Hepatitis E virus genome in stools of hepatitis patients during large epidemic in north India

Ray, Ranjit; Talwar, G. P.; Aggarwal, Rakesh; Salunke, Pooja; Naik, S. R.; Mehrotra, Nitin

doi:10.1016/0140-6736(91)90667-e

Cited by 84 publications

(38 citation statements)

References 7 publications

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“…The serological tests showed that hepatitis A or B virus was not responsible for the epidemic in Kanpur. Using a reverse transcriptionpolymerase chain reaction based on the sequence of a previously described HEV clone (ETI.1) (9), we demonstrated the presence of the HEV genome in 6 of 10 stool samples obtained from persons affected in the epidemic (10). The epidemiological features of the Kanpur epidemic resemble those reported for previous HEV epidemics (1-3), i.e., a high attack rate among adult males but relatively few cases involving children.…”

Section: Discussionsupporting

confidence: 59%

A large waterborne viral hepatitis E epidemic in Kanpur, India

Naik

Aggarwal²,

Salunke³

et al. 1993

Indian J Pediatr

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In 1991 the largest epidemic of viral hepatitis E yet reported occurred in Kanpur (population, 2.1 million), India. The incidence of icteric hepatitis from December 1990 to April 1991 among the inhabitants of 420 randomly sampled houses in seven of the city's 50 wards was 3.76% (138 out of 3666 individuals), i.e., an estimated 79091 persons in the city as a whole were affected. The attack rate was higher for males than females (5.3% versus 3.3%; P = 0.013) and for adults than children aged <10 years (4.26% versus 1.29%; P = 0.0006). The incidence of hepatitis was higher in those city wards that were supplied with drinking-water consisting of a mixture of river Ganges and tubewell water than in those wards supplied only with tubewell water (5.6% versus 1.2%; P = 106). In the mixed-water areas, the incidence decreased as the drinking-water source changed from only tap to both tap and handpump, to only handpump (7.8%, 6.8%, and 4.3% respectively; P = 0.023). None of the sera collected from 41 hepatitis patients during the epidemic showed evidence of hepatitis virus A or B.There were two peaks in the epidemic (in February and April 1991). The first peak was probably caused by faecal contamination of river water, indicated by water analysis data, and the second, by inadequate chlorination of water in a reservoir. There was no evidence of secondary intrafamilial spread.

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Section: Discussionsupporting

confidence: 59%

A large waterborne viral hepatitis E epidemic in Kanpur, India

Naik

Aggarwal²,

Salunke³

et al. 1993

Indian J Pediatr

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“…HEV is excreted in feces of infected persons [Ray et al, 1991], and hence, sewage of human origin may contaminate drinking water supplies. In fact, using epidemiological and water quality data, several HEV outbreaks have been attributed to contamination of drinking water sources with sewage .…”

Section: Discussionmentioning

confidence: 99%

“…An alternative possibility for the reservoir site is persons with sporadic or subclinical HEV infection. HEV-infected persons are known to excrete HEV in large quantities in their feces [Ray et al, 1991]. This virus in the sewage of human origin may then contaminate the drinking water supplies.…”

Section: Introductionmentioning

confidence: 99%

Presence of hepatitis E virus in sewage in Northern India: Frequency and seasonal pattern

Ippagunta

Naik

Sharma

et al. 2007

Journal of Medical Virology

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Outbreaks of acute hepatitis E, associated with consumption of contaminated drinking water, are frequent in India. Sewage is a major source for contamination of surface water. Data on the presence of hepatitis E virus (HEV) in sewage in India are limited. The aim of this study was to look for the presence of HEV RNA in concentrates of sewage specimens collected from a major open sewage drain in Lucknow, India during August 2004 to July 2006, by the polymerase chain reaction, using primers specific for human HEV (genotype 1) or Indian swine HEV (genotype 4). Of the 192 sewage specimens tested, 79 (41%) showed presence of human HEV RNA. The positivity rate was higher during the second year (52/103 [51%]) than during the first year (27/89 [30%]; P = 0.005). The seasonal pattern of HEV RNA positivity was as follows: winter months (November to February): 28 of 61 (46%); summer months (March to June): 36 of 66 (55%); and, monsoon months (July to October) 15 of 65 (23%). There was no reported outbreak of hepatitis E in the city during the study period. Swine HEV RNA was not detected in any of the 69 specimens tested. Repeat testing confirmed the reproducibility of the results. In addition, nucleic acid sequencing of six sewage isolates showed that these belonged to HEV genotype 1. The study suggests that HEV infection and fecal viral excretion may be common in HEV-endemic regions throughout the year even during non-epidemic periods.

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“…Enteric viruses, which include the adenoviruses, rotaviruses, noroviruses, astroviruses and picornaviruses, (Griffin et al, 2003) have been associated with waterborne disease outbreaks worldwide (CDC, 2008;Chang et al, 2011;Halliday et al, 1991;Kamizoulis and Saliba, 2004;Ma et al, 2010;Ray et al, 1991;Yan Ye et al, 2012). Though enteric virus infections are generally mild gastroenteritis and diarrhea, they have also been associated with more serious illnesses such as encephalitis, hepatitis, conjunctivitis, as well as an outbreak of hand, food, and mouth disease in China in 2008 (Chang et al, 2011;Fong and Lipp, 2005).…”

Section: Introductionmentioning

confidence: 97%