Please wait while the transcript is being prepared...
0:00
Hi everyone.
My name is Pleuni Pennings,
and I'm an Associate Professor
at San Francisco
State University.
I use population genetic theory
and analysis of patient data
to study the
evolution and spread
of drug resistance in
human pathogens to find
better ways to prevent
drug resistant infections.
Today,
I will talk about the evolution
of drug resistance in HIV,
Mycobacterium tuberculosis,
and Staphylococcus aureus.
The lecture will include
information also
on selective sweeps and
clonal interference.
0:39
According to Wikipedia
drug resistance is the reduction
in effectiveness
of a medication,
such as an antimicrobial,
in treating a disease
or condition.
In other words, we speak
of resistance when
a medication such
as an antibiotic
which normally works on
a pathogen like bacteria
in the sense that it kills it
or it makes that it
cannot replicate,
doesn't work anymore.
The pathogen, bacteria,
viruses or other pathogens
are now resistant
to the medication.
This picture illustrates
drug resistance.
In the upper panel,
we first see how
bacteria multiply,
but then when the patient
takes antibiotics,
the bacteria die.
In the lower panel however,
the bacteria are resistant.
They don't die when the
antibiotics are used.
That means that the antibiotics
cannot cure the patient.
What you see in this
picture as well is
that the genetic material
of the bacterium,
a circular genome,
now has an added red piece
in the lower panels.
This additional piece of
the genome can be a gene
or a set of genes that
cause drug resistance.
Drug resistance
can also be caused
by smaller changes
to the genome.
Sometimes a simple mutation that
leads to a single
letter change is enough
to make a pathogen
resistant to a drug.
We'll see that in HIV and
Mycobacterium tuberculosis.
