Hepatitis E virus (HEV) is an emerging zoonotic virus
of pigs. It has now been reclassified as the only member of the genus Hepevirus,
family Hepeviridae. The viral particle is composed of a non-enveloped
capsid which encloses a single-stranded positive sense RNA genome. Four main genotypes (HEV 1-4) are identified; two of
them circulate among pigs and humans.
HEV was first detected in
pigs in 1997 in United States. The first swine HEV strains shared about 97%
percent similarity with concurrent strains isolated in humans, showing the zoonotic
potential of the virus.
Virtually all swine-producing countries have already
reported the circulation of swine HEV. Although swine infection is spread
worldwide, the cases of human HEV induced hepatitis are far more common in
developing countries, indicating that poor levels of sanitation and inadequate
disposal of swine manure may have an association with the epidemiology of human
infection.
The disease caused by HEV in humans have some similarities
with that caused by the Hepatitis A virus (HAV), including the fecal-oral route
of transmission and the absence of chronification.
The mortality rate is remarkably higher in pregnant
women, where HEV can cause the death
of up to 20% of patients, while in the non-pregnant population HEV induces up to 4% of deaths.
of up to 20% of patients, while in the non-pregnant population HEV induces up to 4% of deaths.
Although HEV seems to be an important agent of human
liver disease, the infection by swine HEV in pigs is subclinical. After infection, pigs become viremic and shed the
virus on theirs feces from 8 days for up to 12 weeks. The immunity raised by
the infection is long lasting and a prior infection with swine HEV prevents the
onset of viremia and fecal shedding of the virus is also diminished in immune animals.
Viruses from all 4 genotypes cause disease in humans,
whereas only genotypes 3 and 4 are found in pigs. Genotype
1 is mainly found in Asia and Africa, during HEV epidemics in humans; genotype
2 was firstly reported in Mexico and was further reported as an endemic virus
in parts of Africa. These genotypes are restricted
to humans. Genotype 3 is worldwide
distributed and has been causing infection in both humans and swines. This genotype
is often associated to epidemics of HEV liver disease in humans in South America
and is also found on swine in this same region. Genotype
3 HEV strains were also found in many other animal reservoirs including wild
boar, rabbits, rats, deer and mongoose. Similarly,
genotype 4 HEV was detected in humans and pigs, as well in wild boars.
The ubiquitous nature
of HEV infection in pigs suggests that contamination of meat products by HEV
and viscera can be quite frequent. Sporadic cases
of acute hepatitis E have been associated with the consumption of raw pork
liver and under-cooked contaminated pork or grilled meats.
The prevalence of HEV in pigs fed on kitchen
residues is higher than in those fed on complete feed, indicating that indirect
contact with infected humans is also a source of infection for pigs. Veterinarians and swine handlers are at higher
risk of infection than the general population.
HEV has the ability to contaminate water bodies and
be transmitted by water. Contaminated water therefore constitutes a major source of HEV infection in humans and the
reason of ubiquity and perpetuation of the infection in pigs.
Outbreaks of HEV in humans tend to be more common in
regions where conditions of water and sewage treatment are poor. HEV has been found
contaminating the effluents of slaughterhouses and the virus is often found in swine
manure storage facilities.
Control measures to avoid the contamination of the
environment, including better management practices to deal with swine manure,
proper cooking of pork liver and development of swine HEV vaccines.
Dr.
Moses Bwana
Post-grad at the University of Nairobi (Veterinary Applied
Microbiology [Virology Option])
Faculty of Veterinary Medicine