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

144 / 152

S140 Abstracts / Journal of Clinical Virology 82S (2016) S1–S142
Abstract no: 218
Presentation at ESCV 2016: Poster 242
High frequency of JC human polyomavirus in
Portuguese wastewaters: A possible source for
human infection
F. Rodrigues ∗, D. Gonc¸ alves , C. Luxo ,
A.M. Matos
1 Laboratório de Virologia, Grupo das Biociências
Clínicas e Aplicadas, Faculdade de Farmácia da
Universidade de Coimbra, Portugal
2 Laboratório de Virologia, Grupo das Biociências
Clínicas e Aplicadas, Faculdade de Farmácia da
Universidade de Coimbra, Centro de Investigac¸ ão em
Engenharia dos Processos Químicos e dos Produtos
da Floresta (CIEPQF), Coimbra, Portugal
Introduction: JC polyomavirus (JCV) is ubiquitous among the
human population worldwide. Primary infection, typically asymp-
tomatic, normally occurs during childhood and is followed by a
lifelong persistent infection. JCV is excreted in the urine of nearly
half of the infected individuals, without any associated clinical
symptom. Under situations of severe immunosuppression, JCVmay
reactivate and induces a rare but fatal demyelinating disease of the
central nervous system known as Progressive Multifocal Leukoen-
cephalopathy (PML). Despite several hypothesis have been raised,
the main mode of transmission remains unknown. The high fre-
quency of urinary excretion of JCV lead several authors to evaluate
its presence in sewage wastewater systems, though, to date no data
have been reported for Portuguese wastewaters. In this order, the
present study represents the first comprehensive assessment of
JCV in Portuguese wastewaters along with its removal efficiency
by wastewater treatment plants (WWTPs), in order to add further
information for a possible way of JCV transmission to occur.
Materials and methods: Fifteen WWTP distributed all across
Portugal and serving 26.3% of theNational populationwere selected
for the present study. Two pairs of influent (WWI) (untreated)
and effluent (WWE) (treated) samples, were collected from each
WWTP, in September and December 2013, making a total of 60
wastewater samples. Viruses were concentrated by ultracentrifu-
gation as previously described nd detection and quantification
of JCV DNA in wastewater samples was obtained by a quantitative
real-time PCR protocol using a set of four amplification primers and
two internal TaqMan probes, previously described
Results: JCV genome was detected in 14 (93%) of the 15 eval-
uated WWTP, in at least one of the collected samples. Ninety per
cent of the tested influent samples revealed detectable JCV DNA,
at relatively high concentrations (mean = 5.48 ± 0.74 log10 GC/L).
The treatment of wastewater was able to completely remove JCV
genome from 14 (52%) of the 27 initial positive assessedWWI sam-
ples. In the remaining 13 initially positive WWI samples, despite
no complete removal was accomplished, a decrease in JCV concen-
tration was observed in the majority of cases.
Discussion: The ubiquity of JCV infection, claims for a common
route of transmission, particularly when seroepidemiological sur-
veys point to childhood as the age for first infection to occur. The
present study reveals the consistent detection of JCV genome in
sewage from the different regions of Portugal. Moreover, nearly
half of the WWTP were not able to completely remove the virus,
which, by this manner will end up incorporating treated sewage
and be distributed to the surrounding environment. Such viruses
may finally contaminate food and water, which may act as vehicles
for JCV transmission through oral route.
Reference
[1] A. Rafique, S.C. Jiang, Genetic diversity of human polyomavirus JCPyV in
Southern California wastewater, J. Water Health (2008),
.
[2] C.F. Ryschkewitsch, P.N. Jensen, E.O. Major, Multiplex qPCR assay for ultra
sensitive detection of JCV DNA with simultaneous identification of genotypes
that discriminates non-virulent from virulent variants, J. Clin. Virol. 57 (2013)
243–248,
Abstract no: 282
Presentation at ESCV 2016: Poster 243
An unusual course of parvovirus B19 infection,
strongly suggestive of virus reactivation
U. Reber ∗, S. Aldabbagh , S. Pietzonka ,
O. Moser , A. Simon , D. Dilloo ,
A. Eis-Hübinger
1 Institute of Virology, University of Bonn Medical
Center, Bonn, Sigmund-Freud-Str. 25, D-53105 Bonn,
Germany
2 Department of Pediatric Hematology and Oncology,
Center for Pediatrics, University of Bonn Medical
Center, Bonn, Germany
3 Division of Pediatric Hematology, Oncology & Stem
Cell Transplantation, University of Aachen, Germany
4 Pediatric Oncology and Hematology, Children’s
University Hospital, Homburg, Saar, Germany
Because of its highly efficient replication in erythroid progenitor
cells, parvovirus B19 (B19V) causes an interruption of the red cell
production which may result in a more or less severe anemia. After
primary infection and elimination of viremia, viral DNA persists
at low levels in multiple tissues, probably for life. It is not clear
whether the persisting virus is able to reactivate.
We present a case of severe B19V infection in a patient with
spherocytosis that was followed by a further episode of severe
anemia with B19V viremia three years later. Nearly full-length
nucleotide sequencing of the B19V genomes detected in blood
during primary infection and after three years revealed complete
identity of the genomes. Although not apodictically proven, this
case demonstrates that, in rare instances, recurrence of B19V infec-
tion might be possible.
Abstract no: 343
Presentation at ESCV 2016: Poster 244
Parvovirus B19: Its real disease associations
A.C.M. Kroes
Leiden University Medical Center, The Netherlands
Parvovirus B19 (B19V or primate erythroparvovirus 1, ssDNA)
is dependent on actively profilerating erythroid precursor cells for
its replication. This particular tropism is determined by the lack of
a viral DNA polymerase and by a receptor expressed on eythroid
cells, globoside. In addition to the childhood disease erythema
infectiosum, as an immunopathological consequence of infection,
all relevant pathology brought about by B19V is explained by the
property of wiping out erythrocyte precursor cells. A severe break-
down of red cell synthesis or aplastic crisis occurs in cases lacking
recruitment from a resting population, like in sickle cell anemia
and in expanding fetal erythropoiesis. In the fetus, this anemia