PubMed · 7416657
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
L M Bernstein, E R Siegel, R S Koff, A D Merritt, C M Goldstein. 1980. The hepatitis knowledge base (short form).. https://doi.org/10.7326/0003-4819-93-1-183
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Five different hepatitis viruses that cause acute and chronic hepatitis in human beings have been identified. Hepatitis viruses are designated by the letters A, B, C, D and E and abbreviated as HAV, HBV, HCV, HDV, and HEV, respectively. Although each belongs to a distinctly different virologic group, they share the feature of hepatotropism, which remains poorly understood. HAV and HEV are transmitted through a fecal-oral route. HDV, also referred to as the delta agent, is a defective, parenterally transmitted virus that uses the hepatitis B surface antigen (HBsAg) of HBV as its envelope. Thus, HDV infection occurs only in patient with HBV infection. Application of molecular biologic techniques has been instrumental in elucidating the genomic sequences of the individual hepatitis viruses and in understanding viral gene expression and mechanisms of viral replication. Knowledge of the genomic structure of these viruses and perfection of molecular biological techniques have also led to clinical applicability of molecular diagnostic techniques. Indeed, these molecular diagnostic techniques have rapidly become the standards against which serologic tests are compared.
The variability of genomes of the hepatitis viruses leads to the development of viral mutants which are of great importance not only for epidemiology and therapy but also for the prevention of infections they cause. Contemporary knowledge indicates that investigation of mutants of hepatitis viruses is not only necessary for the understanding of the epidemiology, spread, elucidation of the severity of the disease and sequelae after acute infection but also for our therapeutic possibilities in different forms of viral hepatitis (VH). The submitted paper reviews the most important mutants of different types of VH (HA, HB, HC, HD, and HE).
Genetic variations in the known human hepatitis viruses are probably the result (a) of high viral replication rates and poor or absent proofreading ability intrinsic to RNA viruses (HAV, HCV, HDV, HEV) and (b) to a DNA virus (HBV) that uses a reverse-transcription mechanism for genomic replication. Nucleotide substitutions, deletions, duplications, insertions, and rearrangements resulting in amino acid changes may have no consequences, may impair replication, change host susceptibility, or may lead to escape from immune attack. Genetic diversity has been identified in each of the known hepatitis viruses. The importance of mutant viruses in pathogenicity, immunity, natural history, clinical outcomes, vaccine production, and responsiveness to treatment has emerged as an area for intensive study.