HDV is a small ribonucleic acid (RNA) virus which is estimated to affect 12-72 million individuals globally. As compared to HBV or HCV, HDV is connected with a more rapid rate of development of cirrhosis of the liver and a high risk of hepatocellular carcinoma (HCC).
HDV is the smallest virus which is known to cause human disease, which contains a single RNA strand. HDV RNA encodes only one protein, the HDV antigen (HDAg), which forms a complex with the RNA which is subsequently encapsulated by HBV surface antigens (HBsAg).
HDV infects liver cells only in the presence of HBV infection because its access into liver cells is dependent on HBsAg-cell membrane binding. HBV is also very important for the production and release of new virions.
HDV can be spread sexually or by injection drug use, both of which account for 70% of all cases, in addition to needlestick injuries. The prevalence of HDV infection is unknown in many nations; however, it exceeds 2% in sub-Saharan Africa, Central Asia, and Eastern Europe. In Mongolia, the prevalence of HDV is 40% among those with HBV infection.
Anti-HDV antibodies can be detected in 4-43% of HBsAg-positive American adults. Individuals with late liver disease, those on hemodialysis, men who have sex with men (MSM), sex workers, those on injection drugs, and those who also have human immunodeficiency virus (HIV) infection are more likely to be infected with HDV.
Acute coinfection with HDV and HBV is detected when both HBsAg and immunoglobulin M (IgM) antibodies to HBV core antigen (IgM anti-HBc) are present along with HDV RNA. HDAg is visible in the serum for only a few days.
In about 95% of infected people, acute coinfection is followed by rapid clearance of both viruses. When a person is already infected with HBV, subsequent infection with HDV leads to chronic coinfection with both viruses in about 90% of people.
HDV infection can become chronic and these people, are likely to progress more rapidly than HBV infection. At the time of diagnosis, 30-70% of chronic HDV cases have cirrhosis, while more than half are likely to die within one decade from liver disease.
The persistence of HDV RNA in the blood is a main risk factor for progression to cirrhosis and death. Other factors which increase the risk of severe outcomes include the genotype of the virus, as genotype 1 is the deadliest, drinking, obesity, diabetes, and serum HBV-DNA levels.
According to the American Association for the Study of Liver Diseases HBV Guidelines, the diagnosis of HDV infection should be actively sought in many different situations.
These contain when the person is positive for HBsAg, especially if there is an active or worsening hepatitis without apparent cause or if cirrhosis is rapidly developing in spite of low viral DNA levels. Individuals from countries with high HDV prevalence, those with high exposure risks, especially MSM, those with HDV-positive household contacts, or those who use injection drugs, should also be screened for HDV.
The diagnosis of HDV is based on the presence of the HDV antibody or HDV RNA, which reflects the past and current infection, respectively. There is disagreement about whether universal or targeted screening represents the better public health method, which may differ with the prevalence of either infection.
HBV infection can be prevented by the HBV vaccine; however, vaccination is not an option when HBV infection has already happened.
Interferon alpha or its pegylated derivative, which has a longer half-life, may be deployed to prevent the rapid progression of liver disease and the onset of severe events, as this agent suppresses HDV replication. The use of interferon alpha provides relief of liver inflammation and prevents fibrosis; however, in 70% of patients, these effects eventually wane.
Interferon alpha is linked with a reduced risk of decompensated liver disease, HCC, liver transplant, and death from about 8.5% annually to 3.3%. This treatment may cause depression, bone marrow suppression and tiredness.
While HBV therapeutics are ineffective against HDV, drug applicants like bulevirtide and lonafarnib are at present being investigated in advanced clinical trials. These agents prevent the virus from entering liver cells and disrupt the assembly of virions, respectively. Moreover, these agents have been shown to clear the virus and produce negative results in almost 60% of HDV-positive patients after 96 weeks of bulevirtide.
In contrast, about 20% of patients experience improvement after 48 weeks of treatment with lonafarnib in combination with ritonavir and pegylated interferon alpha.
In Europe, Bulevirtide was recently approved for the treatment of HDV infection. Pegylated interferon alpha remains the only available therapeutic in other countries.
All who are infected with HDV should be advised to keep their personal hygiene equipment separate to avoid transmission through razors or toothbrushes. Susceptible contacts must be screened for and vaccinated against HBV infection as suitable.
HDV-positive patients with indications for the treatment of chronic HBV should receive HBV nucleoside analogs or pegylated interferon alpha, which suppress the replication of both viruses.
https://www.news-medical.net/news/20240102/Exploring-the-global-health-challenge-of-hepatitis-D.aspx
