Foodborne viral infections

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August 2013

The leading cause of gastroenteritis, foodborne viral infections are primarily due to two types of virus, norovirus which causes gastroenteritis and Hepatitis A virus which causes hepatitis. All foodborne viruses originate from the human intestine and contamination of food occurs either by contamination from an infected food handler during preparation or by contact with sewage, sewage sludge or polluted water, typically during primary production. Symptoms are typically nausea, vomiting, diarrhoea and abdominal pain.

Viruses behave differently to bacteria and this is a concern because current hygiene guidelines usually either have not been validated for foodborne viruses, therefore there is no understanding of the efficacy of the controls on viruses, or the control measures are not effective in controlling these viruses. Hygiene and control measures mainly depend on staff education and good factory and kitchen hygiene; food handlers suffering from symptoms should be excluded from work immediately and all staff made aware of the ease with which viral contamination is transmitted. The use of clean water for irrigation of crops that are likely to be eaten raw and cultivation of molluscan shellfish in sewage-free seawater are also essential to prevent viral contamination of food.


Between 1886 and 1898 viruses were first recognised as organisms different from other disease causing microbes. In 1886, Adolf Mayer was studying tobacco mosaic disease, but tests and attempts to isolate and culture a bacterial agent failed. In 1892, Dmitri Ivanovski demonstrated through an experiment that the disease was either caused by a toxin or by something much smaller than any previously described organism. In 1898 Martinus Beijerinck replicated Ivanovski's experiment and showed that the disease was caused by an infectious life form of some type. This organism became known as tobacco mosaic virus.

First recognised as a vehicle for viruses in 1914, food was identified as the vehicle in an outbreak of raw-milk associated poliomyelitis. Norwalk virus was identified in 1918 following an outbreak in a primary school in Norwalk, Ohio, which affected both children and adults. In the mid-1950s shellfish was identified as the transmission route in Sweden and then in the United States. Following the introduction of molecular methods in the 1990s, viruses were identified as being the leading cause of human gastroenteritis in developed countries.

Many different viruses can cause gastroenteritis, including, noroviruses, adenoviruses, sapoviruses and astroviruses. Symptoms may be similar to gastroenteritis caused by bacteria and parasites. Norovirus and Hepatitis A are the most important viruses causing viral foodborne illness in Europe for the number of outbreaks and people infected (1).

What are foodborne viruses?

Viruses lie at, or beyond, the edge of what is considered to be a living organism due to the lack of metabolic apparatus. They are totally inert, incapable of reproducing or carrying out other metabolic processes and must induce living cells to reproduce the progeny.  Most foodborne viruses are usually approximately spherical and are at the smaller end of the size scale (25−30nm), typically being visible only with an electron microscope. Few have lipid envelopes or other defining structural features.

Viruses may be shed in extremely high numbers (105 to 1011 virus particles per gram of stools) and one vomiting episode due to gastroenteritis may contain 107 particles. Foodborne viruses have a low infectivity dose of 100−150 cells and this combined with the high numbers shed can lead to large outbreaks in a relatively short time. The burden of illness is highest in the elderly and due to an aging population, this is likely to increase(2). In general, foodborne viruses are persistent in the environment and are able to withstand mild food production processes used to inactivate or control bacterial pathogens in  foods(3).


Photo Credit: F.P. Williams, U.S. EPA(13)

Noroviruses are a genetically diverse group of non-enveloped viruses in the Caliciviridae family, important human pathogens causing sporadic cases and epidemic outbreaks, consisting of several serologically distinct groups that have been named after the places where the outbreaks occurred. The 27−35nm viral particles are symmetrically icosahedral. The particles contain a single-stranded,  positive sense RNA genome of 7.5 kb, a single structural protein of about 60 kDa and have a buoyant density of 1.39−1.40 g/ml in CsCl. Infection is through oral ingestion from contaminated food or water with replication occurring in the small intestine causing transient lesions of the intestinal mucosa. Transmission my also occur through aerosols creating during vomiting, which may contribute to the very rapid secondary spread of infection.( 4,5)

The disease is self-limiting (24−48 hours up to 6 days) with a low infection dose of 10−100 virions, mild, and characterised by nausea, vomiting, diarrhoea, myalgias and abdominal pain. Headache and low-grade fever may occur. The primary route of transmission is the faecal−oral route and secondary person-to-person transmission has been documented. Water is the most common source of outbreaks and may include water from municipal supplies, wells, recreational lakes, swimming pools, and water stored aboard cruise ships(6).Shellfish and salad ingredients are the foods most often implicated in norovirus outbreaks. Ingestion of raw or insufficiently steamed clams and oysters poses a high risk for infection with Norovirus. Foods other than shellfish are usually contaminated by ill food handlers.


Rotaviruses are a group of non-enveloped viruses in the Reoviridae family, consisting of 7 species (named A−G). Rotavirus A is endemic worldwide, causing approximately 80% of rotavirus gastroenteritis in humans, particularly through waterborne infection, with rotavirus B and C also being human pathogens. The 70nm viral particles are icosahedral; the particles consist of 11 double-stranded RNA segments surrounded by a two-layered protein capsid and have a buoyant density of 1.36 g/ml in CsCl. Rotaviruses infect intestinal enterocytes, with early events after infection being  mediated by virus−epithelial cell interactions. Recent research has shown that rotaviruses infect cells differently depending on whether or not sialic acid is required for initial binding, and infection alters epithelial cell functions.

Rotavirus gastroenteritis is a self-limiting, mild to severe disease characterised by vomiting, watery diarrheoa and low-grade fever (temporary lactose intolerance may occur). Symptoms usually start 1−3 days after infection with vomiting followed by 3−8 days of diarrhoea caused by an infective dose believed to be 10−100 infectious viral particles; asymptomatic rotavirus excretion may play a role in perpetuating endemic disease with shedding occurring for in excess of 30 days. Diarrhoea without fluid and electrolyte replacement may result in severe diarrhoea and death, particularly among children 6 months to 2 years of age, the elderly and the immunocompromised. Immunity is believed to be built up which reduces the severity of any subsequent infections.  Outbreaks caused by Group B rotavirus have been reported in the elderly and adults with Group C rotavirus being associated with sporadic cases of diarrhoea in children in many countries (7)

Hepatitis A

Hepatitis A 2 virus (HAV) is part of the enterovirus group of the Picornaviridae family and one of 6 forms (A, B, C, D, E, G) which was first identified in 1973. HAV has a single molecule of RNA surrounded by a 27−32nm protein capsid and a buoyant density in CsCl of 1.33 g/ml. Foods can be contaminated with the virus through contact with raw sewage, such as is the case with shellfish, or through contact with contaminated water; transmission is then primarily via the faecal−oral route. HAV replicates exclusively in liver cells, is excreted in bile and shed in the faeces of infected people. Hepatitis A is less common in developed countries with 367 reported cases in England and Wales in 2010; reported cases have been generally decreasing since 1992.

Hepatitis A is a liver infection which is usually a mild illness characterised by symptoms similar to influenza including sudden onset of fever, malaise, nausea, joint pain, dark coloured urine, pale stools, anorexia and abdominal discomfort, followed in several days by jaundice, with complete recovery within 2 months. The illness is usually more severe the older the person is, with infected children under 6 years not experiencing noticeable symptoms. The minimum infectious dose required for HAV infection in humans is unknown, but presumably is 10−100 virus particles with the incubation period being dependent upon the number of particles ingested (fewer particles means a linger incubation period). The incubation period for hepatitis A varies from 10 to 50 days (average 28 days) with a long communicability period from early in the incubation period to about a week after the development of jaundice. The middle of the incubation period (2 weeks before symptoms develop) presents the greatest period of communicability, well before the first presentation of symptoms during peak shedding of the virus. Many infections with HAV are asymptomatic, especially in children. Symptoms are occasionally more severe, particularly in people with pre-existing liver conditions with convalescence taking up to 3 months. Patients suffer from feeling chronically tired during convalescence with an inability to work. Fatality is rare, usually occurring in the elderly. Once the virus has been contracted lifelong immunity develops(8,9,10).

Routine vaccination of all food handlers is not recommended, because their profession does not put them at higher risk for infection.

Hepatitis E

This virus is rare within the EU but is recognised as having increased importance as an emerging infection(11). HEV is a non-enveloped, positive-stranded RNA of approximately 7.5 kb spherical, probably icosahedral shaped virus with a diameter of 27−34 nm. The virion is composed entirely of viral protein and RNA, with a buoyant density of 1.29 g/cm3 in potassium tartrate/glycerol gradients. Although the capsid icosahedral shape, lack of outer lipid envelope and size of the genome resembles other faecally transmitted viruses including HAV and norovirus, hepatitis E has some distinguishing physicochemical and genetic properties which have led to the virus being assigned its own genus (Hepevirus) and family (Hepeviridae). There is a single serotype and at least five genotypes [human, swine (1-4) and avian (5)].

From the intestinal tract, the virus reaches the liver through an unknown route and mechanism. HEV appears to replicate primarily in liver and gall-bladder cells, but has been noted in the small intestine, lymph nodes, colon and salivary glands. The incubation period following exposure can range from 3 to 8 weeks, with a mean of 6 weeks.  The disease usually is mild, asymptomatic and self-resolves in 2 weeks; it is usually seen in age groups 15−40 and can be asymptomatic in children. Symptoms include jaundice, malaise, anorexia, enlarged tender liver, abdominal pain, arthralgia, hepatomegaly, vomiting and fever. Chronic hepatitis has been reported in organ transplant recipients and in patients with active HIV infections. Extended faecal shedding when present occurs for approximately 2 weeks after jaundice develops. Fuliminant hepatic failure has been observed especially in pregnant women where mortality rates rise from less than 1% to 25%. In immunocompromised patients hepatitis E can be persistent and also associated with increased mortality and morbidity in people with progressed liver disease.

Replication and survival

Viruses can be considered to be intracellular parasites on the basis that production of progeny viruses takes place within the host cell. Progeny are formed from the production by the host cell of viral nucleic acid and protein; these viral constituents are capable of ‘self-assembly’ within the cell spontaneously forming viral progeny. Release of the virus is seldom reliant purely on lysis of the host cell and can be released in a number of ways.

Particulate phase

The viral form that is transmitted from cell to cell and from one host to another is called a particle. If the virus particle’s outer layer contacts a homologous receptor on a susceptible cell’s plasma membrane, the virus’s protein coat, or lipid envelope if present, attaches and infection ensues. To be food or water-borne, a virus must be capable of infectivity upon ingestion by the host in a cell type that is accessible from the digestive tract.

Replicative phase

The virus particle attaches and is engulfed by the host cell (usually the whole particle) through what is believed to be a passive process into the cytoplasm – the host cell does all of the work although a high proportion of particles are rejected after coming into contact with a homologous receptor. Uncoating of the protein coat or lipid envelope occurs during the engulfment process with nucleic acid and intrinsic viral enzymes being released into the host cell. As necessary, the viral nucleic acid is transcribed and translated by the cell; this induces production of viral nucleic acid, protein and other constituents required. As quantities are produced, the progeny self-assembly begins; viruses produced in the intestinal tract are called ‘enteric’.

If progeny fully mature within the host cell, then particulate release may not be immediate and the particles may accumulate within the cell; release of the particles is typically gradual rather than the normal bacteriophage ‘burst. Viruses in animal cells may slowly ‘leak’ through the plasma cell membrane or may stay associated with the cell. The replication cycle may take from between 8 hours to over 24 hours in a single cell.

Reservoirs and survival

Enteric viruses are usually resistant to environmental stresses such as heat and acid. The majority are also resistant to freezing and drying, are stable in contact with lipid solvents and may be resistant to ultrahigh hydrostatic pressure. These properties enable foodborne viruses to survive in pickled, marinated and acidic foods. Enteric viruses are capable of surviving and retaining infectivity in marine, estuarine and fresh water for several weeks at 4°C and survival may be increased by attachment to sediment or particulate matter.

Noroviruses are resistant to drying. They can survive on almost any hard surface (including glass, door handles and railings) for up to 12 hours. On carpet, norovirus can survive for up to 12 days. The virus is relatively resistant to high levels of chlorine (up to 10ppm free chlorine) and also varying temperatures. In chilled and frozen environments norovirus may be able to survive for months or even years. Norovirus remains infective after being subjected to pH 2.7 for 3 hours at ambient temperature. While the virus is inactivated by boiling, it can remain infective at 60°C for 30 minutes and can survive some pasteurisation and steaming processes.

Rotaviruses are stable in the environment; in estuaries samples have been founds at levels of 1−5 infectious particles/gallon and can also survive secondary sewage treatment, with a persistent resistance to many of the new physical or chemical technologies for treating wastewater. Rotavirus is resistant to inactivation, with infectivity being unaltered at both low (3.5) and high (11) pH. To kill or inactivate rotavirus from contaminated well water, bringing the water to a rolling boil for one minute is advised. The virus is stable at low temperatures of -20°C and 4°C, with minimal loss of titre after 32 days, and is stable during 6 freeze/thaw cycles. Rotaviruses can survive on human hands for up to 4 hours, are stable for up to 4 days at 37°C and rapidly inactivated at 56°C. Rotaviruses are inactivated by UV light and by disinfectants, including chlorine, hydrogen peroxide and ethanol. Sanitary measures adequate for bacteria and parasites seem to be ineffective in endemic control of rotavirus, with similar incidence rates of rotavirus infection in countries with both high and low health standards.

Hepatitis A is readily inactivated by heating foods to 85°C for 1 minute but is not subject to thermal denaturation at lower temperatures (70°C for up to 10 min). HAV can survive chilled and frozen temperatures for up to 2 years. Disinfection with a 1:100 dilution of household bleach in water (0.5mg free chlorine for 30 minutes), or cleaning solutions containing quaternary ammonium and/or HCl is also effective in inactivating HAV, although the virus is resistant to disinfection by some organic solvents and by a pH as low as 3, acid treatment (pH 1 for 2 h at room temperature) is effective. HAV can survive in the environment for at least 12 weeks at 25°C when excreted in human faeces and remain infectious after 1 month on environmental surfaces at ambient temperatures, three to four hours in faecal matter on a person's hand. It has been found to survive in experimentally contaminated fresh water, seawater, wastewater, soils, marine sediment, live oysters, and creme-filled cookies. Hepatitis A is more resistant to heat and drying than other enteroviruses.

Hepatitis E is considered to be labile when not in the acidic conditions found in the gastrointestinal tract or in faecal material. HEV can withstand thermal inactivation at temperatures near those expected to be found within a rare-cooked steak (approximately 57°C). The levels of viable virus decrease rapidly at higher temperatures. Repeated freezing and thawing can gradually decrease the HEV levels. As HEV does not have a lipid envelope, it can somewhat withstand exposure to alcohols and detergents. HEV does seem especially susceptible to high salt concentration.

Food and water-borne outbreaks

It is difficult to estimate the proportion of foodborne disease caused by viruses due to under-reporting, the lack of surveillance systems and the inability of existing systems to determine the proportion of disease that is transmitted by foodborne routes relative to other common routes.

Increases in population, scarcity of clean water, changes in eating habits such as the increased consumption of food eaten raw and the globalisation of the supply chain are all contributing to the increase and spread of viral foodborne disease(12).


  • May 2005, 2 outbreaks in Denmark were reported from frozen imported raspberries.
  • 2005, an outbreak in France was reported from imported frozen raspberries
  • Food poisoning outbreak caused by norovirus GII/4 in school lunch, Tochigi Prefecture, Japan in December 2007 affecting 18 children and 5 adults, possibly linked to salad
  • January 2009, military base in Germany, 36 cases from norovirus contaminated salad
  • January 2010 in Tennessee, USA – 13 people affected from cake in a restaurant
  • February 2012, Missouri, USA, 139 cases from fruit salad at a banquet
  • January 2012, 334 cases were reported in the United Kingdom, Norway, France, Sweden and Denmark in 65 clusters
  • 10845 laboratory confirmed cases in England and Wales in 2012 (based on provisional data)


  • Water, China 1982
  • April 2000, 19 confirmed cases and 108 self-reported cases in District of Columbia, United States, possibly from line cooks
  • December 2000, outbreak attributed to contaminated water supplies in Tirane, Albania with 2722 children seen at Tirane Hospital
  • 9907 patients in 2005 in Malatya City, Turkey, due to possible contamination of a large water depository from a water well, which supplied drinking water to two major districts of the city
  • 15,500 human foodborne rotavirus cases are estimated to occur in the United States each year.

Hepatitis A

  • Clam associated outbreak in Shanghai in 1988 with 280,000 people affected due to contamination and inadequate cooking
  • More than 50 residents in South Cambridgeshire, UK in 1991 where the vehicle was believed to be bread
  • 213 cases in Maine, United States in 1997 attributed to frozen strawberries
  • November 2005 in France 111 cases were reported due to consumption of Oysters
  • 2011,7 people believed to have contracted HAV from sun dried tomatoes in UK

Hepatitis E has been the cause of sporadic cases and epidemic forms with the primary vehicle being ingestion of faecally contaminated drinking water.

  • New Delhi in 1955 following the contamination of the city's drinking water when 29,000 cases of icteric hepatitis occurred.
  • Indian subcontinent (1975, 1978, 1980) and USSR (1983): several major outbreaks.


As enteric viruses are passed through the faecal−oral route, foods typically associated with food and waterborne viruses can occur at any point in cultivation, harvesting, processing, distribution, or processing/preparation. Water, shellfish and salads are the most frequent sources.

Foods implicated in outbreaks include:

  • Molluscan shellfish including oysters, cockles, musselsFoods that require handling and no further cooking, which are contaminated by infected food handlers
    • Salads
    • Fruits
    • Hors d'oeuvres.
    • Cold cuts
    • Sandwiches
  • Vegetables - Green onions, Sun dried tomatoes
  • Fruit - Strawberries, Raspberries
  • Drinking water
  • Fruit Juices
  • Milk and milk products
  • Undercooked wild boar meat, deer meat
  • Pig liver sausage
  • Pork livers
  • Salad dressings and cake icings in which viruses can become evenly distributed
Isolation methods

Detection and isolation of food or waterborne viruses is limited by the non-routine nature of testing for these viruses in food (virus particles require living host or tissue to replicate), long incubation of some Hepatitis A virus meaning that the implicated food is often unavailable, difficulty or inability to culture in laboratory cell cultures and the level of virus particles in a contaminated food is usually very low.

Specialist laboratories may achieve detection using cell culture and complex extraction methods but techniques previously available are not suitable for routine application and recovery rates remain poor.

Detection methods






Immune electron microscopy


Enzyme immunoassay

Latex agglutination




Polyacrylamide gel electrophoresis




Norovirus is recognised in human stool specimens by enzyme-linked immunosorbent assays and commonly through PT-PCR to detect and differentiate noroviruses in vomit and stools.  Immune electron microscopy and antibody tests can be used to identify norovirus in serum.

Rotavirus diagnosis may be made by rapid antigen detection of rotavirus in stool specimens. Strains may be further characterised by reverse transcriptase polymerase chain reaction (RT-PCR). Electron microscopy and polyacrylamide gel electrophoresis (PAGE) are used in some laboratories.

Hepatitis A is typically diagnosed by finding IgM-class anti-HAV in serum collected during the acute or early convalescent phase of disease.

Hepatitis E is diagnosed by immune electron microscopy, in feaces of acutely ill patients or by molecular detection of genomic RNA in serum or feaces. Additional diagnostic tests that are used in research studies (due to the specialised facilities required) are RT-PCR and immune electron microscopy.

Good Industry Practice

Controls to reduce the risk of foodborne transmission of foodborne enteric viruses should focus on:

  • Use of potable water for irrigation and processing
  • Use of shellfish from approved waters
  • Active monitoring of shellfish production areas for contamination events
  • Thorough cooking of shellfish prior to consumption (85−90°C for 4 minutes or steamed for 90 seconds)
  • Excluding employees suffering from gastro-enteritis for 48 hours after symptoms have ceased and 1−2 weeks after the onset of jaundice
    • Norovirus: exclude symptomatic food handlers from the entire food business site (not just food handling duties and areas) even if norovirus is only suspected. Once excluded, they should remain away for a further 48 hours from when symptoms stop or from the end of any treatment of the symptoms with medicine such as anti-diarrhoeal drugs19.
      • If their symptoms do not develop, return to work is possible after 24 hours from contact with the infected person
    • Hepatitis A: most infectious in the period before symptoms appear, but are still infectious during the first week of illness. Food handlers with this infection should therefore remain off work for seven days after the onset of jaundice and/or other symptoms. Any food handler who develops jaundice for an unknown reason should be excluded immediately and seek medical advice.
  • Effective training in personal hygiene – practical advice about hand washing techniques and education on when to seek medical attention
  • Thorough cleaning with an effective sanitiser following any vomiting episode in a food processing environment
    • Destroying any food that may have become contaminated through aerosols and cleaning up and disinfecting thoroughly over a wide area after someone has been sick in or near a food handling area is therefore very important,
  • Easy access to hand washing and sanitary facilities for all employees (including field workers)
  • Discourage children from areas where food is harvested or processed
  • Correct disposal procedures for sanitary waste
  • Potable water or chlorinated water should be used for rinsing produce or for making ice for packing
References and further reading
  1. Vasickova P, Dvorska L, Lorencova A, Pavlik I (2005). Viruses as a cause of foodborne diseases: a review of the literature. Vet Med Czech 50 (3), 89–104.
  2. US National Library of Medicine. Accessible from:
  3. FAO/WHO [Food and Agriculture Organization of the United Nations/World Health Organization]. 2008. Microbiological hazards in fresh leafy vegetables and herbs: Meeting Report. Microbiological Risk Assessment Series No. 14. Rome.
  4. Blacklow NR (1996). Chapter 65. Norwalk virus and other calciviruses. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston.
  5. Public Health Agency of Canada (2012). Norovirus. Available from:
  6. US Department of Health and Human Services. Norovirus (Norwalk Virus). Available from:
  7. Estes MK, Kang G, Zeng CQ, Crawford SE, Ciarlet M (2001). Pathogenesis of rotavirus gastroenteritis. Novartis Found Symp 238, 82−96; discussion 96−100.
  8. NHS Choices (2012). Hepatitis A. Available from:
  9. Public Health England (2011). Hepatitis A laboratory reports by age group (in years), England and Wales, 1992–2010, provisional. Available from:
  10. World Health Organisation. Hepatitis A. Available from:
  11. FSA Panel on Biological Hazards (BIOHAZ) (2011). Scientific Opinion on an update on the present knowledge on the occurrence and control of foodborne viruses. EFSA Journal 9(7), 2190 [96 pp.] Available from:
  12. Goyal SM, editor (2006). Viruses in Foods. Springer US.
  13. United States Environmental Protection Agency. Microbial mugshots. Available from:

Further reading

Koopmans M,  Duizer E (2004). Foodborne viruses: an emerging problem. International Journal of Food Microbiology 90 (1), 23–41.

Oogane T, Hirata A, Funatogawa K, Kobayashi K, Sato T, Kimura H (2008). Food poisoning outbreak caused by norovirus GII/4 in school lunch, Tochigi prefecture, Japan. Jpn J Infect Dis 61 (5), 423−424.

Westrell T, Dusch V, Ethelberg S, Harris J, Hjertqvist M, Jourdan-da Silva N, Koller A, Lenglet A, Lisby M, Vold L (2010). Norovirus outbreaks linked to oyster consumption in the United Kingdom, Norway, France, Sweden and Denmark, 2010. Euro Surveill 15 (12), pii=19524. Available from:

Korsager B, Hede S, Bøggild H, Böttiger BE, Mølbak K (2005). Two outbreaks of norovirus infections associated with the consumption of imported frozen raspberries, Denmark, May−June 2005. Euro Surveill 10(6), E050623.1.

Wadl M, Scherer K, Nielsen S, Diedrich S, Ellerbroek L, Frank C, Gatzer R, Hoehne M, Johne R, Klein G, Koch J, Schulenburg J, Thielbein U, Stark K, Bernard H (2010). Food-borne norovirus-outbreak at a military base, Germany, 2009. BMC Infect Dis 10, 30.

Food Standards Agency (2009). Food Handlers: Fitness to Work Regulatory Guidance and Best Practice Advice For Food Business. Available from:

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