine slaughterhouses work-
ers when compared with the general population, suggesting that
this professional group may be at higher risk for HEV infection.
Aims:
The aim of this study was to investigate if there was
also an occupational risk of zoonotic HEV infection in Portuguese
swine slaughterhouseworkers based on the differences of anti-HEV
seroprevalence rates between these professionals and the general