Short report: phylogenetically distinct hepatitis E viruses in Pakistan.

Cuyck-Gandre, H. Van; Zhang, H Y; Tsarev, Sergei A.; Warren, Richard L.; Caudill, Jeffrey D.; Snellings, Norma J.; Bégot, L; Innis, Bruce L.; Longer, Charles F.

doi:10.4269/ajtmh.2000.62.187

Cited by 40 publications

(29 citation statements)

References 17 publications

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“…The significance of HEV seropositivity in these animal species needs to be determined. The recent identification of numerous genetically distinct strains of HEV in several countries where hepatitis E is endemic (4,13,38,39,40) and nonendemic (8,11,12,31,32,41,42) has led to a hypothesis that these novel strains of human HEV may be of animal origin (22). The present study confirmed that one human-HEV strain (US-2 strain) was transmissible to pigs (25), although the clinical manifestations and course of disease were different from those observed in the single human reported to be infected with this strain (8,18,31).…”

Section: Discussionmentioning

confidence: 99%

Comparative Pathogenesis of Infection of Pigs with Hepatitis E Viruses Recovered from a Pig and a Human

et al. 2001

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Specific-pathogen-free pigs were inoculated with one of two hepatitis E viruses (HEV) (one recovered from a pig and the other from a human) to study the relative pathogenesis of the two viruses in swine. Fifty-four pigs were randomly assigned to three groups. Seventeen pigs in group 1 served as uninoculated controls, 18 pigs in group 2 were intravenously inoculated with the swine HEV recovered from a pig in the United States, and 19 pigs in group 3 were intravenously inoculated with the US-2 strain of human HEV recovered from a hepatitis patient in the United States. Two to four pigs from each group were necropsied at 3, 7, 14, 20, 27, or 55 days postinoculation (DPI). Evidence of clinical disease or elevation of liver enzymes or bilirubin was not found in pigs from any of the three groups. Enlarged hepatic and mesenteric lymph nodes were observed in both HEV-inoculated groups. Multifocal lymphoplasmacytic hepatitis was observed in 9 of 17, 15 of 18, and 16 of 19 pigs in groups 1 to 3, respectively. Focal hepatocellular necrosis was observed in 5 of 17, 10 of 18, and 13 of 19 pigs in groups 1 to 3, respectively. Hepatitis lesions were very mild in group 1 pigs, mild to moderate in group 2 pigs, and moderate to severe in group 3 pigs. Hepatic inflammation and hepatocellular necrosis peaked in severity at 20 DPI and were still moderately severe at 55 DPI in the group inoculated with human HEV. Hepatitis lesions were absent or nearly resolved by 55 DPI in the swine-HEV-inoculated pigs. All HEVinoculated pigs seroconverted to anti-HEV immunoglobulin G. HEV RNA was detected by reverse transcriptase PCR in feces, liver tissue, and bile of pigs in both HEV-inoculated groups from 3 to 27 DPI. Based on evaluation of microscopic lesions, the US-2 strain of human HEV induced more severe and persistent hepatic lesions in pigs than did swine HEV. Pig livers or cells from the livers of HEV-infected pigs may represent a risk for transmission of HEV from pigs to human xenograft recipients. Since HEV was shed in the feces of infected pigs, exposure to feces from infected pigs represents a risk for transmission of HEV, and pigs should be considered a reservoir for HEV.Hepatitis E virus (HEV) is the leading cause of enterically transmitted non-A, non-B hepatitis in people in many developing countries (21,28,30). Transmission is thought to be primarily by the fecal-oral route, and waterborne epidemics are characteristic of hepatitis E (1, 28, 30). Clinical disease due to HEV infection is rarely diagnosed in industrialized countries, and most cases of HEV infection in industrialized countries occur in people who have traveled to regions where the disease is endemic (10,21,28,30). Clinical cases occur predominantly in developing countries in Asia, Africa, and Mexico (1, 2, 28, 30). However, sporadic cases of acute hepatitis E in people in the United States and other industrialized countries have recently been reported (7,8,11,18,20,22,31,32,42). Hepatitis E generally affects young adults and usually is not fatal, although mortality r...

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Section: Discussionmentioning

confidence: 99%

Comparative Pathogenesis of Infection of Pigs with Hepatitis E Viruses Recovered from a Pig and a Human

et al. 2001

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“…Genotype 1 contains sequences of isolates found mainly in Asia (4,40,44,51). Genotype 2 contains a sequence of an isolate from an outbreak in Mexico (16).…”

Section: Introductionmentioning

confidence: 99%

Molecular characterization of swine hepatitis E virus from Southeastern Brazil

Paiva

Tzaneva

Haddad

et al. 2007

Braz. J. Microbiol.

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Despite serological evidences of presence of hepatitis E virus (HEV) in humans or other animals, until this study the virus had not been detected and molecular characterization of the isolate that circulates in Brazil had not been described. Thus, we collected stool samples of young pigs and tested for presence of HEV RNA by RT-PCR, using primers for partial amplification of ORF2 sequence. Phylogenetic analysis with sequence obtained from the amplified products revealed that the HEV isolate identified here was most closely related to HEV isolates of genotype 3, which is commonly detected in HEV infected pigs. Nucleotide sequence analyses carried out with the entire amplified fragment, ORF2/ORF3 overlapping and ORF2 non-overlapping sequences showed highest identities with the US isolate of genotype 3. Similarly, amino acid sequence analyses done with the entire amplified fragment, ORF2 non-overlapping, ORF2 and ORF3 overlapping sequences also showed highest identities with the genotype 3 isolate. Presence, in Brazil, of HEV of genotype 4, which also infects pigs, as well as HEV strains that infect humans still remain to be detected and characterized.

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“…In contrast, an isolate from the present outbreak that occurred in 1988 in Abbottabad was genetically related to south Asian isolates from India, Burma, and Nepal. 21 Therefore, at least two genetically distinguishable isolates of HEV have caused outbreaks of hepatitis E in the Pakistani military.…”

Section: Introductionmentioning

confidence: 99%

Epidemic of hepatitis E in a military unit in Abbotrabad, Pakistan.

Bryan¹,

Iqbal²,

Tsarev³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

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Abstract. An outbreak of hepatitis caused by hepatitis E virus (HEV) in Abbottabad, Pakistan was traced to fecal contamination of a water system. Of 109 men hospitalized with hepatitis, 104 (95%) had serologic evidence of acute hepatitis E (IgM antibody to HEV [anti-HEV]), three (3%) probably had acute hepatitis E (high titers of IgG anti-HEV without IgM), and two had acute hepatitis A. Among a subset of 44 men with acute hepatitis E from whom three serum specimens were obtained over a four-month period, the anti-HEV IgG geometric mean titers (GMTs) decreased from 1,519 during the outbreak to 657 at four months. The IgM anti-HEV was detected in 40 (91%) of 44 sera obtained at admission (GMT ‫ס‬ 533 during acute disease), but in only six (14%) four months later. The prevalence of anti-HEV in this population before the outbreak was estimated to be 30%. The presence of IgG anti-HEV appeared to protect against clinical hepatitis or development of serologic evidence of new infection with HEV. This is the second major epidemic of hepatitis E in the Pakistani military confirmed by an anti-HEV enzyme-linked immunosorbent assay (ELISA). Evidence that pre-existing antibody as measured by this ELISA protects against disease is important for assessment of vaccine development.

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Short report: phylogenetically distinct hepatitis E viruses in Pakistan.

Cited by 40 publications

References 17 publications

Comparative Pathogenesis of Infection of Pigs with Hepatitis E Viruses Recovered from a Pig and a Human

Comparative Pathogenesis of Infection of Pigs with Hepatitis E Viruses Recovered from a Pig and a Human

Molecular characterization of swine hepatitis E virus from Southeastern Brazil

Epidemic of hepatitis E in a military unit in Abbotrabad, Pakistan.

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