Hepatitis D
It has been proposed that HDV may have originated from a class of plant pathogens called viroids, which are much smaller than viruses.
Its nucleotide sequence is about 70% self-complementary, allowing the genome to form a partially double-stranded, rod-like RNA structure.
[18] Like hepatitis B, HDV gains entry into liver cells via the sodium taurocholate cotransporting polypeptide (NTCP)[19] bile transporter.
HDV recognizes its receptor via the N-terminal domain of the large hepatitis B surface antigen, HBsAg.
[20] Mapping by mutagenesis of this domain has shown that amino acid residues 9–15 make up the receptor-binding site.
[21] After entering the hepatocyte, the virus is uncoated and the nucleocapsid translocated to the nucleus due to a signal in HDAg.
However, editing by cellular enzyme adenosine deaminase acting on RNA (ADAR) changes the stop codon to UGG, allowing the large-HDAg to be produced.
HDAg-S is produced in the early stages of an infection and enters the nucleus and supports viral replication.
[31][32][33] Thus RNA editing by the cellular enzymes is critical to the virus' life cycle because it regulates the balance between viral replication and virion assembly.
Researchers Georges Abou Jaoudé and Camille Sureau published an article in 2005 that studied the role of the antigenic loop, found in HDV envelope proteins, in the infectivity of the virus.
However, HDV is much more common in the immediate Mediterranean region, sub-Saharan Africa, the Middle East, and the northern part of South America.
[41] Those who get tattoos or body piercings should do so using sterile equipment to prevent the transmission of hepatitis B and D via infected bodily fluids.
[40] Those with hepatitis B or D should also not share razors or other personal care items which may have been contaminated by potentially infectious bodily fluids.
[40] Screening for hepatits D requires testing for anti-HDV antibodies, which indicate past exposure to the virus or current infection.
If anti-HDV antibodies are present, then active HDV infection is confirmed by measuring hepatitis D RNA levels.
[42] Current established treatments for chronic hepatitis D include conventional or pegylated interferon alpha therapy.
[48][49] Bulevirtide may be given with pegylated interferon alpha as the two are thought to have a synergistic effect, leading to greater treatment response rates.
[51] Other treatments for hepatitis D which are currently under development include pegylated interferon lambda (λ), which binds to receptors on the hepatocyte surface leading to an intracellular signaling cascade via the JAK-STAT signaling pathway and activation of anti-viral cell mediated immunity.
[52] The prenylation inhibitor lonafarnib prevents hepatitis D viral particle assembly by inhibiting the farnesylation of the L-HDAg.
[42] Persistent HDV viremia is the most important risk factor for disease progression in those with co-infection or superinfection.
[42] Other factors that are responsible for a poor prognosis in chronic hepatitis D include male sex, older age at time of infection, alcohol use, diabetes, obesity and immunodeficiency.
However, the prevalence is decreasing in many higher income countries due to hepatitis B vaccination programs (although rates remain high in some groups such as those who inject drugs or immigrants from HDV endemic regions).
[42][56] Infection with HDV is a major medical scourge in low income regions of the globe in which HBV prevalence remains high.
Subsequent experiments in chimpanzees showed that the hepatitis delta antigen (HDAg) was a structural part of a pathogen that required HBV infection to produce a complete viral particle.
These symptoms arise from a fulminant hepatitis which may kill in less than a week, and which characteristically affects children and young adults, and more males than females.
[citation needed] The main discovery of delta virus and HBV association was done by Gilberta Bensabath, of the Instituto Evandro Chagas, of Belém, state of Pará, and her collaborators.
