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Virology Research Journal
|
Volume 2
Page 45
allied
academies
IMMUNOLOGY AND CELL BIOLOGY
BACTERIOLOGY AND INFECTIOUS DISEASES
&
Global Summit on
Global Congress on
J u n e 2 5 - 2 6 , 2 0 1 8 | A m s t e r d a m , N e t h e r l a n d s
Joint Event on
2005-2007 GLOBAL SPREAD OF H5N1: CAUSATIVE ROLE OF BODY
BURDEN DIOXIN IN UP-REGULATING GENE OF INFLUENZA VIRUS NS1
PROTEIN IN CHICKEN AND HUMANS IN SOUTHEAST ASIA
I B Tsyrlov
Xenotox, Inc., USA
A
gonist-induced recognition of a cognate DNA enhancer dioxin responsive element (DRE) does epitomize wide range of
mammalian genes expression mediated via the Ah receptor pathway. The same was postulated also for viral DRE-containing
genes expression caused by 2,3,7,8-TCDD (dioxin) in infected human cells. In this study, such mechanistic concept applied to
type A influenza virus nonstructural protein 1 binding protein (NS1BP) induction in humans and chicken. The data are presented
at genetic, cellular, and population levels. Primers for mutation analysis were constructed for two DRE identified within enhancer
region of the IVNS1ABP gene. Treatment of HeLa cell line with 0.1 nM of dioxin resulted in substantial increase of NS1BP protein
level. This might add to influenza virus A non-structural protein 1 (NS1) inhibitory effect on cellular interferons, which determines
antiviral resistance of emerging H5N1 virus. 2005-2007 H5N1 outbreaks among poultry in China and Vietnam might partially
relate to chicken NS1BP, as outbreaks occurred in areas highly contaminated by dioxin-like compounds. Minimal dose of TCDD
upregulating human IVNS1ABP gene was estimated moderately above current TCDD blood level in general population. So, in
human groups in Southeast Asia exposed to TCDD, its body burden might facilitate spreading of H5N1 if avian flu pandemic were
to occur.
xenotoxit@optonline.netVirol Res J 2018, Volume 2