Also called hepatitis delta virus.
A defective, hypotropic pathogenic agent.
Prevalence unknown but estimated between 62 and 72 million people worldwide are infected with HDV, representing 1% of the global population.
HDV is endemic in Mongolia, other parts of Asia, Africa, southern and eastern Europe, the Middle East, and Brazil.
RNA virus is replication defective and can cause infection only when it is encapsulated by HBsAg.
HDV is a satellite RNA virus that requires hepatitis B virus surface antigen for entry into hepatocytes and for propagation.
HDV, is transmitted by the parental route through infectious body fluids.
IV drug uses are at highest risk for infection, because of contaminated syringes.
Prevalence in 13 to 14.6% of HBV carriers.
It is estimated to affect between 10 and 20 million persons worldwide.
In the US 5 to 10% of persons positive for HBsAG are also seroprevalence positive anti-HDV antibody which means that HDV infection meets threshold for designation of an orphan disease, occurring in less than 200,000 persons.
High risks in intravenous drug users and those with high risk sexual behavior.
Its prevalence is decreasing as the worldwide implementation of HPV vaccination programs grow, reducing the number of carriers who are susceptible to HDV.
because of HPV vaccination, there is now an age related prevalence shift to older persons.
It is the most severe and progressive form of viral hepatitis in humans.
HDV is the smallest viral pathogen infecting humans.
It is a defective virus because it does not encode its own envelope proteins and requires the presence of HBV for virion assembly, replication, and transmission.
There are eight genotypes, and has a circular, single-stranded RNA of approximately 700 nucleotides.
Patients infected with HDV always have a simultaneous HBV infection either acquired as an acute co-infection or as a superinfection with chronic HBV.
Long term coinfection with HBV & HDV is considered to be the most serious type of chronic viral hepatitis.
Compared to monoinfection with HBV, HBV-HDV, coinfection accelerates the course of disease, increases the risk of cirrhosis, hepatocellular carcinoma, need for early transplant, and early death.
It is dependent on the genetic information from HBV for its multiplication and causes hepatitis only in the presence of HBV.
A single-stranded, circular RNA, which is the smallest virus known to infect humans.
Occurs with acute coinfection with HBV, with the latter established first to provide the HBsAg needed for development of complete hepatitis D virions.
Can occur as a super infection of a chronic carrier of HBV with a new inoculum of HDV and results in disease 30-50 days later.
The coinfection with HBV results in hepatitis process that ranges from mild to fulminant disease.
Fulminant disease is more likely with coinfection of D and B hepatitis than with HBV alone.
Clinically indistinguishable from acute HBV infection.
HDV infection is associated with an increased risk of acute liver failure, especially in intravenous drug users.
Approximately 90% of patients with acute HDV – HBV co-infection clear their infection spontaneously, but the acquisition of HDV as a superinfection typically results in a chronic HDV infection.
Chronic HDV infection has a viremia that lasts more than six months and frequently results in a severe clinical course.
Chronic HDV-HBV coinfection progresses to cirrhosis in 70 to 80% of cases within 5 to 10 years.
Chronic HDV infections are associated with a 3 to 6 fold increase in hepatocellular carcinoma, compared to HBV.
The diagnosis involves specific serological testing.
All HBsAG positive persons should be tested.
Testing should be done only in patients who are HBsAG positive.
Persistent severe HD viremia is the most important risk factor for progression and chronic hepatitis C, and is almost invariably severe.
Treatment for chronic HDV is a 12 month course of Peglated interferon: sustained responses occur in only 25% and relapse rates are high.
Oral anti-viral drugs for the treatment of HBV infection, are effective as monotherapy in suppressing HBV replication, but they do not effectively suppress HDV replication.
Bulvevirtude in a randomized phase 3 trial for chronic hepatitis D reduced HDV RNA levels and ALT levels in patients with chronic hepatitis D.
Lonaformib has been shown to decrease HDV RNA levels.
The optimal endpoint for treatment is the loss of HBsAG, which is only a rare achievement.