Untitled - D Ank Unlimited

hepatitis B virus protein X 320 hepatitis, non-A, non-B (C) (NANBH)
HBc, a thymus-independent response, appears in the early
phases of the infection together with hepatitis B surface
antigen (HBsAg) and HBeAg. Anti-pre-S1 also appears
early in the infection, together with a potent major histocompatibility
complex (MHC) class-I-restricted cytolytic T
lymphocyte (CTL) response specific for numerous epitopes
of the structural and nonstructural proteins of the virus.
CTLs are critical for viral clearance as are cytokines,
interferon (IFN-γ), and tumor necrosis factor (TNF-α). In
the early phase of acute hepatitis B, nucleocapsid antigens,
hepatitis B core antigen (HBcAg), and HBeAG induce a
powerful MHC class-II-restricted T helper cell proliferative
response. The MHC class II locus DRB1*-1302 is associated
with recovery. The CD4 response has a significant role
in recovery. When the virus is eliminated from the liver,
HBeAg is lost from the serum and anti-HBe is detected. A
short time thereafter, HBsAg is lost and anti-HBs antibodies
appear. The immune response fails to eliminate HBV in
selected patients who become chronically infected. HBsAg
isolated from infected serum or created by recombinant
DNA technology represents a successful immunogen in
inducing protective immunity against HBV infection.
hepatitis B virus protein X
Refer to HBx.
hepatitis C virus immunity
Hepatitis C virus (HCV)-infected subjects develop specific
antibodies whose clinical and biological significance remains
to be determined. They are not protective. Most anti-HCV
positive sera are also RT–PCR (reverse transcription–polymerase
chain reaction)-positive. Antibodies to the envelope
glycoproteins may have neutralizing activity. The cellular
immune response against recombinant viral antigens has
been investigated in proliferation and cytotoxicity assays.
Chronic progressive liver disease may be linked to T H2
cytokine profiles from liver-derived T cells. HCV-specific
cytotoxic CD8 + T cells have been found in HCV-infected
patients. HCV escapes surveillance by the immune system
by altering its antigenic determinants. Problems for vaccine
development include diversity of HCV genotypes and subtypes
in the hypervariability of HCV species within the host.
hepatitis D virus
Refer to δ agent.
hepatitis E virus (HEV)
Enteric non-A, non-B hepatitis. A single-stranded RNA virus
that has an oral–fecal route of transmission and can introduce
epidemics under poor sanitary conditions where drinking
water is contaminated and the population is poorly nourished.
hepatitis E virus immunity
Immunity against hepatitis E virus (HEV), a self-limiting
disease that resembles hepatitis A, consists of an immunoglobulin
M (IgM) antibody response against HEV in the
acute phase of the disease. Once a peak titer is reached, it
declines to undetectable levels 5 months after the immune
response begins. IgG titers reach their height during the early
convalescent phase and decline during the following months.
Half of post-infection patients reveal undetectable levels of
HEV-specific IgG although some still reveal IgG antibodies 2
to 14 years following infection. HEV-specific IgG antibodies
prevent reinfection and clinical hepatitis E in young adults.
hepatitis (immunopathology panel)
Assays that are very useful for establishing the clinical and
immune status of a patient believed to have hepatitis. The
N
Concentration
HBeAg
Exposure
to
Antigen
1
HBsAg
Onset of
Disease
C48 C61
Onset of
Recovery
Complete
Recovery
Hepatitis serology.
HBe/a
HBc/α & HBc/β
Capsid assembly domain
C107
Anti-HBs
HBe/b
Anti-HBe
Anti-HBc
Nucleic acid
binding domain
panel for acute hepatitis may include hepatitis B surface antigen
(HBsAg), antibody to hepatitis B core antigen (anti-HBc),
anti-hepatitis B surface antigen (anti-ABs), anti-hepatitis A
(IgM), anti-HBe, and anti-hepatitis C. The panel for chronic
hepatitis (carrier) includes all but the anti-hepatitis A test.
hepatitis, non-A, non-B (C) (NANBH)
The principal cause of hepatitis that is transfusion-related.
Risk factors include intravenous drug abuse (42%), unknown
risk factors (40%), sexual contact (6%), blood transfusion
(6%), household contact (3%), and health professional occupations
(2%). In the United States, 150,000 cases per year
are reported. Of those, 30 to 50% become chronic carriers
and 20% develop cirrhosis. Parenteral NANBH is usually
hepatitis C, and enteric NANBH is usually hepatitis E.
150
Arg region
C185
HBV core polypeptide. The 185-residue p21.5 polypeptide (genotype A) is
shown with the amino terminus (N) at the left and the carboxyl terminus
(C) at the right. The open region depicts the hydrophobic assembly domain
(a.a.s 1–149; open); the Arg-rich nucleic acid binding region is also
known as the protamine domain (a.a.s 150–185; shaded). Hatched ovals
indicate the approximate locations of the HBe/a and HBe/b antigenic
determinants. The shaded rectangle portrays the capsid-specific HBc/α
and HBc/β epitopes that supposedly overlap HBe/a. Also indicated are the
four Cys residues 48, 61, 107, and 185 (vertical bars).
w.t.
∆172
∆162
∆157
∆149
∆149R4
TTVV RRRDRGR SPRRRTP
TTVV RRRDRGR SPRRRTP SPRRRRSQ S
TTVV RRRDRGR
TTVV RRRDRGR Sqc
TTVV
150 160 170 180
TTVV RRRR
SPRRRT
SPRRRRSQ SPRRRRSQ SRESQC
I II III IV
The protamine region of p21.5 contains four Arg-rich repeats that mediate
interactions between the core protein and nucleic acid. Shown are the
C terminal amino acid sequences (residues 150–185) of wild-type (w.t.)
p21.5 (top) and a series of truncated core proteins with defined endpoints.
C