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

145 / 152

Abstracts / Journal of Clinical Virology 82S (2016) S1–S142 S141
presents as fetal hydrops, without fetal blood transfusion often
causing intrauterine death. A temporary arrest of erythropoiesis
occurs in all infected individuals, leading to disappearance of retic-
ulocytes. This is usually too short in duration to lead to a decline of
hemoglobin levels.
The initial phase of B19V infection is characterized by a brisk
viremic peak of an exceptional magnitude, amounting to 1012 viral
particles/ml or more. This viremia is likely the result of massive
replication in the bone marrow. Several studies have found evi-
dence of B19V DNA persisting in a wide array of tissues. This has
enabled historical analysis of viral genotypes in skeletal remains.
Viral persistence in tissues not known to support viral replication
could be understood by less specific uptake processes during the
viremic peak and subsequent cellular persistence of DNA, which is
not actively degraded.
Independently from these observations in the last decades
some additional pathological associations of B19V infection were
described. These associations were based on the detection of
viral DNA in affected tissues or on the occurrence of viral DNA
in blood. The most frequently reported additional association of
B19V infection concerns a role in various cardiac disorders, mainly
myocarditis and cardiomyopathy. As these findings were described
in prestigious cardiology journals, B19V was included among the
possible causes of myocarditis. From a virological point of view,
this association is difficult to interpret. There is no clear evidence
of viral protein expression or an immune response and there are
no epidemiological clues of infection, like concomitantly occurring
erythema infectiosum. In addition, the nature of cardiac disorders
presumably brought about by B19V appears rather variable.
For these reasons, several authors assumed that passive release
of B19VDNAof any damaged tissue harboring persisting virus could
well be an explanation for the findings. Still, confusion on the pos-
sible role of B19V in a number of disorders remains. Recently, in the
Sanquin/LUMC research group it was found that simple enzymatic
treatment of B19V DNA positive blood samples provided evidence
of the existence of two different states: stable, compatible with
protected viral particles or vulnerable, possibly consisting of naked
DNA. If confirmed, this would enable differentiation of the B19V
DNA findings into those directly related to viral replication and
those possibly emerging from passive tissue release. This is essen-
tial to determine the real disease associations of this infection. In
this way, the case of B19V underlines the importance of a plausi-
ble pathogenesis before assuming a causal role, solely based on the
finding of viral nucleic acid.
Abstract no: 51
Presentation at ESCV 2016: Poster 245
Occurrence, phase and status of human
parvovirus B19 infection in patients with
myalgic encephalomyelitis/chronic fatigue
syndrome
Santa Rasa ∗, Svetlana Chapenko ,
Angelika Krumina , Zane Zazerska ,
Modra Murovska
1 A. Kirchenstein Institute of Microbiology and
Virology, R¯ıga Stradin¸ ˇs University, Latvia
2 Department of Infectology and Dermatology, R¯ıga
Stradin¸ ˇs University, Latvia
Introduction: Myalgic encephalomyelitis/chronic fatigue syn-
drome (ME/CFS) is chronic, multifactorial diseasewith unexplained
etiology. Human parvovirus B19 (B19) is immunomodulating
single-stranded DNA virus belonging to Erythrovirus genus, Par-
voviridae family, Parvovirinae subfamily and is considered as
possible pathogen in development of ME/CFS he aim of this
study was to estimate frequency and activity phase of B19 infec-
tion, viral load, status of infection and clinical symptoms in patients
with ME/CFS.
Materials and methods: 200 patients (65% female and 35%
male, mean age 38 ±12 years) with according to CDC criteria diag-
nosedME/CFS and 104 age and gender matched apparently healthy
individuals were enrolled in this study. Presence of B19 specific IgM
and IgG class antibodies were analysed by recomWell and recom-
Line Parvovirus B19 IgM and IgG kits (Mikrogen Diagnostik). B19
NS1 gene sequence was detected with nested PCR and viral load
was estimated by Parvovirus B19 Real-TM Quant (Sacace Biotech-
nologies) real-time PCR kit.
Results:B19-specific IgG class antibodieswere found in 140/200
(70%) patients with ME/CFS and in 60/89 (67.4%) analysed appar-
ently healthy individuals. None of control individuals, though
16/200 (8%) patients with ME/CFS had IgM class antibodies
(p = 0.0038). Persistent B19 infection in latent phase had 24/200
(12%) patients and 8/104 (7.7%) apparently healthy individuals,
whereas in active phase – 34/200 (17%) ME/CFS patients and
2/104 (1.9%) control individuals (p < 0.0001). Elevated viral loadwas
detected in 20/58 ME/CFS patients and in none of 10 apparently
healthy individuals with B19 infection (p = 0.0276). B19 viral load
varied from<10 copies tomedian1044 (IQR3180-503.6) copies/106
cells.
Analysing B19 specific antibody reaction patterns, results show
that 29.3% of patients had infection status after infection (months),
30.7% – past infection (months to years), 12% had status infection
long ago, 6.7% – after infection (weeks to months) and one patient
had acute infection status. Such typical ME/CFS clinical symptoms
as impaired memory, subfebrility, lymphadenopathy and multi-
joint pain was observed more often in patients with persistent B19
infection in active than in latent phase. In 93.3% of patients onset of
symptoms has occurred 8.3 ± 1.7months ago and in 6.7% of patients
symptoms had started before 2.4± 0.5 years.
Conclusions: Results demonstrate finding of human parvovirus
B19 persistent infection in active phase significantly more frequent
and with higher B19 load among patients with ME/CFS than appar-
ently healthy individuals indicating on implication of B19 infection
in pathogenesis of ME/CFS. Therefore markers of active B19 infec-
tion could be used as one of biomarkers in ME/CFS diagnostics.
Association of persistent B19 infection in active phase with part
of typical ME/CFS clinical symptoms shows possible B19 involve-
ment in disease development and reactivation of B19 may be a risk
factor for ME/CFS.B19 infection statuses and onset of symptoms
allow suggesting the feasible role of B19 infection as a trigger factor
for ME/CFS.
Reference
[1] A.S. Bansal, A.S. Bradley, K.N. Bishop, S. Kiani-Alikhan, B. Ford, Chronic fatigue
syndrome, the immune system and viral infection, Brain Behav. Immun. 26 (1)
(2012) 24–31.
[2] F. Barah, S. Whiteside, S. Batista, J. Morris, Neurological aspects of human
parvovirus B19 infection: a systematic review, Rev. Med. Virol. 24 (3) (2014)
154–168.