Hepatitis D (Delta Agent) The hepatitis D virus (HDV) is an infectious RNA agent.

Biological expression of
this agent in man requires the concomitant obligatory association of hepatitis B surface antigenemia.
HDV can cause both acute and chronic hepatitis. Clinically, HDV hepatitis may be indistinguishable from
other forms of acute and chronic viral hepatitis, although on average, it is more severe. The mortality of
icteric acute HDV hepatitis ranges from 2-20% (the mortality for HBV is approximately 1%). Likewise,
chronic delta hepatitis tends to be more severe than chronic HBV and HCV infection. Approximately 75%
of patients with chronic delta hepatitis have been found to develop cirrhosis and complications of portal
hypertension as contrasted with a 25% incidence of such complications in patients with chronic HBV
infection. In some patients with chronic delta hepatitis infection, the disease is rapidly progressive and
cirrhosis develops within a few years of onset of infection. The prevalence of delta hepatitis infection in
chronic hepatic B carriers with primary hepatocellular carcinoma is low. It has been suggested that since
delta is almost invariably pathogenic it leads to the dire complications of cirrhosis and portal
hypertension, eventuating in death or receipt of a liver transplant before the requisite period of time
necessary for cancer of the liver to develop has elapsed. Acute HDV occurs in two forms coinfection and
superinfection. Coinfection refers to the simultaneous introduction of HBV and delta infection into the
host. It is generally benign, although on occasion it is fulminant. Simultaneous acute HBV and HDV
progresses to chronic liver disease in less than 5% of patients. In patients with coinfection, the HBsAg is
positive, the IgM anti-HBc is positive and IgM antiHDV is positive in low titer. The pattern of elevation in
serum aminotransferase levels is often biphasic. In contrast to coinfection, superinfection with delta
often results in severe and fulminant disease and a high frequency of progression to chronic disease in
those surviving. Chronic active hepatitis is found in 90% of patients and simultaneous post-necrotic
cirrhosis is present in approximately 50% of such patients. Most cases of chronic delta hepatitis probably
arise from superinfection. The serological course is characterized by presence of hepatitis B surface
antigenemia, positive IgG antiHBc, and the presence of IgM anti-HDV. This antibody is often present in
high titer (greater than 1 in 100) and sustained in contrast to the short-lived anti-HDV that is present in
low tier in patients with coinfection. The diagnosis of delta infection can be made by testing the serum
for anti-HDV, assaying for HDV RNA in the serum, and by performing immunoperoxidase staining for
hepatitis D virus antigen in liver tissue specimens. New assays, such as molecular hybridization for HDV
RNA should simplify the diagnosis of HDV in the future. HDV infection should be suspected and
appropriate serological testing performed in patients with severe acute hepatitis B virus infection,
patients with severe chronic hepatitis B virus infection, and in chronic hepatitis B surface antigen carriers
who develop on exacerbation of their liver disease. The epidemiology of delta infection can be
summarized as follows: A. Endemic delta virus infection is common in the mid-east and the
Mediterranean High prevalence rates have been documented in Korea, South America. and Romania In
contrast prevalence rates of HDV are low in the United States, South Africa. North Africa, Northern
Europe, and China. B. HDV as a disease afflicting certain high risk populations-notably intravenous drug
"addicts" and hemophiliacs. HDV is supposedly rare in gay men and health-care workers, although a
number of fulminant cases of delta infection among gay men have been described in recent years Since
delta hepatitis infection is inextricably linked to type B hepatitis, prevention of delta hepatitis can be
achieved by preventing hepatitis B virus infection. The widespread use of the HBV vaccines should result
in the curtailment of this virulent pathogen. There is no proven therapy for delta hepatitis.
Corticosteroids are not beneficial in this disease. Although interferon appears to inhibit hepatitis D virus
replication, and may result in improvement in serum aminotransferase levels during active therapy,
discontinuation of therapy with alpha-interferon is almost always followed by a significant clinical
relapse. Hepatic transplantation has been performed in some