Recent research
published by Princeton researchers has made large strides in understanding how
viruses act in their inert phase and how biochemical coordination of dynamic
phase can be closely related to the host cells that they infect. This work
showed a viral strain VP882 (which is now one of many of its kind) that is
capable of entering dynamic phase only when its bacterial host(s) have achieved
quorum. It is upon this widespread biochemical quorum signaling that VP882 has
been shown to enter the dynamic phase via microscopy of viral protein
localization, killing its current host cells. This work practically creates a
whole new field of study for virologists, as now the biochemical motivation of
the viral inert to dynamic transition can be thoroughly evaluated. Further, it
was shown that this switch can be flipped by using the supplementing these same
quorum sensing molecules into the media and that this effect results in the
death of bacterial hosts. This technology
suggests two major possibilities for this new sub-field of virology: the
application of phage therapy in the prevention and treatment of bacterial
biofilm-reliant infections (like complex urinary tract infections; cUTI, and
acute bacterial skin and skin structure infections; ABSSSI) and the harnessing
of the viral mechanism to help advance phage therapy mechanisms.
Many of the
bacterial infections that must be combatted in patients rely on bacteria with
mechanisms to avoid the immune system. Most of these systems for subverting the
immune system rely on the ability of bacteria to produce small molecules that
allow for them to communicate with other bacteria in the local region. This
process, called quorum sensing, allows for bacterial cells (particularly in
cUTI and ABSSSI) to collectively start producing a thick and relatively
impermeable extracellular matrix at interfaces (solid-liquid, liquid-air,
solid-air). These communities are then protected from immune mechanisms within
the biofilm. While the cells on the outside of this film have reduced
proliferative capacity, the inner population is rapidly dividing. In both of
these types of infections, the dispersal of this now dangerous number of a
single type of bacteria begins to infect non-resident tissues and can lead to
serious infection. The idea that viruses can live inside of bacteria and kill
them only when they undergo quorum sensing to form these dangerous biofilms is
novel and immensely useful. In this case, the researchers were able to show
that this virus is widely infective to bacteria. If this infectivity could be
tuned to specific quorum sensing molecules, this population of viruses is a
potentially effective prophylactic for populations at risk for these types of
infections (burn victims, transplant patients, immunocompromised patients).
This was a truly astounding discovery, and I for one will be watching closely
to see how this work develops.
~Kyle Enriquez
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