MMWR Paper on Hepatitis B
Microbiology 212-A
April 27, 2012

Hepatitis B virus (HBV) is a DNA virus that affects the liver and belongs to the Hepadnaviridae group (Takkenberg, Weegink, Zaaijer, & Reesink, 2010). According to an article in Vox Sanguines, an international journal of transfusion medicine, (Takkenberg, Weegink, Zaaijer, & Reesink, 2010) “about 400 million people worldwide are chronically infected with HBV, and 2 billion people have serological evidence of past or present HBV infection”. HBV, formerly known as serum hepatitis (Huether & McCance, 2008), has eight genotypes (A-H) with genotype D being associated with viral or acute hepatitis B and prevalent mainly in Europe, North Africa, and the United States (Takkenberg, Weegink, Zaaijer, & Reesink, 2010). The virus is about 40nm in diameter, partially double stranded and circular, and has an envelope which is host cell derived (The Board of Trustees of the University of South Carolina, 2011). HBV functions by entering into the nucleus of a hepatocyte and then is transcribed into viral RNA. It is then transported out to the cytosol where transcription occurs and new DNA strands are made that can form new viruses (Takkenberg, Weegink, Zaaijer, & Reesink, 2010). Hepatitis B virus needs to get past the first lines of defense and enter into the body with transmission primarily coming through exposure to blood or body fluids (Adams, Holland, Jr., & Urban, 2011). Main risk factors for infection include intravenous drug use, intercourse with a person infected by HBV, and health care workers who could face exposure from caring for infected individuals (Adams, Holland, Jr., & Urban, 2011). Manifestation of HBV can range from absence of any symptoms through fulminating hepatitis. Acute hepatitis usually goes through three phases, as described in Understanding Pathophysiology (Huether & McCance, 2008): “Prodromal phase – begins about 2 weeks after exposure and ends with the appearance of jaundice; marked by fatigue, anorexia, malaise, nausea, vomiting, headache, hyperalgia, cough, and low-grade fever; infection is highly transmissible during this phase. Icteric phase – begins 1-2 weeks after prodromal phase and lasts 2-6 weeks; jaundice, dark urine, and clay-colored stools are common; liver is enlarged, smooth, and tender, and percussion causes pain; this is the actual phase of illness. Recovery phase – begins with resolution of jaundice, about 6-8 weeks after exposure; symptoms diminish, but liver remains enlarged and tender; liver function returns to normal 2-12 weeks after the onset of jaundice.”
Transmission of HBV from a blood transfusion has become increasingly rare as screening processes have improved and become routine over the past two decades (Lai, Ratziu, Yuen, & Poynard, 2003). Viral HBV is usually symptomatic and can be diagnosed with serological analysis for a specific hepatitis antigen, which for HBV is simply HBsAg (Huether & McCance, 2008). Treatment for acute HBV is also mostly symptomatic with the vast majority of cases, upward of ninety percent, resolving themselves and complete recovery is attained (Adams, Holland, Jr., & Urban, 2011). Physical activity may be limited along with a diet low in fat and high in carbohydrates if any blockage of bile has occurred (Huether & McCance, 2008). The most effective way of preventing infection with HBV is through advance immunization. With the achievement of growing the HBV in a laboratory being made in 1986; by growing liver cells and then infecting them as the HBV cannot grow on its own but must invade appropriate cells and then reproduce the virus, (Schmeck Jr., 1986) greater understanding of the virus along with better defenses such as vaccines have made fighting HBV a more achievable task. Most healthcare workers or those that are exposed to blood or body fluids are vaccinated; and universal vaccination of children before they enter school is being considered or has been adopted in some states (Adams, Holland, Jr., & Urban, 2011). For those who have reasonable belief they may have been exposed to HBV, immunoglobins can be started as soon as possible after exposure. Looking at the data provided by CDC (Department of Health and Human Services, 2011) during 2010-2011 there is an average incidence of HBV of 8 (per 10 million people) in 2010 and 6 (per 10 million people) in 2011 (appendix C). This decrease of 2 (per 10 million people) from 2010-2011 may just be a coincidence and further analysis of data over a larger period of time would be needed. The decrease of 2 persons may not seem like a lot; however with continued education, vaccination, and awareness of prevention, this could indeed signify a downward trend of acute HBV. The trend of occurrence over the course of each year, 2010 and 2011, shows a steady increase without any major spike or deviations (appendix A & B). With the transmission of HBV being mainly from drug use and exchange of fluids between infected individuals (sexually), there is no factor that should cause a spike. Continuing preventative measures will promote lowering the incidence of occurrence, however until a cure is found HBV will still register a minimal number of cases a year.

References
Adams, M. P., Holland, Jr., L. N., & Urban, C. Q. (2011). Pharmacology for nurses: A pathophysiologic approach (Third ed.). Upper Saddle River, NJ: Pearson Education, Inc.
Department of Health and Human Services. (2011, December 11). Morbidity and mortality weekly report. Retrieved March 20, 2012, from Center for Disease Control and Prevention: http://wonder.cdc.gov/mmwr/mmwr_reps.asp?mmwr_year=2010&mmwr_week=01&mmwr_table=2E
Huether, S. E., & McCance, K. L. (2008). Understanding pathophysiology (Fourth ed.). St. Louis, MO: Mosby, Inc.
Lai, C. L., Ratziu, V., Yuen, M.-F., & Poynard, T. (2003, December 20/27). Viral hepatitis B. The Lancet, 362, 2089-2094.
Schmeck Jr., H. M. (1986, October 10). Virus technique may aid liver disease fight. The New York Times.
Takkenberg, R. B., Weegink, C. J., Zaaijer, H. L., & Reesink, H. W. (2010). New developments in antiviral therapy for chronic hepatitis B. Vox Sanguines, 98(4), 481-494.
The Board of Trustees of the University of South Carolina. (2011, May 24). Virology chapter eighteen hepatitis viruses. Retrieved May 24, 2012, from Microbiology and Immunology on-line; University of South Carolina School of Medicine: http://pathmicro.med.sc.edu/virol/hepatitis-virus.htm