

Abstracts / Journal of Clinical Virology 82S (2016) S1–S142
S19
EV specimens in 2015mostly by sequencing. Survey revealed issues
related to EV typing/characterisation mostly in those countries
which rely only on virus neutralisation.
Discussion:
Our survey demonstrated some form of non-polio
EV surveillance throughout the EU/EEA region but only partial
HFMD and EV-D68 surveillance activity in the region. Virus iso-
lation is known to be less sensitive for EV detection than molecular
methods, and depends on cell lines used. It should also be noted
that most emerging EV types are refractory to isolation and anti-
bodies used in neutralisation assays are unlikely available. Hence
it is important to aim for introduction of molecular methods for
EV typing/characterisation throughout the region. We will develop
European algorithms for non-polio EV identification to strengthen
the European enterovirus laboratory preparedness.
http://dx.doi.org/10.1016/j.jcv.2016.08.034Abstract no: 43
Presentation at ESCV 2016: Oral 34
Neurotrophic potential of Saffold virus and the
effects of its leader protein in the central
nervous system of a mouse model
Mookkan Prabakaran
∗
, Shawn Zheng Kai Tan
Temasek Life Sciences Laboratory, Singapore
Background:
Saffold virus (SAFV) is a human cardiovirus
belonging to the
Picornaviridae
family. Since its discovery in 2007,
11 genotypes of SAFV have been identified and it has been shown to
be ubiquitous and causes infection early in life. Information about
SAFV infection tends to be concentrated on respiratory and gas-
trointestinal tract infections, however, there has been increasing
interest in SAFV infection of the central nervous system (CNS) due
to clinical cases of SAFVwith neurological symptoms (Nielsen et al.,
2012; Zhang et al., 2015) and also its close relation to Theiler’s
murine encephalitis virus (TMEV). Compared to TMEV, SAFV has
a truncated Leader (L) protein, a protein essential for the establish-
ment of persistent CNS infections.
Methods:
In order to study the replication kinetics and patho-
genesis of SAFV and its L protein, we generated an infectious cDNA
clone of SAFV and chimeric SAFV containing L gene of TMEV DA
strain. For
in vivo
pathogenicity study, we established a mouse
model for SAFV infection and then studied SAFV and chimeric SAFV
infections in the central nervous system.
Results:
We showed that both SAFV and chimeric SAFV are able
to infect Vero and Neuro2a cells well, but only chimeric SAFV was
able to infect RAW264.7. We then showed that AG129 mice lacking
IFN- / and IFN- receptors provide a good animal model for SAFV
infection, and further identified the locality of the infection to the
ventral horn of the spine and several locations in the brain. Next,
we showed that SAFV infects both neuronal and glial cells in the
brain, causing apoptosis in both. Lastly, we showed that SAFV does
not cause persistent infection nor demyelination in this model.
Conclusion:
Overall, our results provide a strong basis on which
the mechanisms underlying Saffold virus-induced neuropathogen-
esis can be further studied.
http://dx.doi.org/10.1016/j.jcv.2016.08.035Abstract no: 175
Presentation at ESCV 2016: Oral 35
Torque Teno Virus in liver tranplant patients in
Scotland, UK
C. Crossan
1 ,∗
, S. Warren
1, K. Simpson
2,
J. Davidson
2, A. Stanley
3, K. Bantouvakis
1,
L. Scobie
11
Glasgow Caledonian University, Glasgow, UK
2
Scottish Liver Transplant Unit, Edinburgh Royal
Infirmary, Edinburgh, UK
3
Glasgow Royal Infirmary, Glasgow, UK
Torque Teno Virus is a small (approximately 3.8 kb) single
stranded DNA virus first identified in a patient with non A-G hep-
atitis. Despite the circumstances of its discovery, its role as an
aetiological agent of hepatitis remains uncertain and it has been
shown to be a widely prevalent virus globally, including amongst
health individuals. However, previous studies have found a higher
viral load in immunosuppressed patients, such as those receiv-
ing post-transplant immunosuppression, and it has been suggested
that TTV viral load could prove a useful indicator of immunosup-
pression. Given this and TTV’s anecdotal association with hepatitis,
a study was undertaken to assess the TTV viral load of liver trans-
plant patients in comparison to control patients. Serum samples
from patients attending the Scottish Liver Transplant Unit (
n
= 93,
M
:
F
1:0.89, age range; 22–81 mean age = 57) and samples from
non-hepatic patients attending Glasgow Royal Infirmary (
n
= 50,
M
:
F
1:3.54, age range; 19–86 mean age = 61) were assayed for TTV
using a pan-TTV qPCR and genotyped using Genogroup specific
conventional PCRs. Whilst it was found that transplant patients
have a higher mean viral load in comparison to the control group
(3.8
×
10
6
vs 1.0
×
10
4
) the difference was not statistically sig-
nificant (
p
= 0.9007). In addition, variables such as age, sex, time
since transplant and reason for transplant were assayed for sig-
nificance but no correlation with viral load was identified. This
lack of significance may be due to the sample size and work is
ongoing to expand this. The genogrouping assays showed that all
5 Genogroups were present in both the liver transplant patient
and control groups. However, Genogroup 3 was the most com-
mon in the liver transplant patient group whilst Genogroup 4 was
the frequently identified Genogroup in the control group. The sig-
nificance of this is being further investigated, with a correlation
between Genogroup and viral load being one possible explanation.
The differences recorded in viral load between the liver transplant
patient and control group, and the various variables within the
patient group, deserve further investigation, in particular as pre-
vious studies have reported statistically significant increased viral
loads in patients receiving other forms of solid organ transplant and
it would be beneficial to identify if liver transplant patients show
a similar pattern or not. Also further investigation into the various
patient subgroups could elucidate the route of transmission of TTV
and its pathogenic role, if any. Lastly the variation in Genogroup
incidence between the patient and control group is an interesting
and novel finding that warrants further research.
http://dx.doi.org/10.1016/j.jcv.2016.08.036