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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.2016.08.034

Abstract 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.2016.08.035

Abstract 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

1

1

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