Originality: the peripheral nervous system. Upon infection VZV

Originality:

This was a follow up study which was performed based on the
known relevance of leukocyte migration in Varicella zoster virus (VZV) spread
and subsequent pathogenesis, thus possible modulation of leukocyte migration by
VZV was investigated. The study found that cell-free VZV does indeed enhance
chemokine activity, which increases pathogenesis as expected. This however is partially dependant on glycoprotein C
(gC), other factors are currently unknown.  This report also contains the first
description of vCKBP in VZV. VZV rSgC can be considered novel due to it binding
a large number of chemokines specifically from the CXC and CC superfamilies’
and due to it enhancing their activity, phenomenon previously only observed n
HSV glycoprotein C. This report though not making a huge difference to the
knowledge state of this field, it opens up questions and hopefully will
encourage more research into the mechanisms of dissemination used by VZV.

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Reasons for
Undertaking Study:
The study focused on Varicella zoster virus (VZV), a virus which
establishes latency in the neurons of the peripheral nervous system. Upon
infection VZV modifies the activity of important immune components such as T
cells and leukocytes, but despite its importance in pathogenies relatively
little study has been done to investigate the mechanism of VZV dissemination
throughout the body. The article aims to address the influence of VZV on
leukocyte migration in particular due to glycoprotein C.

 

 

Main Conclusions of Study:
The report has found that cell free VZV does enhance chemokine activity and
this is partially dependent on gC. Glycoprotein C was identified as being involved
in the recruitment of leukocytes by VZV. Data shows that VZV gC does enhance
leukocyte migration through the modulation of chemokine activity, which could
facilitate VZV infection of host leukocytes and dissemination of the virus. In
addition as chemokines are known to induce pain, enhancement of their activity
may play a role in VZV associated pathology. 
Results also show that VZV gC is a vCKBP that interacts with high
affinity.  VZV rSgC binds to a broad
range of CXC and CC chemokines with nanomolar affinity and therefore acts as a
novel vCKBP.

 

Flaws of Study:

Though not
many flaws come to mind some minor issues were had with the layout of figures
and their clarity. E.g. Figure 1, graph C.

Also while
an interesting study it seems to only scrape the surface of this area of
research, the report itself admitted little is known about the mechanisms of
VZV dissemination.

 

Future Directions of Study:
What is the role of gC-protein mediated chemokine enhancement in vivio?
What other factors play a role in VZV mediated enhancement of leukocytes and to
what extent?
Does VZV gC enhance leukocyte migration to the initial site of infection?

 

Overall Opinion of Paper:

The article
was an interesting look into what seem to be a neglected area of research. Though
it may not have a large impact I believe it does represent a positive
contribution to the body of knowledge dealing with understanding the mechanism
of VZV dissemination.

 

 

Level of difficulty:

6