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• W2040658891 abstract "Hepatitis E is a disease caused by infection with hepatitis E virus (HEV). The virus has four genotypes, named 1 to 4, with one shared serotype. Genotypes 1 and 2 infect only humans, whereas genotypes 3 and 4 primarily infect several mammalian animals, with occasional transmission to humans. Evidence of infection with HEV has been found in most parts of the world, with two distinct epidemiological patterns. In areas with high disease endemicity, primarily developing countries in Asia and Africa, the disease occurs as outbreaks and as sporadic cases of acute hepatitis, and is caused exclusively by infection with genotypes 1 or 2 HEV, which is acquired through fecal-oral route, usually through contamination of water supplies. The disease in these areas occurs most commonly in young adults, and is particularly severe in pregnant women and persons with pre-existing chronic liver disease; chronic infection has not been reported. In areas with lower endemicity, which are mainly developed areas with robust water supply and sanitation systems, occasional sporadic cases of locally-acquired genotype 3 or 4 HEV infection are observed. The affected persons are often elderly and have other coexisting illnesses. The reservoir of infection in these areas is believed to be in animals, such as pigs, wild boar and deer, with zoonotic transmission to humans, possibly through consumption of undercooked meat. Also, in these areas, persistent HEV infection has been well documented among immunosuppressed persons such as organ transplant recipients, and is believed to lead to chronic liver injury, including liver cirrhosis. Further work is needed to better understand the biological basis underlying these widely-differing epidemiological patterns. Hepatitis E is a disease caused by infection with hepatitis E virus (HEV). The virus has four genotypes, named 1 to 4, with one shared serotype. Genotypes 1 and 2 infect only humans, whereas genotypes 3 and 4 primarily infect several mammalian animals, with occasional transmission to humans. Evidence of infection with HEV has been found in most parts of the world, with two distinct epidemiological patterns. In areas with high disease endemicity, primarily developing countries in Asia and Africa, the disease occurs as outbreaks and as sporadic cases of acute hepatitis, and is caused exclusively by infection with genotypes 1 or 2 HEV, which is acquired through fecal-oral route, usually through contamination of water supplies. The disease in these areas occurs most commonly in young adults, and is particularly severe in pregnant women and persons with pre-existing chronic liver disease; chronic infection has not been reported. In areas with lower endemicity, which are mainly developed areas with robust water supply and sanitation systems, occasional sporadic cases of locally-acquired genotype 3 or 4 HEV infection are observed. The affected persons are often elderly and have other coexisting illnesses. The reservoir of infection in these areas is believed to be in animals, such as pigs, wild boar and deer, with zoonotic transmission to humans, possibly through consumption of undercooked meat. Also, in these areas, persistent HEV infection has been well documented among immunosuppressed persons such as organ transplant recipients, and is believed to lead to chronic liver injury, including liver cirrhosis. Further work is needed to better understand the biological basis underlying these widely-differing epidemiological patterns. ‘Hepatitis E’ is the term used to describe liver disease resulting from infection with ‘hepatitis E virus’ (HEV). This virus consists of non-enveloped icosahedral virions measuring 27–34 nm in diameter, which contain a single-stranded RNA molecule with positive polarity surrounded by a viral capsid.1Holla R.P. Ahmad I. Ahmad Z. Jameel S. Molecular virology of hepatitis E virus.Semin Liver Dis. 2013; 33: 3-14Crossref PubMed Scopus (82) Google Scholar, 2Ahmad I. Holla R.P. Jameel S. Molecular virology of hepatitis E virus.Virus Res. 2011; 161: 47-58Crossref PubMed Scopus (189) Google Scholar Its RNA genome has short untranslated regions at either end and three open reading frames that encode for (i) a polyprotein predicted to contain regions with enzymatic activities required for viral replication (ORF1), (ii) the viral capsid protein (ORF2), and (iii) a small phosphoprotein (ORF3) whose exact function remains unclear though several roles have been proposed.1Holla R.P. Ahmad I. Ahmad Z. Jameel S. Molecular virology of hepatitis E virus.Semin Liver Dis. 2013; 33: 3-14Crossref PubMed Scopus (82) Google Scholar, 2Ahmad I. Holla R.P. Jameel S. Molecular virology of hepatitis E virus.Virus Res. 2011; 161: 47-58Crossref PubMed Scopus (189) Google Scholar Hepatitis E as a distinct entity was first suspected nearly 30 years ago, when a waterborne outbreak of acute hepatitis in the Kashmir valley in India was found to be related neither to hepatitis A virus nor to hepatitis B virus.3Khuroo M.S. Study of an epidemic of non-A, non-B hepatitis. Possibility of another human hepatitis virus distinct from post-transfusion non-A, non-B type.Am J Med. 1980; 68: 818-824Abstract Full Text PDF PubMed Scopus (543) Google Scholar Around the same time, sera from previous outbreaks of acute hepatitis in India, including a large outbreak in New Delhi that occurred during the year 1956,4Viswanathan R. Infectious hepatitis in Delhi (1955–56): a critical study: epidemiology.Indian J Med Res. 1957; 45: 1-29PubMed Google Scholar were also found to lack markers of acute hepatitis A or B.5Wong D.C. Purcell R.H. Sreenivasan M.A. Prasad S.R. Pavri K.M. Epidemic and endemic hepatitis in India: evidence for a non-A, non-B hepatitis virus aetiology.Lancet. 1980; 2: 876-879Abstract PubMed Scopus (353) Google Scholar The confirmation of these observations came in 1983 through demonstration at immune electron microscopy of spherical virus-like particles in stool specimens collected from a human volunteer who had ingested a pooled fecal suspension from patients with acute hepatitis in Afghanistan.6Balayan M.S. Andjaparidze A.G. Savinskaya S.S. et al.Evidence for a virus in non-A, non-B hepatitis transmitted via the fecal-oral route.Intervirology. 1983; 20: 23-31Crossref PubMed Scopus (645) Google Scholar For nearly 15 years after its discovery, HEV was believed to infect only humans, and to circulate only in areas with weak water supply and sanitation systems that facilitate fecal-oral transmission. This seemed to fit well with the observations that hepatitis E was endemic in several developing countries, and that nearly all the cases with HEV infection in the developed countries were related to travel to disease-endemic countries.7Wu J.C. Sheen I.J. Chiang T.Y. et al.The impact of traveling to endemic areas on the spread of hepatitis E virus infection: epidemiological and molecular analyses.Hepatology. 1998; 27: 1415-1420Crossref PubMed Scopus (47) Google Scholar, 8Schwartz E. Jenks N.P. Van Damme P. Galun E. Hepatitis E virus infection in travelers.Clin Infect Dis. 1999; 29: 1312-1314Crossref PubMed Scopus (45) Google Scholar Further, it was thought that the infection was short-lasting, manifesting mostly as self-limited viral hepatitis with occasional severe cases that presented with fulminant hepatic failure (FHF). However, during the late 1990s, a few cases with HEV infection were reported among residents of developed countries who had not traveled to countries where hepatitis E was endemic.9Kwo P.Y. Schlauder G.G. Carpenter H.A. et al.Acute hepatitis E by a new isolate acquired in the United States.Mayo Clin Proc. 1997; 72: 1133-1136Abstract Full Text Full Text PDF PubMed Scopus (156) Google Scholar, 10Schlauder G.G. Dawson G.J. Erker J.C. et al.The sequence and phylogenetic analysis of a novel hepatitis E virus isolated from a patient with acute hepatitis reported in the United States.J Gen Virol. 1998; 79: 447-456PubMed Google Scholar, 11Erker J.C. Desai S.M. Schlauder G.G. Dawson G.J. Mushahwar I.K. A hepatitis E virus variant from the United States: molecular characterization and transmission in cynomolgus macaques.J Gen Virol. 1999; 80: 681-690PubMed Google Scholar Around the same time, HEV-like genomic sequences were identified in specimens from animals, in particular pigs.12Meng X.J. Purcell R.H. Halbur P.G. et al.A novel virus in swine is closely related to the human hepatitis E virus.Proc Natl Acad Sci U S A. 1997; 94: 9860-9865Crossref PubMed Scopus (934) Google Scholar Further work prompted by these observations has led to a major change in our understanding about HEV and its epidemiology, including the routes of transmission and clinical outcomes. Thus, we now know that HEV has a fair degree of genomic heterogeneity, has a wide host range with frequent cross-species transmission,13Meng X.J. Zoonotic and foodborne transmission of hepatitis E virus.Semin Liver Dis. 2013; 33: 41-49Crossref PubMed Scopus (157) Google Scholar circulates in most parts of the world, and causes persistent infection in some persons.14Kamar N. Selves J. Mansuy J.M. et al.Hepatitis E virus and chronic hepatitis in organ-transplant recipients.N Engl J Med. 2008; 358: 811-817Crossref PubMed Scopus (955) Google Scholar Despite the fact that HEV was discovered only in late 20th century, its origin appears to be fairly ancient. Even in geographical areas where currently hepatitis E is infrequent, epidemics of acute hepatitis with features resembling those of HEV infection were common place during the 18th and 19th centuries.15Teo C.G. Fatal outbreaks of jaundice in pregnancy and the epidemic history of hepatitis E.Epidemiol Infect. 2012; 140: 767-787Crossref PubMed Scopus (55) Google Scholar Further, a molecular-clock analysis of the currently-available HEV genomic sequences suggests origin from a common ancestor that existed between 500 and 1300 years ago.16Purdy M.A. Khudyakov Y.E. Evolutionary history and population dynamics of hepatitis E virus.PLoS One. 2010; 5: e14376Crossref PubMed Scopus (85) Google Scholar A detailed review of the structure, genomic organization and replication strategy of HEV are available in another piece in this issue of the Journal.17Panda S.K. Varma S.P.K. Hepatitis E: molecular virology and pathogenesis.J Clin Exp Hepatol. 2013; 3: 114-124Abstract Full Text Full Text PDF Scopus (17) Google Scholar HEV is classified in genus Hepevirus and family Hepeviridae.18Meng X.J. Anderson D.A. Arankalle V.A. et al.Hepeviridae.in: King A.M.Q. Adams M.J. Carstens E.B. Lefkowitz E.J. Virus Taxonomy: Classification and Nomenclature of Viruses: Ninth Report of the International Committee on Taxonomy of Viruses. Elsevier, San Diego2011: 1021-1028Google Scholar It consists of a group of closely-related viruses that, besides humans, infect other mammals such as pigs, rabbits, rats, deer, and mongoose.19Meng X.J. From barnyard to food table: the omnipresence of hepatitis E virus and risk for zoonotic infection and food safety.Virus Res. 2011; 161: 23-30Crossref PubMed Scopus (224) Google Scholar Based on analysis of viral genomic sequences, HEV isolates from various mammalian hosts cluster into at least four separate groups, known as genotypes 1 to 4, with several subgenotypes in each.20Purdy M.A. Khudyakov Y.E. The molecular epidemiology of hepatitis E virus infection.Virus Res. 2011; 161: 31-39Crossref PubMed Scopus (70) Google Scholar, 21Okamoto H. Genetic variability and evolution of hepatitis E virus.Virus Res. 2007; 127: 216-228Crossref PubMed Scopus (261) Google Scholar The genotypes differ in host specificity and geographical distribution (Figure 1). The genotype 1 and 2 strains of HEV infect only humans, and are restricted to areas where HEV disease is very common. In contrast, genotype 3 and 4 strains have a wider geographical spread, and a broader host range, causing frequent infection in several mammalian species with occasional transmission to humans, causing clinical disease. HEV-like genomic material has also been identified in birds, including chickens and turkeys.22Haqshenas G. Shivaprasad H.L. Woolcock P.R. Read D.H. Meng X.J. Genetic identification and characterization of a novel virus related to human hepatitis E virus from chickens with hepatitis-splenomegaly syndrome in the United States.J Gen Virol. 2001; 82: 2449-2462Crossref PubMed Scopus (285) Google Scholar These isolates of HEV are genetically more divergent than the mammalian HEV isolates, appear incapable of transmission to mammals, and are placed in a separate genus named as ‘avian HEV’.18Meng X.J. Anderson D.A. Arankalle V.A. et al.Hepeviridae.in: King A.M.Q. Adams M.J. Carstens E.B. Lefkowitz E.J. Virus Taxonomy: Classification and Nomenclature of Viruses: Ninth Report of the International Committee on Taxonomy of Viruses. Elsevier, San Diego2011: 1021-1028Google Scholar More recently, genomic sequences resembling HEV have also been reported in a virus cultured from cutthroat trout, a species of freshwater fish.23Batts W. Yun S. Hedrick R. Winton J. A novel member of the family Hepeviridae from cutthroat trout (Oncorhynchus clarkii).Virus Res. 2011; 158: 116-123Crossref PubMed Scopus (148) Google Scholar Despite their fairly extensive genetic heterogeneity, the various HEV genotypes that infect mammals show serological cross-reactivity, with existence of a single serotype. This implies that one vaccine should offer protection against all the HEV genotypes that infect humans. Serological data suggest that HEV infection occurs in most parts of the world.24Aggarwal R. The Global Prevalence of Hepatitis E Virus Infection and Susceptibility: a Systematic Review. World Health Organization, Geneva2010http://whqlibdoc.who.int/hq/2010/WHO_IVB_10.14_eng.pdfGoogle Scholar However, two distinct epidemiological and clinical patterns are observed, with differences in the frequency of disease, virus genotypes causing human infection, routes of transmission, affected population groups and disease characteristics (Table 1).25Aggarwal R. Hepatitis E: historical, contemporary and future perspectives.J Gastroenterol Hepatol. 2011; 26: 72-82Crossref PubMed Scopus (82) Google Scholar, 26Aggarwal R. Naik S. Epidemiology of hepatitis E: current status.J Gastroenterol Hepatol. 2009; 24: 1484-1493Crossref PubMed Scopus (219) Google Scholar Each of these patterns is described below.Table 1Comparison of epidemiological features of hepatitis E in high-endemicity and low-endemicity areas.Adapted from: Aggarwal R, Jameel S. Hepatitis E. Hepatology 2011; 54: 2218–2226.CharacteristicsAreas with high-endemicity rateAreas with low-endemicity rateHuman diseaseLarge outbreaks, and a large proportion of cases with sporadic acute hepatitisA small number of cases with sporadic acute hepatitisCharacteristics of diseased personsYoung, otherwise healthy, males > femalesMostly elderly, often with other comorbid conditions, males > femalesPrevalent causative viral genotypesMostly genotypes 1 and 2, a few cases of genotype 4 in ChinaGenotype 3, occasionally genotype 4Reservoir of infectionHumanMost likely animals (pigs, wild boars, deer)Route of transmissionFecal-oral, primarily contamination of water suppliesConsumption of undercooked meat (pig or deer), close contact with animalsRelationship with pregnancyHigh disease attack rate and risk of fulminant disease among pregnant womenNo reports of severe disease among pregnant womenChronic infectionNo reports of chronic hepatitis EChronic infection with hepatitis E virus reported among immunosuppressed persons, primarily organ transplant recipients receiving immunosuppressive drugs Open table in a new tab This epidemiologic pattern is observed primarily in developing countries in the Indian subcontinent, Southeast and Central Asia, the Middle East, and northern and western parts of Africa (Figure 2).25Aggarwal R. Hepatitis E: historical, contemporary and future perspectives.J Gastroenterol Hepatol. 2011; 26: 72-82Crossref PubMed Scopus (82) Google Scholar, 26Aggarwal R. Naik S. Epidemiology of hepatitis E: current status.J Gastroenterol Hepatol. 2009; 24: 1484-1493Crossref PubMed Scopus (219) Google Scholar In these areas, hepatitis E occurs as distinct outbreaks of acute hepatitis, as well as frequent sporadic cases. Two small outbreaks were also reported in Mexico during 1986–8727Velazquez O. Stetler H.C. Avila C. et al.Epidemic transmission of enterically transmitted non-A, non-B hepatitis in Mexico, 1986–1987.JAMA. 1990; 263: 3281-3285Crossref PubMed Scopus (182) Google Scholar; however, no further outbreaks have since been reported from North America. Large outbreaks of hepatitis E occurred frequently in China during 1980s and early 1990s, but none have been reported in the recent years, suggesting a transition from the high-endemicity pattern to the low-endemicity pattern. The outbreaks of hepatitis E vary in size, and can be large, affecting several hundred to several thousand cases each.3Khuroo M.S. Study of an epidemic of non-A, non-B hepatitis. Possibility of another human hepatitis virus distinct from post-transfusion non-A, non-B type.Am J Med. 1980; 68: 818-824Abstract Full Text PDF PubMed Scopus (543) Google Scholar, 4Viswanathan R. Infectious hepatitis in Delhi (1955–56): a critical study: epidemiology.Indian J Med Res. 1957; 45: 1-29PubMed Google Scholar, 28Naik S.R. Aggarwal R. Salunke P.N. Mehrotra N.N. A large waterborne viral hepatitis E epidemic in Kanpur, India.Bull World Health Organ. 1992; 70: 597-604PubMed Google Scholar, 29Zhuang H. Cao X.-Y. Liu C.-B. Wang G.-M. Enterically transmitted non-A, non-B hepatitis in China.in: Shikata T. Purcell R.H. Uchida T. Viral Hepatitis C, D and E. Excerpta Medica, Amsterdam1991: 277-285Google Scholar Most of the outbreaks in endemic areas can be traced to contamination of drinking water supplies with human fecal matter. These outbreaks often follow heavy rainfall and floods, which facilitate mixing of human excreta with sources of drinking water,3Khuroo M.S. Study of an epidemic of non-A, non-B hepatitis. Possibility of another human hepatitis virus distinct from post-transfusion non-A, non-B type.Am J Med. 1980; 68: 818-824Abstract Full Text PDF PubMed Scopus (543) Google Scholar, 4Viswanathan R. Infectious hepatitis in Delhi (1955–56): a critical study: epidemiology.Indian J Med Res. 1957; 45: 1-29PubMed Google Scholar or occur during dry summer months when water flow in rivers and streams is reduced, with consequent increase in concentration of fecal contaminants.28Naik S.R. Aggarwal R. Salunke P.N. Mehrotra N.N. A large waterborne viral hepatitis E epidemic in Kanpur, India.Bull World Health Organ. 1992; 70: 597-604PubMed Google Scholar, 30Corwin A.L. Tien N.T. Bounlu K. et al.The unique riverine ecology of hepatitis E virus transmission in South–East Asia.Trans R Soc Trop Med Hyg. 1999; 93: 255-260Abstract Full Text PDF PubMed Scopus (57) Google Scholar In Southeast Asia, disposal of human excreta into rivers is common, and water from the same rivers is used for drinking, cooking and personal hygiene at downstream locations; this may account for the frequent recurrence of outbreaks.30Corwin A.L. Tien N.T. Bounlu K. et al.The unique riverine ecology of hepatitis E virus transmission in South–East Asia.Trans R Soc Trop Med Hyg. 1999; 93: 255-260Abstract Full Text PDF PubMed Scopus (57) Google Scholar Another mode of contamination of water supplies in developing countries is at the level of peripheral water distribution system.31Sailaja B. Murhekar M.V. Hutin Y.J. et al.Outbreak of waterborne hepatitis E in Hyderabad, India, 2005.Epidemiol Infect. 2009; 137: 234-240Crossref PubMed Scopus (37) Google Scholar This happens when old, leaky water pipes pass through soil that is contaminated with sewage, and water supply is intermittent. The negative pressure produced in pipes during periods of no flow allows inward suction of surrounding contaminants. In recent years, several outbreaks of hepatitis E have been reported from areas with conflict, violence and major human displacement.32Guthmann J.P. Klovstad H. Boccia D. et al.A large outbreak of hepatitis E among a displaced population in Darfur, Sudan, 2004: the role of water treatment methods.Clin Infect Dis. 2006; 42: 1685-1691Crossref PubMed Scopus (141) Google Scholar, 33Teshale E.H. Howard C.M. Grytdal S.P. et al.Hepatitis E epidemic, Uganda.Emerg Infect Dis. 2010; 16: 126-129Crossref PubMed Scopus (118) Google Scholar In these outbreaks too, limited availability of facilities for safe drinking water and proper disposal of human feces, for instance in refugee camps, have been the main factors responsible for spread of HEV infection. In addition to water, contaminated food may be expected to serve as a vehicle for transmission of HEV in areas where the disease is highly-endemic. However, few food-borne outbreaks have been reported. This may be related to the inherent difficulty of relating an outbreak to a particular meal or food item, because of a relatively long and variable incubation period (2–10 weeks) of hepatitis E. The outbreaks of hepatitis E vary widely in time-course. Several outbreaks, particularly those that follow a short and well-defined period of water contamination, have been unimodal lasting only a few weeks, indicating absence of secondary (person-to-person) spread.3Khuroo M.S. Study of an epidemic of non-A, non-B hepatitis. Possibility of another human hepatitis virus distinct from post-transfusion non-A, non-B type.Am J Med. 1980; 68: 818-824Abstract Full Text PDF PubMed Scopus (543) Google Scholar, 4Viswanathan R. Infectious hepatitis in Delhi (1955–56): a critical study: epidemiology.Indian J Med Res. 1957; 45: 1-29PubMed Google Scholar However, some other outbreaks have been multi-peaked and have lasted for over a year; in these, the secondary peaks have generally been related to continued water contamination, rather than to person-to-person transmission.28Naik S.R. Aggarwal R. Salunke P.N. Mehrotra N.N. A large waterborne viral hepatitis E epidemic in Kanpur, India.Bull World Health Organ. 1992; 70: 597-604PubMed Google Scholar Some workers have recently suggested existence of secondary spread34Teshale E.H. Grytdal S.P. Howard C. et al.Evidence of person-to-person transmission of hepatitis E virus during a large outbreak in Northern Uganda.Clin Infect Dis. 2010; 50: 1006-1010Crossref PubMed Scopus (112) Google Scholar; however, these data have been questioned.35Aggarwal R. Hepatitis E virus and person-to-person transmission.Clin Infect Dis. 2010; 51 (author reply 8–9): 477-478Crossref PubMed Scopus (6) Google Scholar During the outbreaks, overall attack rates have varied widely from 1% to above 15%; this is most likely related to the intensity of water contamination. During waterborne outbreaks of hepatitis E, where exposure to the virus may be ubiquitous, disease attack rates are the highest among adolescents and young adults, and are lower among children.36Aggarwal R. Clinical presentation of hepatitis E.Virus Res. 2011; 161: 15-22Crossref PubMed Scopus (113) Google Scholar This observation is probably explained at least partly by a higher proportion of asymptomatic infections, than to rarity of infection, in children. Men are generally affected more often than women, possibly due to their greater risk of exposure to contaminated water; however, a greater propensity for clinical disease among those infected cannot be ruled out. A typical feature of hepatitis E outbreaks is the occurrence of a higher disease attack rate and a higher mortality rate among pregnant women. During a large epidemic in Kashmir, India, the disease attack rates were 8.8%, 19.4%, and 18.6% among pregnant women in the first, second, and third trimesters, respectively; these rates were significantly higher than those among non-pregnant women (2.1%) and men (2.8%).37Khuroo M.S. Teli M.R. Skidmore S. Sofi M.A. Khuroo M.I. Incidence and severity of viral hepatitis in pregnancy.Am J Med. 1981; 70: 252-255Abstract Full Text PDF PubMed Scopus (425) Google Scholar In addition, the risk of development of FHF among those with symptomatic hepatitis E was higher among pregnant women (22%) than among men (2.8%) and non-pregnant women (0%). Once FHF appears, the mortality rate appears to be similar among pregnant women with hepatitis E and pregnant women with other causes of severe liver injury.38Bhatia V. Singhal A. Panda S.K. Acharya S.K. A 20-year single-center experience with acute liver failure during pregnancy: is the prognosis really worse?.Hepatology. 2008; 48: 1577-1585Crossref PubMed Scopus (151) Google Scholar However, since HEV infection during pregnancy is associated with high rates of symptomatic disease and FHF, it accounts for a large proportion of cases with liver failure among pregnant women in the endemic areas.36Aggarwal R. Clinical presentation of hepatitis E.Virus Res. 2011; 161: 15-22Crossref PubMed Scopus (113) Google Scholar The reason underlying the association of hepatitis E and pregnancy is unknown, though immunological or hormonal factors have been proposed.39Pal R. Aggarwal R. Naik S.R. Das V. Das S. Naik S. Immunological alterations in pregnant women with acute hepatitis E.J Gastroenterol Hepatol. 2005; 20: 1094-1101Crossref PubMed Scopus (105) Google Scholar, 40Bose P.D. Das B.C. Kumar A. Gondal R. Kumar D. Kar P. High viral load and deregulation of the progesterone receptor signaling pathway: association with hepatitis E-related poor pregnancy outcome.J Hepatol. 2011; 54: 1107-1113Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar, 41Navaneethan U. Al Mohajer M. Shata M.T. Hepatitis E and pregnancy: understanding the pathogenesis.Liver Int. 2008; 28: 1190-1199Crossref PubMed Scopus (283) Google Scholar, 42Kar P. Jilani N. Husain S.A. et al.Does hepatitis E viral load and genotypes influence the final outcome of acute liver failure during pregnancy?.Am J Gastroenterol. 2008; 103: 2495-2501Crossref PubMed Scopus (95) Google Scholar Hepatitis E during pregnancy is also associated with prematurity and low birth weight.43Khuroo M.S. Kamili S. Khuroo M.S. Clinical course and duration of viremia in vertically transmitted hepatitis E virus (HEV) infection in babies born to HEV-infected mothers.J Viral Hepat. 2009; 16: 519-523Crossref PubMed Scopus (118) Google Scholar The children born to such mothers frequently suffer from hypoglycemia and jaundice, and have an increased perinatal mortality. In areas where hepatitis E outbreaks occur, a large proportion of cases with acute sporadic hepatitis are related to HEV infection, irrespective of the age group. For instance, in some studies from the Indian subcontinent, HEV infection accounted for up to 70% of adult cases with sporadic hepatitis.44Arankalle V.A. Chobe L.P. Jha J. et al.Aetiology of acute sporadic non-A, non-B viral hepatitis in India.J Med Virol. 1993; 40: 121-125Crossref PubMed Scopus (94) Google Scholar, 45Kar P. Budhiraja S. Narang A. Chakravarthy A. Etiology of sporadic acute and fulminant non-A, non-B viral hepatitis in north India.Indian J Gastroenterol. 1997; 16: 43-45PubMed Google Scholar, 46Chadha M.S. Walimbe A.M. Chobe L.P. Arankalle V.A. Comparison of etiology of sporadic acute and fulminant viral hepatitis in hospitalized patients in Pune, India during 1978–81 and 1994–97.Indian J Gastroenterol. 2003; 22: 11-15PubMed Google Scholar The patients with sporadic hepatitis E in these regions share several epidemiological and clinical characteristics with those observed in patients with epidemic hepatitis E. These include predominant affliction of adolescents and young adults, the association between pregnancy and severe disease, and clinical presentation as acute hepatitis, with occasional cases of FHF.47Khuroo M.S. Duermeyer W. Zargar S.A. Ahanger M.A. Shah M.A. Acute sporadic non-A, non-B hepatitis in India.Am J Epidemiol. 1983; 118: 360-364PubMed Google Scholar In areas where hepatitis E is highly-endemic, only genotype 1 or 2 HEV have been identified from human cases. Since such strains circulate only in humans and have not been identified in animals, the reservoir of infection in these areas appears to reside in humans with HEV infection, either symptomatic or asymptomatic. Genotype 3 and 4 HEV, which circulate in animals, have not been identified in human cases from these areas, providing evidence against zoonotic transmission from an animal reservoir. As indicated above, most outbreaks of hepatitis E have been traced to contamination of drinking water supplies. In contrast, the route of transmission of HEV infection in sporadic cases in highly-endemic areas is less clear, though fecal contamination of water or food appear to be responsible in most cases. Some of the sporadic cases may in fact represent small common point-source outbreak among persons who had come together for a short period of time. Person-to-person transmission of HEV appears to be relatively infrequent, in both epidemic and sporadic settings.48Aggarwal R. Naik S.R. Hepatitis E: intrafamilial transmission versus waterborne spread.J Hepatol. 1994; 21: 718-723Abstract Full Text PDF PubMed Scopus (95) Google Scholar, 49Somani S.K. Aggarwal R. Naik S.R. Srivastava S. Naik S. A serological study of intrafamilial spread from patients with sporadic hepatitis E virus infection.J Viral Hepat. 2003; 10: 446-449Crossref PubMed Scopus (67) Google Scholar During outbreaks of hepatitis E, secondary attack rates among household contacts of patients with hepatitis E cases have been much lower than those observed among susceptible household contacts of patients with hepatitis A, another enterically-transmitted form of hepatitis. Even when multiple cases occur in a family, the time interval between these is shorter than the minimum incubation period, indicating exposure to a" @default.
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• W2040658891 date "2013-06-01" @default.
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• W2040658891 title "Hepatitis E: Epidemiology and Natural History" @default.
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