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Article Review on Hepatitis E Virus and Related Viruses in Wild, Domestic and Zoo Animals

Updated on December 23, 2017

Hepatitis

Article Review on Hepatitis E Virus and Related Viruses in Wild, Domestic and Zoo Animals

1. What is Hepatitis?

Hepatitis refers to an inflammatory condition of the liver. It’s commonly caused by a viral infection, but there are other possible causes of hepatitis. These include autoimmune hepatitis and hepatitis that occurs as a secondary result of medications, drugs, toxins, and alcohol. Autoimmune hepatitis is a disease that occurs when your body makes antibodies against your liver tissue.

Your liver is located in the right upper area of your abdomen. It performs many critical functions that affect metabolism throughout your body, including:

  • Bile production, which is essential to digestion
  • Filtering of toxins from your body
  • Excretion of bilirubin (a product of broken-down red blood cells), cholesterol, hormones, and drugs
  • Breakdown of carbohydrates, fats, and proteins
  • Activation of enzymes, which are specialized proteins essential to body functions
  • Storage of glycogen (a form of sugar), minerals, and vitamins (a, d, e, and k)
  • Synthesis of blood proteins, such as albumin
  • Synthesis of clotting factors

According to the Centers for Disease Control and Prevention (CDC), approximately 4.4 million Americans are currently living with chronic hepatitis B and C. Many more people don’t even know that they have hepatitis. Treatment options vary depending on which type of hepatitis you have. You can prevent some forms of hepatitis through immunizations and lifestyle precautions (A. Kahn and V.Higuera, 2017).

1.1. Types of Hepatitis

Viral infections of the liver that are classified as hepatitis include hepatitis A, B, C, D, and E. A different virus is responsible for each type of virally transmitted hepatitis (A. Kahn and V.Higuera, 2017).

Hepatitis A is always an acute, short-term disease, while hepatitis B, C, and D are most likely to become ongoing and chronic. Hepatitis E is usually acute but can be particularly dangerous in pregnant women. Hepatitis A is caused by an infection with the hepatitis A virus (HAV). This type of hepatitis is most commonly transmitted by consuming food or water contaminated by feces from a person infected with hepatitis A. Hepatitis B is transmitted through contact with infectious body fluids, such as blood, vaginal secretions, or semen, containing the hepatitis B virus (HBV). Injection drug use, having sex with an infected partner, or sharing razors with an infected person increase your risk of getting hepatitis B. It’s estimated by the CDC that 1.2 million people in the United States and 350 million people worldwide live with this chronic disease. Hepatitis C comes from the hepatitis C virus (HCV). Hepatitis C is transmitted through direct contact with infected body fluids, typically through injection drug use and sexual contact. HCV is among the most common bloodborne viral infections in the United States. Approximately 2.7 to 3.9 million Americans are currently living with a chronic form of this infection. Also called delta hepatitis, hepatitis D is a serious liver disease caused by the hepatitis D virus (HDV). HDV is contracted through direct contact with infected blood. Hepatitis D is a rare form of hepatitis that only occurs in conjunction with hepatitis B infection. The hepatitis D virus can’t multiply without the presence of hepatitis B. It’s very uncommon in the United States. Hepatitis E is a waterborne disease caused by the hepatitis E virus (HEV). Hepatitis E is mainly found in areas with poor sanitation and typically results from ingesting fecal matter that contaminates the water supply. This disease is uncommon in the United States. However, cases of hepatitis E have been reported in the Middle East, Asia, Central America, and Africa, according to the CDC (A. Kahn and V.Higuera, 2017).

1.2. Hepatitis E Virus and Related Viruses in Wild, Domestic and Zoo Animals

1.2.1. Introduction to Hepatitis E

The hepatitis E virus (HEV) represents one of the five major human hepatotropic viruses, in addition to hepatitis A, B, C and D virus. It represents the most common cause of acute hepatitis in humans worldwide (Rein, Stevens, Theaker, Wittenborn, & Wiersma, 2012). After incubation for two to 8 weeks, mild-to-moderate influenza-like symptoms arise at first. The symptoms may thereafter develop to emesis, fever, pain of the limbs or headache and epigastralgia before signs of acute hepatitis can occur. Generally, the case fatality rate is low, ranging between 0.2% and 4% (Kumar, Subhadra, Singh, & Panda, 2013).

However, case fatality rates of up to 25% were observed in pregnant women due to fulminant hepatitis in outbreak areas of endemic regions in China, India, Somalia and Uganda (Kamar et al., 2012). In contrast, only sporadic cases of hepatitis are common in industrialized countries. As the HEV IgG seroprevalence range here between 16% and 53% (Faber et al., 2012), most of these infections seem to be asymptomatic.

1.2.2. Virus and Taxonomy

Hepatitis E virus is a small non-enveloped virus with an icosahedral capsid (Meng, 2010). Recent analyses suggest the presence of an additional outer membrane in a fraction of HEV particles (Yin, Ambardekar, Lu, & Feng, 2016). The virus genome consists of a non-segmented, single-stranded RNA with positive polarity and a length of 6.6–7.3 kb. It contains three major open reading frames encoding a non-structural polyprotein, a capsid protein and a small phosphoprotein (Meng, 2010). Rat HEV and ferret HEV contain an additional open reading frame (ORF4) of still unknown function, which overlaps with ORF1 at its 5′-end (Johne, Plenge-Bönig, et al., 2010; Raj et al., 2012).

There is a large variety of HEV-like viruses identified in animals and humans so far. The current taxonomy (Smith et al., 2014) classifies all of them within the family Hepeviridae. This family is divided into the two genera Orthohepevirus and Piscihepevirus. The genus Orthohepevirus contains four species designated as Orthohepevirus A to D. Orthohepevirus A contains seven genotypes (HEV-1 to HEV-7) and a putative new genotype 8 that can infect humans and/or a wide variety of mammals (Lee et al., 2016; Smith et al., 2014; Woo et al., 2016). Orthohepevirus B consists of avian viruses and is divided into four proposed subtypes (I–IV), which are mainly detected in domestic chicken. Orthohepevirus C includes two genotypes mainly detected in rats (HEV-C1) and carnivores

(HEV-C2). Orthohepevirus D strains have been detected in different bat species. Additional putative new genotypes within the genus Orthohepevirus have been proposed, but not assigned so far. The genus Piscihepevirus contains only one single species: Piscihepevirus A, which has been identified in cutthroat trout and related species.

1.2.3. Transmission Pathways to Human

The transmission pathways of HEV are complex and may involve virus transmissions via faecally contaminated water, blood products, food, environment and direct contact with animals as well as to humans (Figure 2). Some of these pathways are well proven, whereas others are only suspected. Most importantly, the transmission pathways are dependent on the genotype of the virus.

1.2.4. Genotypes of HEV

v Genotypes 1 and 2

HEV-1 and HEV-2 are mainly restricted to humans and have been responsible for large hepatitis E outbreaks in the past. According to the World Health Organization (WHO), one-third of the world’s population— comprising of more than two billion people—are living in areas highly endemic for these genotypes, including South-East Asia, the Middle East, India, Central Asia, Middle America or South America (World Health Organization, 2015). Annually, approximately 20 million HEV infections are reported for Africa and Eastern Asia (Rein et al., 2012).

Contamination of drinking water and food with human excretions is suspected to be the major route of transmission for HEV-1 and HEV-2 (Figure 2, yellow). Low hygienic standards and limited access to clean water therefore represent a high risk for the occurrence of hepatitis E outbreaks in developing countries. In households, sharing of utensils for eating and drinking during an HEV outbreak may also contribute to virus transmission. Direct person-to- person transmission of HEV is possible, although this has been described only rarely.

Infections with HEV-1 are often associated with high mortality rates (15%–25%) in pregnant women (Khuroo, Kamili, & Jameel, 1995). Vertical transmission from infected mothers to their babies has also been described (Khuroo, Kamili, & Khuroo, 2009). To analyse the infection routes of HEV-1 and HEV-2, unravel the disease progression and assess vaccine efficiency, non-human primates served as useful animal models in the past. By this, several primate species have been shown to be susceptible for HEV-1 and HEV-2 including African green monkey, cynomolgus, macaqu (Macaca fascicularis), eastern-owl monkey (Ticehurst et al., 1992; Yugo, Cossaboom, & Meng, 2014) (Aotus trivirgatus), rhesus macaque (Arankalle, Goverdhan, & Banerjee, 1994; Arankalle et al., 1993) (Macaca mulatta), squirrel monkey (Tsarev et al., 1994) (Saimiri sciureus), moustached tamarin (Bradley et al., 1987) (Saguinus mystax mystax) and chimpanzee (Arankalle et al., 1988; Yu et al., 2010) (Pan troglodytes) (Table 1). Experimental infection of cynomolgus monkeys leads to faecal excretion of virus particles and clinical symptoms similar to those observed in humans (Aggarwal et al., 2001; Bradley et al., 1987). Interestingly, even Mongolian gerbils (Meriones unguiculatus) could be infected successfully with HEV-1 via intravenous inoculation (Hong et al., 2015)

v Genotypes HEV-3 and HEV-4

HEV-3 and HEV-4 can be detected in both, humans and animals, and the predominant transmission pathway follows that of a zoonosis. Domestic pig (Sus scrofa domesticus) and wild boar (Sus scrofa) represent the most important animal reservoirs for HEV-3 and HEV-4 (Caruso et al., 2016). Transmission of HEV-3 from deer to humans has also been described repeatedly, although deer most probably undergoes spillover infections from wild boar, rather than being a true HEV reservoir (Anheyer-Behmenburg et al., 2017). A distinct subtype of HEV-3 has been repeatedly detected in rabbits (Oryctolagus cuniculus) and was recently also identified in a few.

Evidence for transmission of HEV-3 and HEV-4 by direct contact of humans with animals has been repeatedly described, although the clinical consequence is not clear in most cases. Several studies have shown that persons with occupational contact to domestic pigs such as slaughterers, pig farmers or veterinarians exhibit significant higher anti-HEV antibody prevalences than the general population (Khuroo et al., 2009). The same has been demonstrated for people with frequent contact with wild boars and their excretions like forestry workers and hunters.

v Other HEV genotypes and HEV-related viruses

Besides HEV-1 to HEV-4, a new potentially human pathogenic HEV genotype (HEV-7) has been described recently. The genotypes HEV-5 and HEV-6 have been detected in wild boar from Japan, but not yet in humans (Takahashi et al., 2011). A putative additional genotype, HEV-8, was detected very recently in farmed Bactrian camels (Camelus bactrianus) from Xinjiang, China, but its zoonotic potential has not been investigated so far (Woo et al., 2016).

1.2.5. HEV Infection in Animals

Serological and/or molecular analyses indicated infections with HEV or HEV-related viruses in a broad spectrum of different animal species. These investigations included farmed animals, pets, laboratory animals, wild animals or animals from zoo-like locations. For some of the animals like domestic pigs, wild boars, chicken or rats, a frequent and continuous detection of specific HEV types at different geographical areas clearly indicates a function of a true animal reservoir. In other animal species, HEV is detected only sparsely, which may rather suggest spillover infections. However, for many animal species, no systematic studies on HEV infections are available. Additionally, there are large differences in the methods used for the identification of HEV infection, which make direct comparisons of the studies difficult.

In some studies, only HEV-specific antibodies were detected, but the causative virus or genotype was not determined. Besides experimental intravenous infections of primates, clinical symptoms due to HEV infection have only been described in chicken infected with avian HEV, whereas all other animal species seem to be infected mainly asymptomatically. In this chapter, we give an overview on the current knowledge on animal species that can be infected with HEV and which may therefore represent sources of infection for humans. As the situation in the typical reservoir animals has already been reviewed extensively, this review mainly focuses on other animal species.

1.2.5.1. HEV Infection in Domestic and Pet Animals

v Domestic and Pet Mammals

Domestic pig represents a major animal reservoir for zoonotic HEV-3 and HEV-4 worldwide, which has already been reviewed explicitly elsewhere (Doceul et al., 2016). The reported anti-HEV IgG seroprevalences in swine herds are usually high, ranging between 23% and 100%, with increasing seroprevalence with higher age (Pavio et al., 2010). Whereas pig is a well-known reservoir animal for HEV, comparatively few studies report evidence of HEV infection in domesticated bovids. HEV-specific antibodies have been found in breeds of domestic cattle (Bos taurus primigenius) like yellow cattle (Yan et al., 2016), Holstein Frisian cattle and other dairy cattle as well as in domesticated wild bovids, such as yak (Bos grunniens) (Xu et al., 2014), buffalo (Syncerus caffer) (El-Tras et al., 2013) or bison (Bison bison). Reported anti-HEV IgG prevalences were 4.4%–6.9% in India, 1.4% in Brazil, 10.4% to 37% in China and up to 15% in the USA. In contrast, HEV-RNA was detected in cattle only in a few studies. HEV-4 strains were identified in Holstein cows kept on a mixed farm together with pigs in Southwest China and in yellow cattle from Eastern China (Huang et al., 2016; Yan et al., 2016). As mixed raising of domestic livestock is popular in the investigated regions of China and the detected strains are closely related to pig strains, spillover infections are a likely explanation for the observed findings. Hepatitis E virus-specific antibodies have also been detected in goat (Capra hircus aegagrus) and sheep (Ovis aries).

HEV-7 sequences were first reported from three dromedaries sampled in the United Arab Emirates (UAE) in 2013 (Woo et al., 2014). Later, a retrospective study investigated 2,438 dromedaries from UAE, Somalia, Sudan, Egypt, Kenya and Pakistan (Rasche et al., 2016). Overall, 45.7% of the sera were anti-HEV antibody positive, which is similar to the HEV-3 seroprevalence of pigs in developing countries (Khuroo et al., 2016; Rasche et al., 2016). RNA of HEV-7 was also detected in a sample collected in 1983 suggesting a long evolutionary history of this virus type in dromedaries (Rasche et al., 2016). As a similar virus strain was also found in a liver transplantation patient, zoonotic potential of HEV-7 must be suspected (Lee et al., 2016). Very recently, a novel HEV genotype, tentatively designated as HEV-8, has been identified in Bactrian camels from a farm in China (Woo et al., 2016).

Ferret and mink are small carnivores of the family Mustelidae, which are kept as pets or farmed as fur-bearing animals. RNA of ferret HEV, belonging to species Orthohepevirus C, was first identified in ferrets kept as household pets at four locations in the Netherlands (Raj et al., 2012). Additionally, the authors detected HEV-specific antibodies in serum from farmed ferrets in the Netherlands. In farmed minks from Denmark, RNA sequences of strains most closely related to but not identical with ferret HEV were detected (Krog, Breum, Jensen, & Larsen, 2013). Pet dogs (Canis lupus familiaris) and pet cats (Felis catus silvestris) are obviously susceptible to infections with HEV or HEV-like viruses, as repeatedly evidenced by serological analysis (Table 2). However, as only antibodies have been detected so far, the distinct viruses causing the infection are unknown. Rabbits are commonly farmed in many countries for meat consumption, fur production and as pets. In Virginia, USA, farmed rabbits from eight breeds were investigated for anti-HEV antibodies and HEV-RNA (Cossaboom et al., 2011). The IgG seroprevalence was 36.5%, and rabbit HEV-RNA was detected in serum and faeces in 22% of 85 rabbits. IgG seroprevalences in farmed Rex rabbits from China were reported between 55% and 57% (Geng et al., 2011; Zhao et al., 2009).

Rabbit HEV-RNA was detected in 7.5% (serum) and 7.0% (faeces) of these animals. Furthermore, IgG seroprevalences in New Zealand White rabbits from two US vendors were reported 40% and 50%, respectively (Birke et al., 2014). Additionally, rabbit HEV-RNA was detected in 5% of Japanese White rabbits and Rex rabbits from China (Xia et al., 2015). Rabbits from France, slaughtered for consumption, had a rabbit HEV-RNA prevalence of 7% in liver specimens (Izopet et al., 2012). Rabbit HEV strains are related to other HEV-3 strains but represent a distinct subtype. However, this subtype has been recently also detected in a few human patients from France (Abravanel et al., 2017; Izopet et al., 2012). In addition, a rabbit HEV strain very closely related to one of these French human patient isolates was also identified in a pet house rabbit (Caruso et al., 2015). Domesticated horses (Equus caballus ferus) were investigated sparsely for HEV. In one study, 200 sera from work horses in Egypt were surveyed for the presence of HEV (Saad et al., 2007). 13% of sera were positive for anti-HEV IgG antibodies and 4% also for HEV-RNA. The detected sequences were closely related to human HEV-1 isolates from Egypt from 1993/1994. Another study investigated 101 horses from Eastern China for the presence of anti-HEV IgG antibodies (Zhang, Shen, Mou, Gong, et al., 2008). 17.8% of these horses were seropositive, and even 2% were positive for HEV-3-RNA. These descriptions are indicative for accidental spillover infections.

v Domestic and Pet Birds

Avian HEV, which belongs to the species Orthohepevirus B, was initially described in barnyard fowl (chicken) from the United States, in 2001. Interestingly, barnyard fowl infected with avian HEV can reach clinical manifestations (Haqshenas et al., 2001; Morrow et al., 2008; Payne, Ellis, Plant, Gregory, & Wilcox, 1999). Clinical signs of an acute infection with avian HEV comprise hepatomegaly, splenomegaly, kidney modifications, growth depressions, decline of laying performance, accumulation of abdominal blood fluid, hepatic vasculitis and amyloidosis as well as increased deaths among poultry (Agunos et al., 2006; Morrow et al., 2008). Avian HEV is widespread in chicken flocks worldwide (Gerber, Trampel, & Opriessnig, 2014). The reported seropositive rates in chicken flocks are high: 95.1% in Taiwan, 71% in the USA, 90% in Spain and 57% in Korea (Gerber et al., 2014; Hsu & Tsai, 2014; Huang et al., 2002; Peralta, Biarnés, et al., 2009). The HEV-RNA prevalence is similarly high, with 72-100% reported in one study from the USA (Gerber et al., 2014). Experimental cross-species transmission of avian HEV from chicken to turkeys (Meleagris gallopavo) has been reported (Sun et al., 2004). Avian HEV does not seem to have a potential for transmission to humans. Using an experimental infection approach with rhesus macaque as a model, avian HEV was unable to infect primates (Huang et al., 2004). HEV-specific antibodies were detected in domestic farmed duck (Anas platyrhynchos domesticus) and pigeon (Columba livia domestica) from Eastern China, with anti-HEV IgG prevalences of 12.8% and 4.4%, respectively (Zhang, Shen, Mou, Gong, et al., 2008).

Pet birds can also be infected with HEV. In 2014, 685 serum samples of three pet bird species from China were investigated (Cong et al., 2014). This included the Eurasian siskin (Carduelis spinus), the Oriental skylark (Alauda gulgula) and the black-tailed grosbeak (Coccothraustes migratorius). Collectively, 8.31% birds were positive for avian HEV-specific antibodies. In the same year, another study investigated four parrot species from China and two of them were positive for avian HEV-specific antibodies: budgerigar (Melopsittacus undulatus) and Alexandrine Parakeet (Psittacula eupatria) (Zhang et al., 2014). The ascertained seroprevalence was 6.43.

1.2.5.2. HEV Infection in Wildlife and Zoo Animals

v Piramates

Primates in the wild

Natural HEV infection in wild-living primates has been reported sparsely so far. A report from the rural Yunnan province, China, describes the testing of 480 stool samples and 92 serum samples of wild rhesus macaques (Huang et al., 2011). The prevalence of HEV-specific IgG was quite high (35.87%), and three of 31 rhesus macaques were even positive for HEV-specific IgM indicating acute infections. However, the authors concluded that “Macaca mulatta may not be a natural reservoir of HEV-4” and that “HEV-4 infection might have been acquired from contact with HEV infected wild boars, wild rats or humans.” Natural infection was also reported in three Indian monkey species: wild rhesus macaques, bonnet macaques (Macaca radiata) and grey langur (Semnopithecus entellus) were reported with HEV IgG seroprevalences of 36.7%, 19.1% and 2%, respectively (Arankalle et al., 1994).

Primates in zoos

In a study from China, 37 faecal samples of chimpanzees from two zoos were tested by RT-PCR for the presence of HEV-RNA (Zhou, Li, & Yang, 2014). Overall, 29.2% of the samples were HEV-RNA positive. The HEV-RNA sequences showed 99% identity to each other. Surprisingly, the detected RNA shared only 45%–58% sequence similarity with known HEV strains. The authors therefore suggested that they had found a novel type of HEV. However, only small RNA fragments were amplified and independent confirmation of the sequences has not been done so far. Natural infection and transmission of HEV-3 has been described in a monkey facility in Japan, housing non-human primates of the species Japanese macaque (Macaca fuscata) and rhesus macaque (Yamamoto et al., 2012). None of the animals showed any clinical signs of illness. Initially, neither IgG nor IgM anti-HEV antibodies could be found in any of the primates. Within 2 years, both IgG (78.5%) and IgM (6.6%) reached their maximum and slowly decrease within another 3 years to 35.3% (IgG) and 0% (IgM). HEV-3 RNA was detected in serum and faeces of these animals.

v Other mammals

Mammals in the wild

Natural HEV infection of wildlife animals has been reported in a variety of mammalian species. Among the affected species, there are ungulates like wild boar, bovids, deer and moose (Alces alces), as well as some carnivores like mink, red fox, mongoose and ferret, but also rodents, lagomorphs and bats. Wild boar are a well-known reservoir for zoonotic HEV strains. This has been already reviewed elsewhere and selected studies are given as examples in Table 2 (Doceul et al., 2016; Johne et al., 2014; Pavio et al., 2015). The reported HEV-specific antibody prevalences range from 3% to 42.7% in the USA and Spain, respectively (De Deus et al., 2008; Dong et al., 2011). Using RT-PCR, HEV-3 was mostly identified, with detection rates up to 68% in wild boar in Germany. HEV-4 has been reported in wild boar from Japan (Takahashi et al., 2014). Also, the single detection of HEV-5 and HEV-6 has been reported in wild boar from Japan (Takahashi et al., 2011). However, these genotypes have not been detected in humans so far. Hepatitis E virus infection has been repeatedly identified in several deer species. The prevalence of HEV-specific antibodies in Europe and Japan ranges from 2% to 35% (Pavio et al., 2010). In Japan, wild Sika deer (Cervus nippon nippon) showed an HEV IgG seroprevalence of 2%, whereas that of Yezo deer (Cervus nippon yesoensis) was 34.8%. Generally, HEV-3 strains that were identified in deer species were closely related to wild boar and human strains (Pavio et al., 2010; Takahashi, Kitajima, Abe, & Mishiro, 2004; Tei, Naoto, Kazuaki, & Shunji, 2003). In a study in Germany, similar strains were detected in wild boar, roe deer (Capreolus capreolus) and red deer (Cervus elaphus) from the same hunting area (Anheyer-Behmenburg et al., 2017). As consistently lower prevalences and lower virus loads were detected in the deer species as compared to the wild boar, spillover infections have been proposed as explanation for the deer HEV infections.

1.3. Prevention of HEV

Prevention is the most effective approach against the disease. At the population level, transmission of HEV and hepatitis E disease can be reduced by:

  • maintaining quality standards for public water supplies;
  • establishing proper disposal systems for human feces.

On an individual level, infection risk can be reduced by:

  • maintaining hygienic practices such as hand-washing with safe water, particularly before handling food;
  • avoiding consumption of water and/or ice of unknown purity; and
  • adhering to WHO safe food practices. (WHO, 2017)

1.4. Treatment of HEV

There is no specific treatment capable of altering the course of acute hepatitis E. As the disease is usually self-limiting, hospitalization is generally not required. Hospitalization is required for people with fulminant hepatitis, however, and should also be considered for symptomatic pregnant women. Immunosuppressed people with chronic hepatitis E benefit from specific treatment using ribavirin, an antiviral drug. In some specific situations, interferon has also been used successfully (WHO, 2017).

1.5. Conclusion

Hepatitis E is a human disease mainly characterized by acute liver illness, which is caused by infection with the hepatitis E virus (HEV). Large hepatitis E outbreaks have been described in developing countries; however, the disease is also increasingly recognized in industrialized countries. Mortality rates up to 25% have been described for pregnant women during outbreaks in developing countries. In addition, chronic disease courses could be observed in immunocompromised transplant patients. Whereas the HEV genotypes 1 and 2 are mainly confined to humans, genotypes 3 and 4 are also found in animals and can be zoonotically transmitted to humans. Domestic pig and wild boar represent the most important reservoirs for these genotypes. A distinct subtype of genotype 3 has been repeatedly detected in rabbits and a few human patients. Recently, HEV genotype 7 has been identified in dromedary camels and in an immunocompromised transplant patient. The reservoir animals get infected with HEV without showing any clinical symptoms. Besides these well-known animal reservoirs, HEV-specific antibodies and/or the genome of HEV or HEV-related viruses have also been detected in many other animal species, including primates, other mammals and birds. In particular, genotypes 3 and 4 infections are documented in many domestic, wildlife and zoo animal species. In most cases, the presence of HEV in these animals can be explained by spillover infections, but a risk of virus transmission through contact with humans cannot be excluded. This review gives a general overview on the transmission pathways of HEV to humans. It particularly focuses on reported serological and molecular evidence of infections in wild, domestic and zoo animals with HEV or HEV-related viruses. The role of these animals for transmission of HEV to humans and other animals is discussed. Although still comparatively rare, the total numbers of hepatitis E cases are currently increasing in many industrialized countries. The disease is mostly self-limiting and the patients recover after a few weeks.

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Woo, P. C. Y., Lau, S. K. P., Teng, J. L. L., Cao, K., Wernery, U., Schountz, T., … Yuen, K. (2016). New hepatitis E virus genotype in Bactrian Camels, Xinjiang, China, 2013. Emerging Infectious Diseases, 22(12), 2219–2221

April Kahn and Valencia Higuera, 2017, Hepatitis Website:https://www.healthline.com/health/hepatitis#types

Mohammad S. Khuroo, Mehnaaz S. Khuroo and Naira S. Khuroo , 2016. Transmission Of Hepatitis E Virus In Developing Countries,Open Acess Journal 2016 http://www.mdpi.com/1999-4915/8/9/253/pdf

World Health Organization, 2017. Hepatitis, Website: http://www.who.int/mediacentre/factsheets/fs280/en/

About Hepitis E virus

© 2017 Chala Dandessa Debela

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