|
|
Victor Stollar, MD
 |
Victor Stollar, M.D.
Professor
Office: 732-235-4596
Lab: 732-235-5449
stollar@umdnj.edu
Office: RWJMS 731
Lab: RWJMS 730 |
Publications
Click
Here for PubMed Link to Publications
Lab Staff
Mei-Ling Li |
Adjunct Assistant Professor |
Research Interests
Most of the work in our laboratory during the past year has been with
Sindbis virus (Family Togaviridae, genus alphavirus), a mosquito-transmitted
virus. It was observed many years ago that when chick embryo fibroblasts
were infected with Sindbis virus, and then maintained in a medium with
decreased ionic strength, viral RNA and protein synthesis proceeded normally,
but infectious virus was not released from the cells. Restoration of the
normal ionic strength to the medium led to the release of virus within
several minutes. Thus release of virus appeared to be blocked at a very
late stage, probably just prior to budding. We have been able to isolate
a viral mutant, SVLS29, capable of budding from chick cells maintained
in low ionic strength medium, and identified two mutations responsible
for this phenotype; both were in the region coding for the exodomain of
E2, one of the viral envelope proteins. Further study of this mutant should
be useful for understanding how viruses bud from cell membranes, and why
in certain situations, this process is inhibited by reducing the ionic
strength of the medium.
In the course of looking for a mutant of Sindbis virus, which could
grow in methionine-deprived Ae. albopictus cells, we observed that one
isolate, SVLM17, which was able to grow normally in Ae. albopictus cells
was restricted in chick embryo fibroblasts. As with infected cells maintained
in low ionic strength medium, the restriction was at a late stage in replication.
Interestingly, the mutation responsible for the host restriction of SVLM17
was also in the region which coded for the exodomain of E2. Although in
the case of alphaviruses, the budding process is considered to be driven
mainly by an interaction between the nucleocapsid and the endodomain of
E2, our findings with the mutants, SVLS-29 and SVLM-17 indicate that the
exodomain of E2 also plays an important role in the late stages of viral
maturation.
|
