Hepatitis D (HDV), or the Delta Virus, is a defective RNA virus that only infects only liver cells already inhabited by the hepatitis B virus. HBV is a DNA virus, while delta contains only RNA.
Another peculiarity it has is that it must undergo a step otherwise known only in retroviruses – the use of the reverse transcriptase molecule – to replicate itself. HDV looks a little like some plant viruses, but it is different enough from any other virus that biologists have had to invent a new classification for it. It is the only member of the genus Deltaviridae.
In 1977, a researcher working in Turin, Italy, discovered this new viral strain. At first, he thought it was the HBV, but he soon realized it was something quite different, but yet still definitely a hepatitis virus.
Viruses require an envelope around them in order to survive. The Delta virus takes advantage of the HBV enzymes to supply the envelope it needs for its own replication. Once wrapped in this envelope provided by HBV, HDV can then manufacture a protein and RNA so that it can begin to replicate itself. This allows it to survive outside the liver. Other than using this bit of hepatitis B surface antigen, HDV’s function is independent.
There are three different genotypes of HDV which may have different geographical locations.
Type I is common in North America and Italy.
Type II is common in Japan and Taiwan.
Type III seems to exist only in South America.
There does seem to be some association between genotype III and more severe forms of fulminant infection (occurring suddenly and with great intensity). Stranger yet, HDV seems to reduce the serological markers of HBV, even though the disease gets worse with HDV infection. In other words, this love-hate relationship causes the HBV to help HDV replicate. At the same time, HDV inhibits the replication of HBV. HDV is transmitted in blood as well as sexually. There is also some evidence that it is passed within close family members as in parents and siblings.
When chronic carriers of HBV are superinfected with HDV, a more aggressive illness occurs. Neither Interferon nor transplantation is effective for HDV. Although HDV is the least common of all the hepatitis viruses, it is becoming the most serious since two viruses are now involved.
Vaccination may help prevent both infections, and both can be treated prophylactically with immune globulin after infection, but there is no way to prevent an HDV superinfection of a person already afflicted with chronic HBV infection. Vaccination for HBV will prevent HDV infection.
There is one circumstance under which HDV can be found in the blood without the presence of HBV and that is in patients who have had liver transplants following chronic HBV infection. After surgery, the HDV may reappear but its affects are minor except when an HBV infection is present. Virologists are leaning toward the thought that while HDV does not actually need HBV to survive, it does need it to cause a clinically apparent illness.
HDV infection tends to be no different from other hepatitis virus infections in the beginning. However, it rapidly takes its toll, causing liver failure quicker (usually within a few months to a year or two) for about 15% of the people who contract the disease.
Any treatment other than liver transplant is virtually non-effective. In fact, for some unknown reason, patients who are infected with both HBV and HDV do better after a transplant than those who had an HBV infection alone.
