The hepeviridae include and
especially are the hepatitis
This is a small, nonenveloped,
which contains a linear, single-stranded,
positive-sense RNA genome.
So, again, able to function
like messenger RNA.
This resembles the Norwalk virus
and in fact, if you've seen that
session already, we talked
about the hepatitis E virus
within the caliciviridae family.
However, this session will be important
to compare and contrast
the different hepatitis viruses.
Hepatitis E virus is transmitted
via the fecal-oral route,
and it has similar manifestations
to that of hepatitis A virus.
So, fecal-oral routes, in incubation
period, and then
a short-lived, thankfully,
period of icteric hepatitis, or
However, unlike hepatitis A virus,
the hepatitis E virus
can be quite severe, especially
in pregnant women.
And in those individuals, specifically,
it can cause fulminant hepatitis,
along with a hepatic encephalopathy,
typically over a period of 8 weeks or so.
The scanning electron microscopy
picture you see in front of you
shows the hepatitis E virus in small
form and it clusters just like that
in real life
So, let's now do that hepatitis virus
comparison, starting with hepatitis A.
So just like we talked about
with hepatitis E,
hepatitis A is a fecal-oral transmission,
Many times, it is completely asymptomatic.
But in those patients in whom
it is an acute onset with rapid progression
to fulminant hepatitis, but then
rapid resolution as well.
The mortality rate, the death
rate is very low,
and there's no carrier state.
Also, hepatitis A because it is
so short lived and relatively non-acute,
doesn't have any extra-hepatic manifestations
or other diseases associated
acquired via parenteral, so blood borne
or blood and body fluid exposure, so
parenteral, sexual transmission,
perinatal transmission to infants
born to mothers who are actively
infected with hepatitis B.
The incubation period for
hepatitis B is long;
months to get to the potential
for acute disease,
and potentially years if one has a chronic
infection with hepatitis B to eventually
go to either hepatitis or serotic disease.
In patients who develop the acute
hepatitis, so after a month-
long or even longer incubation period,
they'll develop fever along
with arthralgias, a rash,
and then the acute onset of the hepatitis.
Those patients then may go into a complete
recovery if they develop
or a chronic carrier state, which may
ultimately lead to hepatic carcinoma.
The immediate and medium-term
mortality rate is quite low,
but those patients developing
hepatic carcinoma, of course,
have a much higher mortality rate.
Yes, there is a carrier status, a
prolonged carrier state,
and it's during this time that blood
and body fluid transmission
can still occur to other partners.
Hepatic carcinoma, as mentioned before,
and cirrhosis; long-term,
slowly-onset form of cirrhosis
and liver failure.
And then extra-hepatic manifestations:
aplastic anemia, kidney disease
and then even an inflammatory disease of
mall and large blood vessels
called polyarteritis nodosa.
Hepatitis C, also transmitted via blood
and also body fluid exposure,
although blood transmission via transfusion
is perhaps the currently most
in blood which has not been
A long transmission or a long incubation
period just like hepatitis B,
and also like Hepatitis B,
there can be an acute hepatitis
with liver disease
and/or a long progression to
cirrhosis and carcinoma.
So, think of hepatitis B and C
in a very similar fashion,
similar exposure, similar incubation,
for long-term progression.
Mortality rate for both is quite low,
and the carrier state is quite common
in hepatitis C as well.
And also, the same progression
to hepatic cirrhosis
and hepatic carcinoma.
There are fewer known extra-hepatic
manifestations in hepatitis C
there are for hepatitis B.
This is an interesting one because it's only
been more recently described and its
pathogenesis has yet to be
completely understood or fleshed out.
It can be thought of in the same
lines as hepatitis B,
in that it is a parenteral, you know, so
blood and body fluid exposure,
so parenteral, sexual, perinatal transmission.
But it only appears to cause disease
in combination with hepatitis B.
So, if a patient has previously been infected
with and developed disease from
hepatitis B, and then
gets hepatitis D as a second exposure,
they have a very rapid progression to
fulminant hepatitis with liver failure.
However, if hepatitis B and D are
co-infected, so acquired at the same time,
, then, just like hepatitis B, it's a
very long incubation period.
And then the clinical course, very
much like I described,
just now with hepatitis B.
High mortality rate, especially when
hepatitis D is a second infection.
Yes, there's a carrier state.
Yes, there is association with cirrhosis,
and then the fulminant hepatitis.
And very much like we described
with the hepatitis B
there are additional extra-hepatic
manifestations, such as you see in the slide.
So, hemolytic anemia, again, the
glomerulonephritis for kidney failure,
inflammatory vasculitis, very much
like polyarteritis nodosa
and then skin lesions with lichen planus,
and even in association with
And then our friend hepatitis
E in comparison
sounds very mild and minor after what
we've just described for B, C, and D.
So, just like hepatitis A, hepatitis E,
fecal-oral transmission, short incubation,
is very -- well, I should say, relatively
mild in comparison to the others, unless
the infection occurs in pregnant women
in which there can be a 10% attack rate,
10% risk of fulminant hepatitis.
So, in those pregnant women only,
the mortality is high.
Otherwise, this is a mild,
with no associated additional major impact.
So, that is our friend hepatitis E in
comparison to the other viral hepatitises.
Think of this session as a important review
of the hepatitis viruses as it covers
several of the other sessions that
you may already have watched.