Hepatitis E Virus in Rats, Los Angeles, California, USA - Vol. 17 No. 12 - December 2011 - Emerging Infectious Disease journal - CDC

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Hepatitis E Virus in Rats, Los Angeles, California, USA - Vol. 17 No. 12 - December 2011 - Emerging Infectious Disease journal - CDC

Volume 17, Number 12—December 2011

Research

Hepatitis E Virus in Rats, Los Angeles, California, USA

Article Contents

• Materials and Methods
• Results
• Discussion
• Acknowledgment
• References
• Figure 1
• Figure 2
• Figure 3
• Table 1
• Table 2
• Table 3
• Table 4
• Table 5
• Suggested Citation

Robert H. Purcell, Ronald E. Engle, Michael P. Rood, Yamina Kabrane-Lazizi¹, Hanh T. Nguyen, Sugantha Govindarajan, Marisa St. Claire², and Suzanne U. Emerson 

Author affiliations: National Institutes of Health, Bethesda Maryland, USA (R.H. Purcell, R.E. Engle, Y. Kabrane-Lazizi, H.T. Nguyen, S.U. Emerson); Department of Public Health Services, Los Angeles, California, USA (M.P. Rood); Rancho Los Amigos Hospital, Downey, California, USA (S. Govindarajan); Bioqual, Inc., Rockville, Maryland, USA (M. St. Claire)

Suggested citation for this article

Abstract

The role of rats in human hepatitis E virus (HEV) infections remains controversial. A genetically distinct HEV was recently isolated from rats in Germany, and its genome was sequenced. We have isolated a genetically similar HEV from urban rats in Los Angeles, California, USA, and characterized its ability to infect laboratory rats and nonhuman primates. Two strains of HEV were isolated from serum samples of 134 wild rats that had a seroprevalence of antibodies against HEV of ≈80%. Virus was transmissible to seronegative Sprague-Dawley rats, but transmission was spotty and magnitude and duration of infection were not robust. Viremia was higher in nude rats. Serologic analysis and reverse transcription PCR were comparably sensitive in detecting infection. The sequence of the Los Angeles virus was virtually identical to that of isolates from Germany. Rat HEV was not transmissible to rhesus monkeys, suggesting that it is not a source of human infection.

Hepatitis E virus (HEV) is a major cause of epidemic waterborne and sporadic hepatitis in developing countries. Hepatitis E is caused principally by HEV genotypes 1 and 2 (1). Recently, hepatitis E has been diagnosed with increasing frequency as a cause of sporadic hepatitis in industrialized countries (2). Additionally, a large proportion (<20%) of populations of such countries have antibodies against HEV in the absence of any recognized hepatitis (3–5), and evidence is increasing that these antibodies might be the result of subclinical infections acquired zoonotically.

Strains of HEV representing genotypes 3 and 4, which have been isolated from humans with hepatitis E, regularly infect pigs worldwide (6), and infection in humans caused by eating undercooked meat from domestic pigs, wild boar, and several species of wild deer has been documented (6,7). However, many, if not most, persons who have unexplained antibodies against HEV do not eat undercooked pork or venison, raising the possibility that other animals or modes of zoonotic transmission exist. It is noteworthy that swine handlers in the United States have a higher incidence of antibodies against HEV than do healthy blood donors, even though pork is generally thoroughly cooked in the United States. Therefore, eating pork is unlikely to explain the prevalence of antibodies against HEV in this country.

Numerous species, including rodents, have been found to have antibodies reactive with capsid protein of human HEV strains, and HEV closely related to genotypes 3 or 4 has been recently isolated from rabbits (8), cattle (9), and sheep (10). However, an HEV strain recently isolated from rats was unique and only distantly related to known strains (11). Thus, it is important to understand how this rat virus is related to human infections. Rats are particularly interesting as a potential source of human infections because although they are not a human food, they have a high seroprevalence of antibodies against HEV (12,13) and they are ubiquitous and in close contact with humans everywhere.

We have demonstrated that a high proportion of wild-caught Rattus norvegicus, R. rattus, and R. exulans rats trapped in several US cities (Baltimore, Maryland; New Orleans, Louisiana; and the islands of Oahu and Hawaii, Hawaii) were positive for antibodies against HEV (12). We studied their seroepidemiology but were unable to obtain genomic sequence or to transmit an agent to laboratory rats. Subsequently, in collaborations with the County of Los Angeles Department of Health (Los Angeles, CA, USA) Vector Management Program, we succeeded in transmitting to laboratory rats 2 strains of HEV from rats from Los Angeles but were again unable to obtain genomic sequence (14).

Recent cloning of rat HEV obtained from R. norvegicus rats in Germany and development of more broadly reactive PCR primers (11) prompted us to revisit those experiments. This report describes the partial PCR amplification and characterization of a US strain of rat HEV.

Suggested citation for this article: Purcell RH, Engle RE, Rood MP, Kabrane-Lazizi Y, Nguyen HT, Govindarajan S, et al. Hepatitis E virus in rats, Los Angeles, California, USA. Emerg Infect Dis [serial on the Internet]. 2011 Dec [date cited]. http://dx.doi.org/10.3201/eid1712.110482

DOI: 10.3201/eid1712.110482

¹Current affiliation: Embassy of France, Beijing, People’s Republic of China.

²Current affiliation: National Institutes of Health, Frederick, Maryland, USA.