Polyomavirus infection occurring during childhood
is followed by a lifelong latency in immunocompetent
subjects. The major site of
polyomavirus persistence are the uroepithelial
cells which leads to oral transmission. It has
recently been hypothesized that tonsils could be a
possible reservoir. The role of tonsil, adenoid,
and peripheral blood mononuclear cells (PBMCs)
as possible sites of JCV, BKV, and SV40 latency
in young healthy children was assessed. Two
hundred fifteen fresh specimens, including 57
tonsil, 80 adenoid, and 78 PBMC samples from 80
immunocompetent children (mean age 4.8 years)
were analyzed to determine the viral load by
quantitative real-time PCR. The human herpes
virus 6 (HHV-6) was tested as a lymphotropic
reference virus. Polyomavirus was detected in 5/
80 (6.2%) children while HHV-6 infection affected
27/80 children (33.7%) (P<0.001). SV40 was
detected in one adenoid sample, while footprints
of BKV were found in one adenoid and three
tonsil samples. JCV was never found in all
samples. Polyomavirus sequences were not
detected in the 78 blood samples. One adenoid
and two tonsils from three children (1.4%) were
positive for both polyomavirus and HHV-6.
Infections were characterized by low replication
rates ranging typically from 110e2/5.510e4 to
6.810e3/8.510e4 viral copies/number of cells.
In conclusion, tonsils and adenoids of children
could effectively harbor BKV and SV40, although
only very few cells proved to be infected. Nevertheless,
the low prevalence of polyomavirus, in
comparison with the lymphotropic HHV-6, suggests
that these tissues are unlikely to be the
preferred site of polyomavirus latency, at least
in younger children.
