Hepatitis D (or delta, the Greek letter "D"), is a form of liver
inflammation that occurs only in patients who also are infected
by the hepatitis B virus. Infection by the hepatitis delta virus
(HDV) either occurs at the same time as hepatitis B develops, or
develops later when infection by hepatitis B virus (HBV) has
entered the chronic (long lasting) stage.
Delta hepatitis can be quite severe, but it is seen only in
patients already infected by HBV. In the late 1970s, Italian
physicians discovered that some patients with hepatitis B had
another type of infectious agent in their liver cells. Later the
new virus HDV was confirmed by experimentally infecting
chimpanzees. When both viruses are present, acute infection
tends to be more severe. Furthermore, patients with both
infections are likelier than those with HBV alone to develop
chronic liver disease, and, when it occurs, it is more severe.
About 300 million persons
worldwide carry HBV. Of them, at least 5% probably also have
delta hepatitis. In North America HDV infection appears to be
less frequent: 4% of all patients with acute hepatitis B have
HDV infection. The delta virus causes an estimated 2% of all
cases of acute viral hepatitis in the United States. The rate of
HDV infection varies widely in different parts of the world; it
is a very serious infection in some countries and quite mild in
others. Chronic delta hepatitis is a more serious disease than
either chronic hepatitis B alone or hepatitis C.
Certain individuals-the same ones
who are at increased risk of developing hepatitis B are the
prime candidates to be infected by HDV.
Not infrequently, HDV infection
occurs in patients with chronic HBV infection who also have
hemophilia, a bleeding disease. These patients are at risk
because they require large amounts of transfused blood and blood
products that may contain HDV.
In some areas, one-fourth to
one-half of patients with chronic HBV infection who inject
themselves with illicit drugs become infected by HDV as well.
Drug abusers who share contaminated needles are likely to infect
Patients who get HBV infection by
sexual contact may also be infected by HDV, although the delta
virus is less often spread in this way than is HBV itself.
Between 10 & 25% of homosexual men with chronic HBV infection
harbor the delta virus.
Like hepatitis B, HDV infection may develop in healthcare
workers who are victims of a needle stick, and it also can be
spread within households when personal items such as a razor or
toothbrush are shared.
Causes and Symptoms
The delta virus is a small and
incomplete viral particle. Perhaps this is why it cannot cause
infection on its own. Its companion virus, HBV, actually forms a
covering over the HDV particle. In chronically ill patients
(those whose virus persists longer than six months), the
combined viruses cause inflammation throughout the liver and
eventually destroy the liver cells, which are then replaced by
scar tissue. This scarring is called cirrhosis.
When HBV and HDV infections
develop at the same time, a condition called coinfection,
recovery is the rule. Only 2-5% of patients become chronic
carriers (have the virus remain in their blood more than six
months after infection). It may be that HDV actually keeps HBV
from reproducing as rapidly as it would if it were alone, so
chronic infection is less likely.
When HBV infection occurs first
and is followed by HDV infection, the condition is called
superinfection. This is a more serious situation. Between half
and two-thirds of patients with superinfection develop severe
acute hepatitis. Once the liver cells contain large numbers of
HBV viruses, HDV tends to reproduce more actively. Massive
infection and liver failure are more common in superinfection.
The risk of liver cancer, however, is no greater than from
hepatitis B alone.
As with other forms of hepatitis, the earliest symptoms are
nausea, loss of appetite, joint pains, and tiredness. There may
be fever (not marked) and an enlarged liver may cause discomfort
or actual pain in the right upper part of the abdomen. Later,
jaundice (a yellowing of the skin and whites of the eyes that
occurs when the liver is no longer able to eliminate certain
pigmented substances) may develop.
Who is at risk of hepatitis D?
Chronic HBV carriers are at risk
for infection with HDV. Individuals who are not infected with
HBV, and have not been immunized against HBV, are at risk of
infection with HBV with simultaneous or subsequent infection
with HDV. Since HDV absolutely requires the support of a
hepadnavirus for its own replication, inoculation with HDV in
the absence of HBV will not cause hepatitis D. Alone, the viral
genome indeed replicates in a helper independent manner, but
virus particles are not released.
HDV infection may be diagnosed by detecting the antibody against
the virus. Unfortunately this test cannot detect acute
coinfection or superinfection as early as when symptoms first
develop. Antibody against HDV usually is found no sooner than 30
days after symptoms appear. Until recently, the virus itself
could only be identified by testing a small sample of liver
tissue. Scientists now are developing a blood test for HDV that
should make diagnosis faster and easier. When HDV is present,
liver enzymes (proteins made by the liver) are present in
abnormally high amounts. In some patients with coinfection, the
enzyme levels peak twice, once when HBV infection starts and
again at the time of HDV infection.
How to prevent hepatitis D?
Since HDV is dependent on HBV for
replication, control of HDV infection is achieved by targeting
HBV infections. All measures aimed at preventing the
transmission of HBV will prevent the transmission of hepatitis
D. HBV vaccination is therefore recommended to avoid HBV-HDV
The vaccine against hepatitis B
also prevents delta hepatitis, since it cannot occur unless HBV
infection is present. Hopefully, a vaccine can be developed that
will keep delta infection from developing in chronic HBV
carriers. However, if a person already has HBV infection, any
exposure to blood should be strictly avoided. A high level of
sexual activity with multiple partners is also a risk factor for
However, there is no effective measure to prevent HDV infection
of chronic HBV carriers, and prevention of HBV-HDV
superinfection can only be achieved through education to reduce
risk behaviors. Promising research results indicate that in some
woodchucks immunized with recombinant purified HDAg-S complete
protection is possible. Hepatitis B Ig and HB vaccine do not
protect HBV carriers from infection by HDV.
The virus exists throughout the
world and infection is always associated with serum that is
positive for HBsAg. The presence of anti-Delta antibody in a
subject who is negative for HBsAg but positive for anti-HBs
indicates a previous infection. The infection is endemic in
Southern Europe, Africa, the Middle East and, probably, Latin
America. Delta is present in most of the countries of the world
where it has been looked for, the one possible exception being
China and Japan. Most of the countries of the Far East at the
moment appears to have quite a low incidence of Delta with the
exception of Taiwan. In Taiwan, it was reported that 26% of all
acute hepatitis cases have Delta antigen in the serum. Similarly
in India where 14% of all acute cases are reported positive for
The transmission of the Delta
agent mirrors that of HBV, being primarily parenterally
transmitted. Sexual transmission appears to be less efficient
mode of transmission as there is a lower incidence of Delta
infection in homosexuals compared to IV drug abusers.
"Clustering" occurs within families, the spread within families
appear to be horizontal rather than vertical. Although vertical
transmission can occur, it does not appear to be an important
means of transmission.
The infection is observed particularly frequently among drug
addicts, who are repeatably exposed to inoculation with HBV
infected blood. This epidemiological category is currently
responsible for the spread of virus into Northern Europe and the
USA eg. In Sweden, there was no trace of Delta infection before
1973 but since then, the annual incidence amongst HBsAg positive
drug addicts have progressively increased, reaching a rate of
72% in 1981. There is also a significant risk of infection in
haemophiliacs who receive commercial factor VIII concentrates.
Approximately 50% of these patients appear to contract the
infection and develops liver disease. In the US, Delta infection
was found in 20 - 53% of IV drug abusers, 40 - 80% of
haemophiliacs, and 8 - 20% of homosexuals and dialysis patients
who are known HBsAg carriers.
Immunological Aspects of Delta Infection
Against the background of an HBV
infection, the initial stage of Delta infection is marked by the
appearance of the Delta antigen in the liver, this is quickly
followed by a phase where the Delta antigen is present in the
blood, usually for a brief period and at pre-clinical levels.
Consequently, in most cases, Delta antigen is not detected in
the blood. The extent of the antibody response against the Delta
agent depends on the extent and duration of the presence of
Delta anigen in the blood. therefore, in a normally short acute
coinfection, the response is usually limited to a brief
appearance of anti-Delta IgM and a low, sometimes undetectable
titre of IgG. If the infection is sustained, as in most cases of
superinfection, the appearance of Delta IgM is followed by high
titres of Delta IgG.
If the infection is resolved, then the Delta antigen in the
liver as well as the serum is eliminated. Delta-IgG, when it is
present, is the only sign of former infection. If the infection
becomes chronic, as is very likely in the case of superinfection,
the Delta antigen will persists in the liver whilst it will be
rapidly eliminated from the serum. Delta IgG should persists at
high levels, Delta IgM will also persists for a longer period of
time than acute infection. In practice, the Delta antigen/antiboby
system behaves in a similar way to the core antigen/antibody
system of Hepatitis B.
Coinfection with HBV is
necessary for the Delta agent. Those who are immune to hepatitis
through vaccination or natural infection will also be immune to
HDV. Infection may occur in 2 ways :-
HBV of a patient not previously exposed to HBV.
Super-infection of a
In the case of coinfection, the synthesis of the
defective virus must necessarily follow the appearance in the
circulation of the HBsAg induced by the coinfecting HBV. Hence
one may see more than one rise in liver transaminase and there
may be 2 peaks of ALT, although not always. The synthesis of the
Delta agent cannot continue after the elimination of HBsAg. The
clinical appearance is that of normal hepatitis B. Delta antigen
is rarely detected in the serum, though anti-Delta IgM is found
in the serum and lasts 2 - 6 weeks. Anti-Delta IgG may be
present in a low level or perhaps not detectable at all. In
general, the clinical course of acute hepatitis B is more severe
in the presence of Delta coinfection. There is a much increased
likelihood of developing fulminant hepatitis.
The most common form of Delta
infection is superinfection of a known HBsAg carrier and it is
where Delta infection produces its most deleterious effects.
Preexisting HBsAg in the circulation captures the Delta virus,
even if it is in small amounts and intensifies its synthesis
immediately. Delta infection of a previously healthy carrier may
induce an acute hepatitic picture. Infection in a carrier with
preexisting hepatitis will aggravate the clinical picture.
Primary Delta infection in a HBsAg
carrier is often severe, with a significantly higher number of
fulminant hepatitis cases. The most serious aspect of
superinfection by Delta is its tendency to become chronic and
for the acute hepatitis to progress into chronic hepatitis
(chronic active or persistent hepatitis and cirrhosis). At least
70 -90% of superinfected carriers develop chronic infection.
(70% of such patients develop chronic active hepatitis, 20%
cirrhosis and a minority chronic persistent hepatitis). In an
outbreak in Venezuela, there was a 23% mortality rate and 80% of
survivors went on rapidly to develop chronic active hepatitis
and to cirrhosis. In an Italian study, where the progression
rate of acute HBV to chronic active hepatitis without Delta is 1
- 2%, it was 2.4% in coinfections and 91% in superinfections.
The rapid evolution of chronic hepatitis Delta may explain the
rare occurrence of Delta markers in patients of hepatocellular
Delta superinfection in a HBsAg carrier should induce a quick
rise in liver enzymes. Delta antigen appears in the serum
followed by Delta IgM and Delta IgG. In contrast to acute
coinfection, Delta IgG can reach very high levels. Acute Delta
superinfection is accompanied by a drop in HBsAg in the HBV
carrier, sometimes to undetectable levels so that true diagnosis
could be masked. The serum picture remains the same whether the
infection becomes chronic or not. However, in the case of the
infection becoming chronic, Delta antigen persists in the liver
and can be detected by immmunoperoxidase or immunofluorescence
HDV infection may be diagnosed by
detecting the antibody against the virus. Unfortunately this
test cannot detect acute coinfection or superinfection as early
as when symptoms first develop. Antibody against HDV usually is
found no sooner than 30 days after symptoms appear. Until
recently, the virus itself could only be identified by testing a
small sample of liver tissue. Scientists now are developing a
blood test for HDV that should make diagnosis faster and easier.
When HDV is present, liver enzymes (proteins made by the liver)
are present in abnormally high amounts. In some patients with
coinfection, the enzyme levels peak twice, once when HBV
infection starts and again at the time of HDV infection.
Detection of Delta Ag in the
liver - Liver biopsy specimens may be stained for Delta Ag
by immunofluorescence or immunoperoxidase techniques. This
method is particularly useful in the diagnosis of chronic
Serology - Serum Delta Ag, anti-Delta IgM,
anti-Delta IgG or Total anti-Delta may be determined by
competitive or antibody capture radioimmunoassays. The
results must be interpreted in context with the HBV serology
HBsAg Total IgM HBeAg Anti-HBe Total IgM Anti-HBs
1. + +
+ + - +
2. + +
- +or- +or- + + -
3. + +
- +or- +or- + - -
4. - +
- - + +
5. - + - -
+or- + - +
Acute coinfection with HBV and
Delta. (Probably cure).
Acute Delta superinfection
(anti-Delta low), or chronic Delta superinfection
Recovery from acute Delta
superinfection (anti-Delta low), or, rarely, chronic Delta
superinfection (anti-Delta level high), usually without
Previous HBV and Delta
infection with probable recovery.
Recovery from HBV and Delta infection.
The Delta antigen
appears in the serum before or early in the course of clinical
illness (a few days to a month or so), and thus it is often
missed. However, if it is detected, it would indicate an acute
attack. (One case has been reported where there is persistent
Delta Ag in the serum. The patient concerned is a IV drug abuser
who is also HIV positive.) It is recommended that the following
should be tested for Delta infection :-
All drug abusers with
jaundice, whether or not HBsAg positive, because of
possibility of suppression of surface antigen.
All HBsAg positives (perhaps
this is the easiest thing to do from an administrative
HBsAg carriers with chronic
All fulminant hepatitis even if HBsAg
Is there a vaccination for HDV?
Infection with HDV can be prevented by vaccinating those at risk
with the hepatitis B vaccine. However, those who already have
hepatitis B cannot prevent infection with HDV because there is
no HDV vaccine.
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