Important note: Information in this article was accurate in October 2003. The state of the art may have changed since the publication date.
Treatment Issues: Newsletter of Experimental AIDS Therapies - Volume 17, Number 10, October 2003
Bob Huff
Susan Goldstein and colleagues from the Centers for Disease Control (CDC) have projectedthat if everyone born in 2000 were considered as a single cohort, and none were vaccinated for HBV, over their lifetimes they would experience 64.8 million HBV infections resulting in 9.7 million chronic infections. In this imaginary cohort there would be 1.4 million deaths from chronic infection and 65,000 deaths due to acute hepatitis B. Perinatal infection would contribute 21 percent of these deaths, infections occurring between birth and age 5 would account for 48 percent, and infections acquired after the age of 5 would lead to 31 percent of the deaths. They estimate that HBV infection would be responsible for 1.3 percent of the deaths of all people born in 2000.
They then modeled the effect that vaccination would have on these estimates. Infant vaccination with 90 percent 3-dose coverage starting within 24 hours of birth could prevent 84 percent of these projected HBV-related deaths.
Preventable HBV in a U.S. Prison
Despite general agreement that healthcare in prison settings is terrible, remarkably little research appears at the major infectious disease conferences to document the results of treatment or the epidemiology of disease behind bars. William Bower, of the CDC in Atlanta, presented a poster at the IDSA conference in San Diego that tracked the molecular epidemiology of HBV transmission in a Georgia state prison. Prisons are prime settings for transmitting HBV through sexual activity, shared needles, shared tattooing equipment or in fights. The CDC recommends hepatitis B vaccination for all inmates in correctional facilities without evidence of immunity.
A baseline serologic survey was conducted in June of 2000 of 1,124 participating prisoners. Of these, 11 were found with acute HBV infection, 11 had chronic infection and 208 had a resolved infection for a total of 230 or 20.5 percent of the sample. This left 894 inmates susceptible to infection. A year later, in June of 2001, a second survey of the susceptible inmates was conducted with 653 of the 894 remaining at the facility. Of these, 503 of 653 (77 percent) consented to retesting. One year after the baseline survey, 18 new infections were detected, with one of these a chronic infection. This results in an annual infection rate of 3,579 per 100,000 persons in this prison.
DNA sequence analysis identified 11 different strains within three HBV genotypes. Eight of the chronically infected and one of the acutely infected inmates had unique strains. But ten of the sequences represented the other two strains, with one of those found in four inmates with chronic infection. The other shared strain was found in six inmates, two with chronic and four with acute infection. Three of these acute infections turned up in the June 2000 survey and one in 2001. Two inmates with acute infection reported having sex with one of the inmates with chronic infection.
This study is remarkable for a number of reasons. First, it documents the sexual transmission of disease within a correctional facility, a phenomenon that is rarely acknowledged by corrections officials who then deny the need for providing condoms inside. It also confirms that, with an annual incidence of HBV infection in this facility over 120 times that of the estimated national incidence, prisons are incubators of infectious disease. It also shows the role that an individual can play in sparking an epidemic. Finally it shows that a prison in Georgia, willing to collaborate with the CDC in its research, routinely ignores its recommendation that all inmates be vaccinated against hepatitis B.
HBV in EuroSIDA
The EuroSIDA cohort reported on the impact that chronic HBV infection has on AIDS progression and response to antiretroviral therapy. Of 5,833 individuals in EuroSIDA tested for HBV surface antigen, 530 (9%) were found positive. The incidence of all-cause and liver-related death was greater in those with chronic HBV than in others (12 vs. 2.6 and 0.5 vs. 0.2/100 patient years, respectively). The authors conclude that HBV antigen status did not impact virological or immunological response in 1752 patients receiving HAART. This confirms previous reports that, although HBV may not make HIV worse, coinfection with HBV increases the risk of dying from liver disease in people with HIV.
Goldstein S, et al. Hepatitis disease burden: global estimates and reduction from vaccination. 41st IDSA, 2003, San Diego.. Abstract 583.
Bower W, et al. Molecular epidemiology of hepatitis B virus transmission in a United States correctional facility. 41st IDSA, 2003, San Diego.Abstract 585.
Konopnicki D, et al. Hepatitis B (HBV) in the EuroSIDA Cohort: prevalence and impact on mortality, AIDS progression and response to HAART. European AIDS Conf 2003 Oct 25-29;9:F9/3 (abstract no. 46).
| HIV | HBV | HCV | |
| EPI | Slowly progressing disease, with ~10 years to life threatening stage. High mortality if untreated. Transmitted by blood, sex, and from mother to child. Not easy to transmit |
Slowly progressing disease with ~40 years to life threatening stage. 5% to 25% mortality if untreated. Transmitted by blood, sex, and from mother to child. Extremely easy to transmit |
Slowly progressing disease with ~20 years to life threatening stage. Uncertain mortality if untreated. Transmitted by blood, sex, and from mother to child. Easy to transmit |
| Therapy | No vaccine available. Viral eradication not possible. |
Effective vaccine is available. Eradication is unlikely. |
No vaccine available. Viral eradication is possible. |
| Lifetime therapy required. | Lifetime therapy required to control chronic, replicating disease. | Duration of therapy ranges from 6 months to 1 year for ~50% success rate. |
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| Viral suppression with therapy offers clinical benefits. Immune recovery is possible. |
Therapy may offer clinical benefits. Recovery from liver damage is possible. Conversion from chronic replicating to inactive state is possible. |
Therapy may offer clinical benefits despite failure to eradicate. Recovery from liver damage is possible. |
|
| Disease progresses if therapy is halted. | Life-threatening flares are possible if therapy is halted. | Disease progression is possible if therapy is halted. |
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| Retrovirus | Hepadnavirus | Flaviviridae virus | |
| Virology | Contains 2 strands of RNA. | Usually contains 2 circular strands of DNA | Contains 1 strand of RNA. |
| Infects immune cells using CD4 receptors by fusion with cell membrane. The genetic material (RNA) is uncoated in the cytoplasm. DNA is transrcibed by RT in the cytoplasm then delivered to the nucleus and integrated into the nuclear DNA. |
Infects liver cells using an uncertain receptor. Cell membrane fusion is likely. The genetic material (DNA) is delivered directly into the nucleus where it resides as circular DNA. Pre-genomic RNA is exported to the cytoplasm and reverse transcribed to genomic DNA |
Infects liver cells using uncertain receptors. Fusion occurs within a vesicle The genetic material (RNA) is uncoated in the cytoplasm and never enters the nucleus. Templates for the genomic RNA are produced in the cytoplasm |
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| New virus is produced when the cell divides. RNA exported from the nucleus and viral proteins produced in the cytoplasm are packaged using cellular membrane. |
New virus is produced when the cell divides. Viral proteins are produced in the ER and packaged with genomic DNA in the Golgi. |
New virus production is stimulated by infection. Viral proteins are produced and packaged with genomic RNA in the cytoplasm using vesicle membranes. |
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