Hepatitis D: Implications for Sexuality

I recently saw a patient whose boyfriend had just been diagnosed with hepatitis D. Neither of them had ever heard of this form of hepatitis before, and I am uncertain about what guidance to give them regarding the implications for sexual behavior.

Hepatitis D virus (HDV) is an RNA virus that is structurally unrelated to hepatitis A virus, hepatitis B virus (HBV), or hepatitis C virus. HDV was discovered in 1977 by an Italian gas-troenterologist who was studying liver biopsies. HDV, also called the hepatitis delta virus, causes a unique infection that requires the assistance of viral particles from hepatitis B in order to replicate and infect other hepatocytes. The clinical course varies, and ranges from an acute self-limited infection to chronic and severe liver symptoms¹. Like HBV, HDV has the potential to cause progressive signs and symptoms (S/S) such as cirrhosis and liver failure².

As a viroid, HDV is a single-stranded circu¬lar RNA molecule with some double-stranded attachments³. The virus includes an RNA genome, an HDV-concealed anti¬gen, and a lipoprotein envelope created by HBV. The structure combines HDV and HBV by having the surface antigen of the HBV (HBsAg) comprise the framework of the outer layer, whereas the inner ribonucleo¬protein configuration provides space for the HDV to thrive¹. HDV infection can occur only in a person already infected with HBV; without the HBV envelope, virion assembly, and secretion, HDV cannot survive⁴. A per¬

son can be infected by HBV and HDV simultaneously or by HBV first.

Hepatitis D is clinically indistinguishable from other forms of hepatitis. After expo¬sure to HDV, the incubation period is 21-45 days. Although up to 90% cases of HDV are asymptomatic, patients may experi¬ence S/S such as jaundice, fatigue, vague abdominal pain, confusion, pruritus, loss of appetite, nausea, vomiting, and joint pain⁵. More progressive S/S may include scleral icterus, fever, right-upper-quadrant pain, dark “tea-colored” urine, and petechiae with bruising⁶.

To determine whether or not a patient is infected with HDV, blood testing must be performed. HBsAg and immunoglobulin M for hepatitis B core antigen (IgM anti-HBc) must be present. Additional assays include serum HDAg; serum HDV RNA; anti-HDV antibody, and tissue markers for HDV infection. Commercially available assays used in the United States to make a diag¬nosis of HDV are microplate-based enzyme-linked assay or radioimmunoassay for anti-HDV antibody, which is positive in either the acute or the chronic form of HDV infection¹.

Although several HDV genotypes exist, the most prevalent one found in the United States is genotype 1, which is usually associated with the chronic form of HDV infection. With simultaneous HBV/HDV infection, the viral load can be very high, resulting in hepatic compromise that may intensify to cirrhosis or fulminant liver fail¬ure in approximately 1% of cases^1,6-8. The goal of HDV treatment is to prevent replication and achieve long-term suppres¬sion of replication processes in both of the hepatitis viruses. Treatment will normalize the serum alanine transaminase level, which, in turn, improves hepatic necroin¬flammatory activity, allowing healing and cell regeneration. Improvement is mani¬fested by decreasing HDV RNA serum lev¬els and falling levels of liver HDAg¹.

Both HDV and HBV can be transmitted through body fluids, including blood, semen, vaginal fluids, and saliva, although the risk of transmitting the viruses through kissing alone is exceedingly low and the “efficiency” for transmission via unpro¬tected sexual intercourse is less for HDV than for HBV^2,6. Perinatal transmission is rare, with no cases reported in the United States to date. HDV is highly associated with parenteral transmission through transfusions or intravenous (IV) drug use⁶. An estimated 15 million persons are infected with HDV worldwide⁹. HDV infec¬tion prevalence in the United States is much lower; approximately 70,000 US adults are infected with chronic HDV, among whom about 1000 die as a result of the disease each year⁹.

Education and research on HDV are ongoing. According to what is known to date, the best way for women to avoid contract¬ing HDV is by observing safe-sex practices and avoiding illicit IV drug use. Latex con-doms must be used during vaginal, anal, and oral sex, and sex partners must avoid any possible transfer of bodily fluids through shared toy use. Unless the con¬dom is used correctly, it may not be 100% effective at preventing the virus from being transmitted⁴. Women may also con-sider becoming vaccinated with Engerix-B or Recombivax HB to prevent hepatitis B¹⁰.These recombinant DNA injections are given in three doses. After the series has been completed, approximately 90% of healthy adults cultivate protective antibod¬ies, resulting in full immunity to HBV¹⁰.

Kelly Apgar is a full-time student at Widener University in Chester, Pennsylvania. She is working toward an EdD degree in human sexuality. She plans to graduate in 2012. Kelly received her MS in science education from Nova Southeastern University in Fort Lauderdale-Davie, Florida, and her BS from Eckerd College in St Petersburg, Florida. Kelly resides in Bloomfield, New Jersey, with her two dogs.

References

1. Negro F, Lok ASF. Pathogenesis and clinical manifes¬tations of hepatitis D virus infection. In: Esteban R, Bonis PAL, eds. UpToDate. February 1, 2008. Available at: http://www.uptodate.com
2. Mayo Clinic Staff. Hepatitis B. Causes. October 3. 2008. Available at: http://www.mayoclinic.com/health/ hepatitis-b/DS00398/DSECTION=causes
3. Tritz R. Prions and Viroids. 2000. Available at: http://www.kcom.edu/faculty/chamberlain/Website/Lects /prions.htm
4. Lok ASF. Hepatitis D virus infection and liver trans¬plantation. In: Brown RS Jr, Bonis PAL, eds. UpTo Date. November 25, 2008. Available at: http://www.uptodate.com
5. Worman HJ. The Hepatitis D Virus. 2000. Available at: http://www.thailabonline.com/hepatitisd.htm
6. Lacey SR. Hepatitis D. October 31, 2006. Available at: http://emedicine.medscape.com/article/178038-overview
7. Krogsgaard K, Kryger P, Aldershvile J, et al. Delta-infection and suppression of hepatitis B virus replication in chronic HBsAg carriers. Hepatology. 1987;7(1):42-45.
8. Smedile A, Rosina F, Saracco G, et al. Hepatitis B virus replication modulates pathogenesis of hepatitis D virus in chronic hepatitis D. Hepatology. 1991;13(3):413¬416.
9. Farci P, Mandas A, Coiana A, et al. Treatment of chronic hepatitis D with interferon alfa-2a. N Engl J Med. 1994;330(2):88-94.
10. Immunization Action Coalition. Hepatitis B Vaccine. 2008. Available at: http://www.vaccineinformation.org/ hepb/qandavax.asp