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Most adults clear the virus, but babies and young children are more likely to get chronic hepatitis B. It is not intended to be and should not be interpreted as medical advice or a diagnosis of any health or fitness problem, condition or disease; or a recommendation for a si test, doctor, care provider, procedure, treatment plan, product, or course of action. I am a medical anomaly. This is called chronic hepatitis B. My personal philosophy and method is to be selective about the people I choose to date. If you have or suspect you may have a health problem, consult your health care provider. A number of bat infecting species have also been described. The virus is one of the smallest enveloped animal viruses with a virion diameter of 42 nm, but forms exist, including filamentous and spherical bodies lacking a core. Good thing she responsible me. The function of the protein coded for by gene X is not fully understood, but some evidence suggests that it may function as a transcriptional transactivator.
Main article: In addition to causing hepatitis, infection with HBV can lead to and. It has also been suggested that it may increase the risk of. Roles in disease Viral infection by hepatitis B virus HBV causes many changes due to direct action of a protein coded for by the virus, , and to indirect changes due to a large increase in ROS after infection. HBx appears to dysregulate a number of cellular pathways. HBx causes dysregulation in part by binding to genomic DNA, changing expression patterns of miRNAs, affecting histone methyltransferases, binding to protein to activate transcription, and cooperating with histone methylases and demethylases to change cell expression patterns. HBx is partly responsible for the approximate 10,000-fold increase in intracellular ROS upon chronic HBV infection. Increased ROS can be caused, in part, by localization of HBx to the mitochondria where HBx decreases the mitochondrial membrane potential. In addition, another HBV protein, , also increases ROS through interactions with the. The increase in ROS after HBV infection causes inflammation, which leads to a further increase in ROS. ROS cause more than 20 types of DNA damage. Oxidative DNA damage is mutagenic. In addition, repair of the DNA damage can cause epigenetic alterations at the site of the damage during repair of the DNA. By the time accumulating epigenetic and mutational changes eventually cause progression to , epigenetic alterations appear to have a larger role in this than mutations. Only one or two genes, and perhaps , are mutated in more than 20% of liver cancers while 41 genes each have repressing gene expression in more than 20% of liver cancers, with seven of these genes being hypermethylated in more than 75% of liver cancers. HBx also alters that can affect gene expression. Several thousand protein-coding genes appear to have HBx-binding sites. In addition to protein coding genes, about 15 and 16 are also affected by the binding of HBx to their promoters. Each altered microRNA can affect the expression of several hundred messenger RNAs see. The hepatitis B virus is classified as the type species of the , which contains three other species: the Ground squirrel hepatitis virus, , and the Woolly monkey hepatitis B virus. The genus is classified as part of the family, which contains two other genera, the and a second which has yet to be assigned. This family of viruses have not been assigned to a viral order. Viruses similar to hepatitis B have been found in all apes , , and , in , and in a suggesting an ancient origin for this virus in primates. The virus is divided into four major adr, adw, ayr, ayw based on antigenic present on its envelope proteins. The viral strains have also been divided into ten genotypes A—J and forty subgenotypes according to overall nucleotide sequence variation of the genome. The genotypes have a distinct geographical distribution and are used in tracing the evolution and transmission of the virus. Differences between genotypes affect the disease severity, course and likelihood of complications, and response to treatment and possibly vaccination. The serotypes and genotypes do not necessarily correspond. Genotype D has 10 subgenotypes. Unclassified species A number of as yet unclassified Hepatitis B like species have been isolated from bats. The structure of hepatitis B virus Hepatitis B virus is a member of the. The virus particle, called Dane particle , consists of an outer envelope and an core composed of. The nucleocapsid encloses the viral DNA and a DNA polymerase that has activity similar to retroviruses. The outer envelope contains embedded proteins which are involved in viral binding of, and entry into, susceptible cells. The virus is one of the smallest enveloped animal viruses with a virion diameter of 42 nm, but forms exist, including filamentous and spherical bodies lacking a core. These particles are not infectious and are composed of the lipid and protein that forms part of the surface of the virion, which is called the surface antigen , and is produced in excess during the life cycle of the virus. The function of this protein is not yet well known, but evidence suggests it plays a part in the activation of the viral transcription process. The early evolution of the Hepatitis B, like that of all viruses, is difficult to establish. The divergence of orthohepadnavirus and avihepadnavirus occurred ~125,000 years ago 95% interval 78,297—313,500. Both the Avihepadnavirus and Orthohepadna viruses began to diversify about 25,000 years ago. The branching at this time lead to the emergence of the Orthohepadna genotypes A—H. Human strains have a most recent common ancestor dating back to 7,000 95% interval: 5,287—9,270 to 10,000 95% interval: 6,305—16,681 years ago. The Avihepadnavirus lack a X protein but a vestigial X reading frame is present in the genome of duck hepadnavirus. The X protein may have evolved from a. A second estimate of the origin of this virus suggests a most recent common ancestor of the human strains evolved ~1500 years ago. The most recent common ancestor of the avian strains was placed at 6000 years ago. Another analysis with a larger data set suggests that Hepatitis B infected humans 33,600 years ago 95% higher posterior density 22,000-47,100 years ago. The estimated substitution rate was 2. A significant increase in the population was noted within the last 5,000 years. Cross species infection to orangutans and gibbons occurred within the last 6,100 years. Examination of sequences in the zebra finch have pushed the origin of this genus back at least to million years ago and possibly to million years ago. Chimpanzee, gorilla, orangutan, and gibbons species cluster with human isolates. Non primate species included the woodchuck hepatitis virus, the ground squirrel hepatitis virus and arctic squirrel hepatitis virus. A number of bat infecting species have also been described. It has been proposed that a New World bat species may be the origin of the primate species. A study of isolates from the circumpolar Arctic human population has proposed that the ancestor of the subgenotype B5 the endemic type found in this population that the ancestral virus originated in Asia about 2000 years ago 95% HPD 900 BC - 830 AD. Coalescence occurred about 1000 AD. This subgenotype spread from Asia initially to and then spread westward within the last 400 years. The oldest evidence of hepatitis B infection dates to. The evidence was obtained from 4,500-year-old human remains. According to the 2018 study, the viral obtained by became the oldest ever recovered from vertebrate samples. It was also found that some ancient hepatitis viral still infect humans, while other became extinct. This disproved the belief that hepatitis B originated in the New World and spread to Europe around 16th century. The genome organisation of HBV. Size The of HBV is made of circular , but it is unusual because the DNA is not fully double-stranded. One end of the full length strand is linked to the viral. The genome is 3020—3320 long for the full length strand and 1700—2800 nucleotides long for the short length strand. Encoding The negative-sense, non-coding strand is complementary to the viral mRNA. The viral DNA is found in the nucleus soon after infection of the cell. The partially double-stranded DNA is rendered fully double-stranded by completion of the + sense strand by cellular DNA polymerases viral DNA polymerase is used for a later stage and removal of a protein molecule from the - sense strand and a short sequence of RNA from the + sense strand. Non-coding bases are removed from the ends of the - sense strand and the ends are rejoined. The viral genes are transcribed by the cellular RNA polymerase II in the cell nucleus from a covalently closed circular DNA cccDNA template. Two enhancers designated enhancer I EnhI and enhancer II EnhII have been identified in the HBV genome. Both enhancers exhibit greater activity in cells of hepatic origin, and together they drive and regulate the expression of the complete viral transcripts. There are four known genes encoded by the genome called C, P, S, and X. The core protein is coded for by gene C HBcAg , and its start codon is preceded by an upstream in-frame AUG start codon from which the pre-core protein is produced. HBeAg is produced by proteolytic processing of the pre-core protein. The DNA polymerase is encoded by gene P. Gene S is the gene that codes for the surface antigen HBsAg. Because of the multiple start codons, polypeptides of three different sizes called large, middle, and small pre-S1 + pre-S2 + S, pre-S2 + S, or S are produced. The function of the protein coded for by gene X is not fully understood, but some evidence suggests that it may function as a transcriptional transactivator. Several elements have been identified in the HBV genome. These include: , and. Genotypes Genotypes differ by at least 8% of the sequence and have distinct geographical distributions and this has been associated with anthropological history. Within genotypes subtypes have been described: these differ by 4—8% of the genome. There are eight known genotypes labeled A through H. Two further genotypes have since been recognised. The current 2014 listing now runs A though to J. Several subtypes are also recognised. There are at least 24 subtypes. Different genotypes may respond to treatment in different ways. Individual genotypes Type F which diverges from the other genomes by 14% is the most divergent type known. Type A is prevalent in , and , including the. Type B and C are predominant in ; type D is common in the Mediterranean area, the and ; type E is localized in sub-Saharan Africa; type F or H is restricted to Central and. Type G has been found in and. Genotypes A, D and F are predominant in and all genotypes occur in the with frequencies dependent on ethnicity. The E and F strains appear to have originated in aboriginal populations of Africa and the New World, respectively. Type Ba has been further subdivided into four clades B2—B4. Type C has two geographically subtypes: Cs C1 in South-east Asia and Ce C2 in East Asia. The C subtypes have been divided into five clades C1—C5. A sixth clade C6 has been described in the Philippines but only in one isolate to date. Type C1 is associated with , and ; type C2 with , and ; type C3 with and ; C4 with ; and C5 with the. A further subtype has been described in ,. Type D has been divided into 7 subtypes D1—D7. Type F has been subdivided into 4 subtypes F1—F4. F1 has been further divided into 1a and 1b. In subtypes F1, F2, and F3 are found in East and West Amerindians. Among South Amerindians only F3 was found. Subtypes Ia, III, and IV exhibit a restricted geographic distribution Central America, the North and the South of South America respectively while clades Ib and II are found in all the Americas except in the Northern South America and North America respectively. Hepatitis B virus replication The life cycle of hepatitis B virus is complex. Hepatitis B is one of a few known viruses which use as a part of its replication process. Attachment The virus gains entry into the cell by binding to receptors on the surface of the cell and entering it by mediated by either or. HBV initially binds to. The pre-S1 segment of the HBV L protein then binds tightly to the cell surface receptor NTCP , encoded by the. NTCP is mostly found in the of. The presence of NTCP in liver cells correlates with the tissue specificity of HBV infection. Penetration Following endocytosis, the virus membrane fuses with the host cell's membrane, releasing the nucleocapsid into the cytoplasm. Uncoating Because the virus multiplies via RNA made by a host enzyme, the viral genomic DNA has to be transferred to the cell nucleus. It is thought the capsid is transported on the to the. The core proteins dissociate from the partially double stranded viral DNA, which is then made fully double stranded by host DNA polymerases and transformed into covalently closed circular DNA that serves as a template for transcription of four viral. Replication The largest mRNA, which is longer than the viral genome , is used to make the new copies of the genome and to make the core protein and the viral RNA-dependant-. Assembly These four viral transcripts undergo additional processing and go on to form progeny virions which are released from the cell or returned to the nucleus and re-cycled to produce even more copies. Release The long mRNA is then transported back to the cytoplasm where the virion P protein synthesizes DNA via its reverse transcriptase activity. University of Southern California, Department of Pathology and Microbiology. Journal of Clinical Oncology. Nat Rev Gastroenterol Hepatol. ICTVdB Index of Viruses. International Committee on Taxonomy of Viruses. Journal of Viral Hepatitis. Journal of Viral Hepatitis. Proceedings of the National Academy of Sciences of the United States of America. In Baron S; et al. Univ of Texas Medical Branch. Retrieved 11 April 2018. Archived from on 2015-07-10. Archived from on 2009-04-13. Cold Spring Harbor perspectives in medicine. Current Opinion in Virology. Molecular and Cellular Biology. American Journal of Therapeutics. Retrieved 11 April 2018. Cold Spring Harbor Perspectives in Medicine. Retrieved 18 February 2015.
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