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0:00
Hello. I'm Kevin Downes,
a Pediatric infectious
disease physician at
the Children's Hospital
of Philadelphia in
the Perelman School of Medicine
of the University
of Pennsylvania.
The topic I will
be discussing is
the management of
cytomegalovirus
or CMV in pediatric solid
organ transplant recipients.
0:18
I have no pertinent disclosures
relevant to this talk
although my institution receives
funding for research
that I conduct.
0:25
A brief outline of this
talk is shown on the slide.
We'll start with
the background of
CMV and review why it's
important in pediatric solid
organ transplant recipients.
We'll then review the key
features to determining
the risk of CMV and
transplant recipients
which ultimately
dictates the use of
specific prevention and
viral monitoring strategies.
We will spend the last
half of the talk reviewing
CMV treatment strategies
and the pros and
cons of available
antiviral therapies.
0:50
CMV is a betaherpesvirinae that
establishes lifelong latency
after primary infection.
It's an extraordinarily
common infection in
all individuals with most adults
infected by the age of 40.
Approximately one in three
are infected by the age of five
although there is significant
variability in the incidence of
CMV infections
geographically and
across different
living environments.
Transmission occurs via
person-to-person spread when
someone comes into contact
with infected body fluids.
Following primary
infection, the virus
is shed in urine and
saliva as well as
other body fluids for weeks
to months and sometimes
even for years making it
very easy to spread
to close contacts.
1:30
Fortunately, in
healthy individuals,
CMV infections are typically
self limited and mild.
It may cause a mononucleosis
type syndrome,
but infections are
often asymptomatic.
However, like all
herpes viruses,
CMV establishes lifelong latency
and is never fully
eradicated from the body.
Although it can reactivate
healthy individuals,
particularly in the settings of
stress on the immune system,
CMV rarely causes complications;
however, in organ
transplant recipients,
management of CMV
becomes a challenge.
Immune control of
CMV is complex and
requires competent host
cellular immune response.
Upon infection, multiple arms of
the innate and adaptive
immune systems
play a role in limiting
viral replication,
but CMV infects
multiple cell types
and employs strategies to avoid
elimination and
establish latency
within a number of host
cell types within the body.
Cellular immune
responses, most notably
CD8+ memory T cells
provide long term protection
against CMV reactivation.
An impairment of this term of
the immune system
is what allows for
CMV replication and ultimately
disease following
organ transplantation.
Although humoral
immune responses
are involved in the
initial infections,
they ultimately play a
limited role in control of
CMV replication and
reactivation long term.
