6 / 13
Page 41
Notes:
allied
academies
Virol Res J 2017 Volume 1 Issue 3
International Virology Conference
October 30-31, 2017 | Toronto, Canada
HTLV antisense proteins role in the nf-κb modulation
Stefania Fochi, Simona Mutascio, Francesca Parolini, Donato Zipeto
and
Maria Grazia Romanelli
PhD student
, Italy
T
he retrovirus HTLV-1 is the causative agent of adult T-cell
leukemia, whereas the genetically related sierotype HTLV-2
is sporadically associated with neurological diseases. The HTLV-
1 genome encodes regulatory proteins, such as the oncoprotein
Tax and the antisense proteins HBZ, involved into T-cells
proliferation and transformation. Tax-1, HBZ, and the HTLV-2
homologs, Tax-2 and APH-2 interact with many host cell factors
imparing cell signaling pathways involved in the mechanisms of
survival, andproliferation, including theNF-κBpathway. The aim
of this study is to investigate the involvement of the regulatory
proteins HBZ and APH-2 in the constitutively Tax-mediated NF-
κB activation. We demonstrated that HBZ and APH-2 differ in
the NF-κB promoter suppression. The APH-2 protein, differently
fromHBZ, localizes into the cytoplasm in presence of Tax, where
it prevents the degradation of the inhibitor IκB, hindering the
nuclear translocation of p65. Unlike HBZ, we found that APH-
2 interacts with the E3 ubiquitin ligase TRAF3, an upstream
inhibitor of the alternative NF-κB pathway. By generating a
TRAF3-KO cell line applying the CRISPR/Cas9 technique, we are
investigating the HBZ and APH-2 activity on the alternative NF-
κB cell signaling. This studymay provide insight into the effect of
host-viral interactions in human viral oncogenesis.
Speaker Biography
Stefania Fochi is a PhD student from Departement of Neurosciences, Biomedicine and
Movement Sciences, University in Verona, Italy.
e:
stefania.fochi@univr.it