الفهرس 
REVIEW OF LITERATUREOnly 14 pages are availabe for public view
Abstract
HCV represents a global health problem affecting a high
range of population worldwide. It is the main cause of liver
inflammation. Meanwhile, hepatitis may be caused by an
autoimmune disorder, in which the body’s immune system attacks
the normal liver cells because it became unable to differentiate
between harmful invaders and healthy liver tissues.
Thus, differentiation between different causes of liver
inflammation due to various etiologies still represents big
challenge. Therefore, this study sought to develop new
immunodiagnostic markers able to differentiate between different
types of inflammation. The study was performed on eighty-one
blood samples collected from the medical unit at the national
research center starting from October 2016 till May 2019.
The samples were divided into seven groups as follow:
group (1); normal: nine healthy control volunteers with no history
of HCV-infection, liver disturbance diseases or autoimmune
diseases.
group (2); HCV: eleven- HCV infected patients with no history of
autoimmune diseases.
group (3); HCV+auto: eleven-HCV infected patients who are
positive for autoimmune markers.
Summary
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group (4); NAFL: four HCV\HBV non infected patients but had
liver disturbance as nonalcoholic fatty liver.
group (5); NAFL+auto: six HCV\HBV non infected patients but
had liver disturbance as NAFL and are positive of autoimmune
marker.
group (6); RA: nineteen patients suffering from RA.
group (7); SLE: twenty-one SLE patients.
The levels of ALT, AST in sera, BAFF, TNF α and IL-10
were measured in plasma while the levels of TLR3, TLR7 were
quantified in lysates of PBMNCs at protein levels and the relative
expression of TLR3, TLR7, TNF; IL-10 in cell lysates was
assessed against GAPDH by qRT-PCR from all groups.
The current study demonstrated the detection of Auto-Abs, such
as ANA and ASMA in patients with NAFL and HCV and their
presence leads to concerns about AIH. Additionally, HCV-Ab titer
can well differentiate between HCV and non-HCV infected
patients, with inability to predict the progression of HCV infection
to AIH. Additionally, a positive correlation between the presence
of Auto-Abs and the increase in BAFF levels was also recorded in
HCV and NAFL patients. At both transcriptional and protein
levels,high expression in the IL-10 levels were detected in the
SLE group. TNFα was upregulated in the NAFL+auto group at
both the protein and transcriptional levels with negative
correlation with IL-10. The AST levels were significantly elevated
Summary
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only in RA patients, with no significant changes in the ALT level
among various patients’ groups.
TLR3 was shown to be unable to differentiate between
HCV and NAFL patients at both the protein and mRNA levels.
Beneficially, TLR3 can differentiate between NAFL and
NAFL+auto at the protein level. Importantly, at the protein level,
TLR7 can well differentiate between HCV and NAFL patients. At
the transcription level, the TLR7 can also differentiate between
the NAFL and the NAFL+auto patients, since a significantly
higher expression of TLR7 in the NAFL+auto patients compared
to healthy individuals, HCV, HCV+auto, NAFL, SLE or RA
patients was observed. Last and not least, TLRs 3 and 7 can
differentiate between the NAFL and NAFL+auto patients.
Further investigations needed to elucidate whether both
TLR 3 and TLR 7 signaling mechanisms worked in tandem
together to establish an antiviral state in HCV infected individuals.