The papillomaviruses are
small and nonenveloped,
with an icosahedral capsid, and,
important to remember,
circular, double-stranded DNA genome.
These are DNA viruses.
And you can see scanning electron microscopy
of them on the right side of the slide.
These viruses are ubiquitous,
but thankfully, they are very
and when so, it's typically in the setting
of an immunosuppressive event.
There are 2 important or medically-
that we'll discuss today,
the BK virus and JC virus.
Awfully unusual names for viruses,
however, each of these viruses
were named with the initials of the
first patient ever described
suffering from infection from those viruses.
Typical infection or pathogenesis
with both viruses
starts with a primary infection, which
is completely asymptomatic,
then latency occurs.
Immunosuppression, as I mentioned before,
is the reason for allowing reactivation,
and there's a cycle between
reactivation and latency
depending on the degree
In the case of JC virus,
with reactivation after immunosuppression,
viremia can occur,
and the virus deposits in the
central nervous system as a
When it does so, then it causes
and we'll talk about the clinical
meaning of that in just a bit.
With the BK virus,
reactivation occurring after
allows the virus to target the kidney
where it creates a urinary tract infection.
And, again, not the typical process
as we would expect with a bacterial
urinary tract infection, but something seen
in the setting of immunosuppression
in a kidney transplant recipient.
Who are the risks -- the people at risk for
developing reactivation of either virus?
These are especially our patients with
immunodeficiencies caused by
HIV infection, who would progress to AIDS.
Those who have received solid organ
transplants, who are receiving
immunosuppression to prevent rejection,
and those patients with other underlying
If we now look at the primary
infections for these viruses,
in general, the population at risk is
all of us.
All of us, either are at risk for, or
may already have acquired
a very completely asymptomatic
infection with either one or
both of the viruses.
If we have any symptoms at all,
they're incredibly mild.
A respiratory illness, very much
like a common cold.
And since we rarely do further
evaluation of a common cold,
there would be no way to know that we
had been infected with one or the other.
If we, then, look specifically at JC virus,
this is the cause of progressive multifocal
most often seen in patients who
due to HIV infection with AIDS.
Progressive multi-focal leukoencephalopathy,
reactivation of the JC virus within
the central nervous system creates
a progressive impairment of speech,
as well as vision, coordination through
as well as cognitive disarray.
Ultimately, this progresses to
paralysis and death,
very much like a very advanced or aggressive
form of Alzheimer's syndrome.
This occurs because there are abnormal,
targeted oligodendrocytes with
reactivation of the virus
that then cause the equivalent
of demyelinating syndrome.
BK virus, again, occurs most often in
renal or kidney transplant recipients,
and this will be at some point
after the primary transplant has occurred,
typically, in the early, post-transplant
immunosuppression is still quite extensive,
and there's been time for the virus to
reactivate within the renal setting itself.
These patients will have a severe
urinary tract infection,
not so much with dysurea, painful urination,
but with a very extensive
to these diseased reactivated cells.
So, one might see incredible
leukocytosis or leukorrhea
in the urine specimen,
as well as viruria, which can be
detected through sampling,
and ultimately, kidney dysfunction.
The challenge is, that an reactivated
BK virus, after a renal transplant,
may manifest as transplant rejection.
In both cases, one we need
to consider whether to
increase or decrease the
early diagnosis of BK virus
is quite important.
So, ubiquitous viruses that most of
us don't need to worry about,
unless we practice either
or transplant medicine,
but when they occur, they need to
be identified quickly.