Journal of Clinical Virology - Volume 82 - Supplement 1 - September 2016

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Abstracts / Journal of Clinical Virology 82S (2016) S1–S142 S11
3.2 × 104 copies/ml) and 180 days after transplantation (median
4.3 × 106 copies/ml; p < 0.001). On the contrary, a slight decrease
on median TTV load was observed between 180 and 360 days after
transplantation (p = 0.06). Forty-seven out of 78 (60.3%) patients
received basiliximab (Simulect) as induction therapy, while 31/78
(39.7%) received antithymocyte globulin (thymoglobuline). No dif-
ferences on peak of viral load or time to reach the peak were
observed in patients according to different induction therapy. In a
series of patients, immunological data were available and therefore
compared to TTV load kinetics. After a slight decrease of T-CD4+, T-
CD8+ cell counts between 15 and 30 days after transplantation, a
significant increase of T-CD4+, T-CD8 + cell counts between 30 and
360 days after transplantation was observed (p < 0.05). The kinet-
ics of TTV DNA load and immune reconstitution showed the same
tendency but no statistically significant correlation was observed
between TTV viremia and lymphocytes levels.
Discussion and conclusions: In conclusion our findings provide
evidence of high positivity rate of KTRs during the first post-
transplant year. The TTV load kinetics showed a sigmoidal-shaped
curve as previously observed by Görzer et al. in lung transplant
recipients o correlation between TTV DNA load level and dif-
ferent induction therapy was observed. Despite the increased level
of immune reconstitution, in about 40% of patients the TTV DNA
load at 360 days after transplantation was >2 log10 DNA copies/ml
with respect to TTV load level in the immediately post-transplant
period. Finally, in near 30% of patients the peak of TTV load was
observed at 360 days after transplantation.
Reference
[1] I. Görzer, P. Jaksch, M. Kundi, T. Seitz, W. Klepetko, E. Puchhammer-Stöckl,
Pre-transplant plasma Torque Teno virus load and increase dynamics after lung
transplantation, PLOS ONE 10 (April (3)) (2015) e0122975.
Abstract no: 344
Presentation at ESCV 2016: Oral 19
Encephalitis caused by a novel adenovirus
“orphan genome” in an adult allogenic SCT
recipient
A. Heim ∗, E. Hage , A. Turki , R. Trenschel ,
S. Ross
1 Institute of Virology, Hannover Medical School,
Hannover, Germany
2 Klinik für Knochenmarktransplantation,
Universitätsklinikum Essen, Germany
3 Virology, University Essen, Essen, Germany
Introduction: Since the addition of a genotype definition to the
classical definition of human adenovirus (HAdV) serotypes and the
use of next generation sequencing for the differentiation of human
adenovirus isolates, the number of HAdV types increased rapidly
from 51 to 72. Fifteen of these 21 newly identified types belong
to species HAdV-D and 12 of these 15 new HAdV-D types were
found to have multiple recombinant genomes. Many of these new
HAdV-D types were isolated from the faeces of adult immunocom-
promised patients suggesting persistent infections of adults and
reactivation after immunosuppression. Persistent infections may
facilitate co-infections with more than one HAdV-D type and this
seems to be a prerequisite for homologous recombination. How-
ever, the virulence of most of these new HAdV-D types seems to
be rather low (with exception of a few types causing epidemic
keratoconjunctivitis, e.g. types 53 and 54) and severe disease man-
ifestations have hardly ever been found to be associated with these
types.
Clinical case and diagnostic virology: A 54 year old male
presented with encephalitis on day 93 post allogenic stem cell
transplantation (SCT). Neurotropic viruses were not detected in CSF
but a high concentration of HAdV DNA (3e5 c/ml) was detected by
quantitative PCR. In contrast to typical acute infections, HAdV DNA
was not detected at other body sites. In peripheral blood, only a low
virus load (below the level of quantification, <1e3 c/ml) was found,
far too lowfor a disseminated infection. Therefore, HAdVencephali-
tis, probably caused by a HAdV reactivation, was diagnosed. In
spite of antiviral therapy with cidofovir the patient succumbed to
encephalitis on day 122.
HAdV typing: Complete genomic sequencing directly from CSF
demonstrated a multiple recombinant HAdV-D genome with a
hexon sequence (including the neutralization epitope) almost iden-
tical to type 25 whereas other parts of the genome were either
related to types 47, 56, 59 or were novel sequence stretches.
According to the rules of HAdV taxonomy, the pathogen should
be labelled as a new HAdV type. However, virus isolation on A549
cells failed and therefore a new type number was not assigned to
this genome.
Discussion and conclusions: Reactivations of species D HAdV
may occur in adults as late complications after allogenic SCT. These
reactivations can be limited to a single organ (e.g. encephalitis)
and thus diagnosis may be difficult. Next generation sequencing
facilitates the identification of novel HAdV types, but new com-
plete genomic sequences can also be generated in cases of failed
virus isolation resulting in an orphan genome (here defined as a
complete genomic sequence without virus isolate). Although the
virulence of many HAdV-D types and “orphan genomes” may be
low in general, these can cause severe opportunistic infections of
immunocompromised patients.
Abstract no: 250
Presentation at ESCV 2016: Oral 20
Molecular and clinical characterization of
Enteroviruses-D68 infections between 2010 and
2015 in Lyon, France using 3D Cell culture and
Next-Generation Sequencing
M. Sabatier ∗, M. Pichon , M. Essaidi-Laziosi ,
D. Falcon , C. Tapparel , I. Schuffenecker ,
B. Lina , L. Josset
1 National Reference Centre on Enterovirus and
Parechovirus, Virology Laboratory, University
Hospital of Lyon, Lyon, France
2 VIRPATH Inserm U1111 – CNRS UMR 5308, Faculté
de médecine Laennec, Lyon, France
3 Faculty of Medicine of Geneva, Department of
Microbiology and Molecular Medicine, Geneva,
Switzerland
Introduction: In August 2014, the United States reported an
outbreak of Enterovirus-D68 (EV-D68) infections, associated with
severe respiratory disease in children. In this study, we investigated
the prevalence and molecular evolution of EV-D68 circulating in
France between 2010 and 2015, in association with clinical data.
Methods: Respiratory samples collected frompatients hospital-
ized in the University Hospital of Lyon between weeks 31 and 51
from 2010 to 2015 and positive for viruses of Picornaviridae family
were screened for EV-D68 using quantitative RT-PCR. We further
propagated EV-D68 in 3D human primary upper airway epithe-