Hepatitis D is a disease caused by a small circular RNA virus (hepatitis delta virus or hepatitis D, HDV). The HDV is regarded as a subset virus satellite, because it can spread only in the presence of another virus, the hepatitis B virus (HBV). The transmission of HDV can occur either through a simultaneous infection by HBV (co-infection) or by infecting someone who already has one carrier of hepatitis B (infection). Whether a co-infection or a superinfection HDV is responsible for more serious complications in cases of infection with HBV alone. Among these complications citing a higher probability of developing liver failure in acute infections and increased risk of developing liver cancer in chronic infections. In combination with the hepatitis B virus, hepatitis D is responsible for the highest mortality rate of all viral hepatitis or 20%.
Structure of the genome and similarities with viroids
The genome of HDV is in the form of a single strand of RNA circular and sealed, wrapped in the negative sense. Due to a sequence of nucleotides that is 70% self-complementary, the genome of HDV form a structure RNA partially double strand which is described as a structure to stick. With a genome of about 1700 nucleotides, HDV is the smallest "virus" capable known to infect animals. However, it was suggested that HDV could find its origin in a class of viruses infecting plants and called viroids. The evidence advanced to support this hypothesis stem from the fact that HDV and viroids have a structure of simple strand of RNA and closed circular-shaped stick. Similarly, HDV and viroids contain RNA sequences capable of exercising the catalytic activity of structures called ribozymes. During viral replication, these are catalytic RNA necessary to produce copies unit fragments of RNA genome before the assembly. Finally, neither the HDV or viroids are able to encode their own polymerases. Failing that, for their replication and viroids HDV require a host of which they can use the RNA polymerase as a matrix. Based on circumstantial evidence, RNA polymerase II was involved in the replication of HDV. Normally, RNA polymerase II uses DNA as a substrate and produces mRNA. Therefore, if the HDV actually uses RNA polymerase II during its replication, it would be the only pathogen known able to convert a DNA polymerase dependent on RNA polymerase dependent.
A significant difference between viroids and HDV is the fact that while viroids do not produce proteins, HDV produces two proteins called the small and large delta antigen (HDAg-HDAg-S and L, respectively). These two proteins are produced from the opening and reading a single matrix. They are the same for 195 amino acids and differ only in the presence of 19 additional amino acids at the end of HDAg C-L. Although 90% of their identical sequences, these two proteins play different roles during an infection. The HDAg-S is produced in the early stages of infection and it is essential to viral replication. HDAg-L, however, is produced during the latter stages of infection, it acts as an inhibitor of viral replication, and it is essential for the assembly of viral particles.
Read also Hepatitis A, Hepatitis C, Hepatitis B