In individuals with chronic Hepatitis B virus (HBV) infection, the Hepatitis D virus (HDV) was first identified in 1977. The HDV nuclear antigen was eventually shown to be a component of a novel pathogen, initially identified...
In individuals with chronic Hepatitis B virus (HBV) infection, the Hepatitis D virus (HDV) was first identified in 1977. The HDV nuclear antigen was eventually shown to be a component of a novel pathogen, initially identified as the delta agent, despite initially being believed to be an unrecognised HBV antigen. HDV is categorised as a hybrid virus since it employs the Hepatitis B surface antigen (HBsAg) as its envelope protein and can only infect people who also have HBV. For unidentified causes, HDV-infected people have suppressed HBV replication.
In this exercise, the presentation, assessment, and management of hepatitis D are described. The inter-professional team's role in the treatment of these patients is also highlighted.
In individuals with chronic Hepatitis B virus (HBV) infection, the Hepatitis D virus (HDV) was first identified in 1977. The HDV nuclear antigen was eventually shown to be a component of a novel pathogen, initially identified as the delta agent, despite initially being believed to be an unrecognised HBV antigen. HDV is categorised as a hybrid virus because it employs the Hepatitis B surface antigen (HBsAg) as its envelope protein, which allows it to only infect people who also have HBV. HBV replication is decreased in people with HDV infection for unidentified reasons.
Acute and chronic inflammation are caused by the hepatitis D virus, which is spread parenterally. Within hepatocytes, hepatitis D replicates autonomously, but it needs hepatitis B surface antigen to spread. Hepatitis D virus direct cytotoxic actions or a host-mediated immune response both cause hepatic cell death.Transmission during pregnancy is unusual. Blood transfusions and intravenous drug usage are risk factors.
Despite the fact that HDV is dependent on HBV, its geographic distribution is different from that of HBV, in part because of the various modes of transmission. Parenteral exposure to blood or blood products is the principal way Ultrasound by which HDV is spread. Vertical transmission is uncommon compared to sexual transmission (even in gay men). HBV carriers who are also super-infected with HDV have mostly provided information on HDV epidemiology. It is believed that HDV infection affects 5% of HBV carriers.
Hepatitis D antigen (HDAg), a lipoprotein envelope from HBV, and an RNA genome make up the structural components of HDV. Only HDAg is encoded by the genome. The terms "long" and "short" refer to two different types of HDAgs. Hepatocytes are where viral replication takes place. Because it transcribes its messenger RNA via the host's RNA polymerase II, the virus is distinctive. While the long HDAg controls viral assembly and also suppresses viral replication, the short HDAg drives viral replication by directly attaching to the HDV RNA. After the HBV envelope has been included, the virus has been fully formed and is then released.
Infection with HDV only happens when HBV is present. Acute hepatitis B and D infection develops from co-infection with both viruses in those who are HBV sensitive. A biphasic course of two peaks of blood alanine aminotransferase (ALT) may be detected in co-infection, which clinically resembles classic acute hepatitis B. This is due to the fact that HDV cannot spread until the HBV infection has been established during the acute confection.
In some instances, more severe cases than acute HBV mono-infection may be seen with a higher risk of liver failure. Only around 5% of individuals develop chronic infection, which is defined as persistence of infection for more than six months, during the acute coinfection with HBV and HDV. The majority of patients recover during this time.
A full-blown superinfection that might manifest as severe acute hepatitis or an aggravation of preexisting chronic hepatitis B can happen in those who are chronic HBsAg carriers. Acute HDV infection may be misinterpreted for a hepatitis B virus flare in patients with chronic HBV infection. If HDV superinfection is not considered as a diagnostic option, clinical presentation and initial investigations in people with previously undetected hepatitis B infection may be misinterpreted for acute HBV infection.
In comparison to HBV/HDV coinfection, the clinical course of a superinfection is frequently more severe. 90% of these people develop chronic hepatitis D because the HBsAg allows for ongoing viral replication. Progressive fibrosis, cirrhosis, hepatocellular cancer, and hepatic decompensation are among the severe morbidity and consequences brought on by chronic HDV infection, which is more common .
Depending on the geographical location, host immunological variables, activity, and genotype of the HDV involved, one of the three viruses—HBV, hepatitis C virus (HCV), and HDV—will predominate over the others in situations of triple infection.
Although the exact method by which HDV causes liver damage is unknown, it is believed to be caused by the host immunological response. From minimal symptoms to fulminant liver failure, the severity of the damage might vary. Hepatocellular carcinoma risk is elevated by HDV superinfection because of its propensity for a quicker course.
The HDV genotype, host immune system, and HBV genotype are just a few of the variables that affect the extent of harm. Traditionally, there are three primary genotypes of HDV: 1, 2, and 3. Other genotypes have been identified as well, however these have not yet been fully characterised. In Western countries, genotype 1 predominates.
Similar to other viral diseases, hepatitis D alters the liver parenchyma histologically. The liver cells become necrotic and inflamed as a result. Acute illness is characterised by cytoplasmic eosinophilia and interlobular infiltration of inflammatory cells (lymphocytes, macrophages). Periportal necrosis, which is a hallmark of chronic hepatitis, is frequently accompanied by nodular alterations.
IgM and IgG class antibodies (anti-HDV) are generated in reaction to HDAg. In terms of appearance and amounts of HDV RNA, HDAg, and anti-HDV as well as HBV indicators, the three infectious patterns—acute HDV/HBV coinfection, acute HDV superinfection, and chronic HDV infection—vary. The presence of HBsAg is crucial for diagnosis since HDV depends on HBV. Acute HBV/HDV coinfection must also be diagnosed in the presence of IgM antibodies to the hepatitis B core antigen (IgM anti-HBc).
The HDAg presentation is early but transient in acute HDV infection, and detection frequently requires repeat tests. If additional HDV infection signs are not present, the development of anti-HDV may be the only means to detect acute HDV. The progression of acute hepatitis D affects the IgM class of Anti-HDV pattern. If HDV infection self-limits, anti-HDV IgM development is
Temporary and delayed
For diagnosing an active HBV infection in the past, HDAg detection was regarded as the gold standard. It is challenging and time-consuming to detect HDAg using the necessary immunoblot technique because anti-HDV creates immunological complexes with HDAg. As a result, the most accurate and feasible test for identifying a current HDV infection is HDV RNA detection through reverse transcriptase-polymerase chain reaction (RT-PCR).
Hepatitis D has few available treatments, and the best course of action is unknown. Acute hepatitis D has no known therapies. Interferon alpha (IFN alpha) has been demonstrated to be effective in the majority of clinical trials, despite the fact that it is not FDA-approved for treating chronic hepatitis D. Expert recommendations state that the optimal agent should be IFN alpha in the pegylated form. For at least a year, treatment is given once every week.
Treatment aims to decrease HDV replication, as seen by the absence of HDV RNA in serum and HDAg in the liver. Normalisation of alanine aminotransferase (ALT) and liver biopsy inflammation are two treatment endpoints. Liver transplantation is the sole treatment option when the condition develops into cirrhosis.