The Emergence of New Hepatitis Viruses
ABSTRACTS & COMMENTARIES
Synopsis: Hepatitis E and hepatitis G viruses are increasingly recognized as health concerns world-wide, with implications for international workers and travelers.
Sources: Janisch Th, et al. Emerging viral pathogens in long-term expatriates (1): Hepatitis E virus. Trop Med Internatl Health 1997;2:885-891; Corwin AL, et al. Short Report: Evidence of worldwide transmission of hepatitis G virus. Am J Trop Med Hyg 1997;57:455-456.
To assess the epidemiologic pattern of hepatitise in different regions and the infection risk to long-term expatriates, 500 serum samples were collected. The subjects were development aid workers and their family members, and they had spent an average of nine years in an HEV-endemic region.
An overall anti-HEV seroprevalence rate of 5.2% was found, with no significant differences between gender or country of upbringing. None of the 77 children and adolescents tested positive for HEV. Furthermore, seroprevalence rate of adults did not increase with increasing number of expatriate years. Of the 26 HEV-positive subjects, five presented with elevated transaminases at the time of sampling, and two others had past diagnoses of non-A-non-B-non-C hepatitis. The Indian subcontinent showed the highest seropositivity for HEV with 10%. Seroprevalence rates from Latin America, East Africa, West and Central Africa, and Asia ranged between 6% and 9%. The Arab countries and the Middle East showed a relatively low seroprevalence rate of 2.1%. Individual countries related to the highest seropositivity include Myanmar, Nepal, Pakistan, Sudan, China, and India.
COMMENT BY LIN H. CHEN, MD
Hepatitis E was identified in the early 1980s to be a calici-like virus.1 It is found in tropical and subtropical regions. There have been outbreaks from numerous countries around the world, including India, Pakistan, Ethiopia, China, and Mexico.2 The transmission of HEV appears to be via the fecal-oral route, with the virus being mainly water-borne. Person-to-person transmission can rarely occur.1 Peak incidence is in young adulthood. Following approximately a 40-day incubation period and a prodromal period of 1-10 days, some patients develop nausea, vomiting, abdominal pain, pruritus, and joint pain.1 Illness is usually mild, with many anicteric cases. However, fulminant hepatitis can develop. Pregnant women in the third trimester seem to be prone to developing severe illness, with a mortality rate reaching 25%.1 No chronic sequelae from hepatitis E infection have ever been identified.
There have been reports of international workers and travelers acquiring hepatitis E abroad.2-4 However, the risk of acquiring infection in long-term expatriates has not been clear. The current report suggests that certain regions may expose the long-term expatriate to increased risk for hepatitis E infection. Now that active immunization against hepatitis A is available, hepatitis E may become a more visible cause of hepatitis associated with travel.
Although some preliminary success has been noted in vaccine development, there is currently no effective immunoprophylaxis for hepatitis E.1,5 Therefore, it remains crucial to educate expatriates and travelers regarding water and food safety. Additionally, hepatitis E should be considered in evaluating the returning traveler with fever and hepatitis. In those with evidence of non-A-C hepatitis, diagnostic tests for anti-HEV can be done by Western blot or enzyme immunoassay. CDC's Hepatitis Branch should be contacted at (404) 639-3048 for information concerning serologic testing.
Hepatitis G
A total of 236 sera from Egypt, Indonesia, Vietnam, and Peru were screened for HGV in addition to HBV and HCV. The subjects included multiply transfused children, adults with chronic liver disease, patients with acute non-A-E hepatitis, and healthy controls and blood donors.
HGV was detected in 11% of the specimens. A high proportion (24-32%) of multiply transfused children from Egypt and Indonesia were found to be HGV-positive. Many of the HGV-positive patients from Indonesia demonstrated coinfection with HBV or HCV. One healthy control (5%) from Indonesia was found to be positive for HGV without evidence for HBV or HCV. Similarly, 20% of the blood donors in Egypt were found to be positive for HGV without evidence for HBV or HCV. However, it was noted that some of these donors were paid donors and illicit drug users.
In addition, 13% of the patients from Peru with chronic liver disease were found to have HGV, although half of these patients also had markers for HBV. One Peruvian patient with acute non-A-E hepatitis tested positive for HGV.
COMMENT BY LIN H. CHEN, MD
An agent for non-A-non-B hepatitis had been isolated from human stool samples and transmitted to monkeys intravenously. It was called HFV (hepatitis French [origin] virus).6 However, this agent has not been confirmed and may have been designated prematurely.7
More recently, the hepatitis G virus (HGV) was isolated from a patient with chronic hepatitis and coinfected with HCV.8 It is an RNA virus in the family Flaviviridae and appears to be the same as GB virus C (GBV-C).7,8 The GB hepatitis agent was isolated from a surgeon (whose initials were GB) and experimentally passed onto tamarins.9 In the process of cloning this agent, two viruses were discovered. These were called GBV-A and GBV-B and were felt to be nonhuman viruses.7 In screening human sera for GBV-A and GBV-B, GBV-C was identified.7,9
Our knowledge about the hepatitis G virus will likely expand rapidly in the near future. It has been found in varying rates among blood donors around the world, from less than 2% in the United States and Japan to 10% in Brazil.7 The report by Corwin et al found HGV among different populations in North Africa, Southeast Asia, and South America. HGV is felt to be transmitted via the parenteral route, including blood products, intravenous drug use, and vertical transmission,7 yet there are also many with no identifiable parenteral risk factors.
The role of HGV in disease is still being explored. Among the suggested presentations are chronic liver disease, acute non-A-E hepatitis, asymptomatic viremia, and coinfection with HBV and HCV.7 The Peruvian population suggested an association of HGV with chronic liver disease as well as acute non-A-E hepatitis.
Detection of HGV infection can be done by polymerase chain reaction. A PCR kit for HGV RNA (Hepatitis G virus probe set) is available in Europe from Boehringer Mannheim GmbH, cat no. 1 782 720.7 It is not yet available in the United States. There is research being done on an enzyme-linked immunosorbent assay (ELISA) to detect antibodies to an HGV envelope protein. This may eventually be useful as a serological marker for past HGV infection.
Given the similar routes of transmission, international workers and travelers at risk for HBV or HCV are likely to be at risk for HGV also. It would be prudent to advise these patients regarding HGV. There is no vaccine available, and data on treatment with interferon are only preliminary.7 Therefore, the only means of preventing hepatitis G infection is to minimize possible exposure.
References
1. Mast EE, Krawczynski K. Annu Rev Med 1996;47: 257-266.
2. Centers for Disease Control. MMWR Morb Mortal Wkly Rep 1993;42(1):1-4.
3. Drabick JJ, et al. Am J Trop Med Hyg 1997;57:449-454.
4. Abid M, et al. J Travel Med 1997;4:187-188.
5. Purcell RH. Hepatitis E virus. In: Fields BN, Knipe DM, Howley PM, et al (eds). Fields Virology, 3rd edition. Philadelphia: Lippincott-Raven Publishers; 1996:2831-2843.
6. Deka N, et al. J Virol 1994;68:7810-7815.
7. Cheung RC, et al. West J Med 1997;167:23-33.
8. Linnen J, et al. Science 1996;271:505-508.
9. Simons JN, et al. Nature Med 1995;1:564-569.
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