Norovirus

Basic Virology

Norovirus is a member of the family Caliciviridae. The human norovirus genome is composed of a linear, positive-sense RNA that is 7.5 to 7.7 kb in length. The genome is covalently linked to the viral protein genome at the 5' end and polyadenylated at the 3' end. Here are three open reading frames (ORFs), designated ORF-1, ORF-2, and ORF-3, encoding eight viral proteins including structural proteins (viral protein 1 (VP1) and VP2). The mature virion contains 90 VP1 dimers with a diameter of 27-35 nm, assembled with icosahedral symmetry and arranged in such a fashion as to create hollows or cup-like structures on the virus surface. The Norovirus can be subdivided into seven genogroups (GI-VII), of which genogroups GI, GII, and GIV have been detected in humans, and can be further subdivided into more than 40 genotypes. GII noroviruses are responsible for approximately 80% to 90% of norovirus infections worldwide.

Pathogenesis

Noroviruses likely infect both enterocytes and intestinal immune cells, such as macrophages, dendritic cells (DCs), B cells, and T cells in gut-associated lymphoid tissues. An infection model for murine norovirus has been proposed that noroviruses can exploit microfold (M) cells to cross the intestinal epithelial barrier to infect immune cells in the intestine, before being trafficked to local lymph nodes and distal sites by DCs.

Cell-associated host glycans including terminal sialic acid and histo-blood group antigens (HBGAs) can facilitate the entry of norovirus and augment the attachment of the virus to cells. Viral receptors are essential to host molecules that specifically bind the virus particle, induce a conformational change in the virus, and actively promote viral entry. However, the human norovirus receptor remains unknown. Following receptor engagement, the virus is endocytosed where receptor binding triggers the minor capsid protein VP2 to form a membrane portal that may enable viral genome release in the cytosol. Eventually, new virus particles are produced and released from the infected cell via replication, translation, and assembly.

Fig.1 The composition and life cycle of human norovirus. (Graaf, 2016)

Epidemiology

Noroviruses affect people of all ages, causing sudden onset, often explosive. They are transmitted fecal-orally via multiple routes including person to person; environment to person; through contaminated food or water, which makes infection control a challenge. Noroviruses contaminate the surrounding environment where they can survive for prolonged periods on surfaces leading to fomite transmission. Norovirus poses particular challenges in closed or semi-closed settings like nurseries, schools, cruise ships, hospitals, or care homes where outbreaks are common, especially during the winter months.

Fig.2 Human norovirus tropism and transmission. (Graaf, 2017)

Symptoms

Norovirus infections cause acute gastroenteritis. The norovirus-associated disease is usually self-limiting, and symptoms such as diarrhea, vomiting, nausea, low-grade fever, and abdominal cramps, usually resolve within two to four days in healthy adults. Constitutional symptoms, including low-grade fever, generalized myalgias, malaise, headache, and chills, frequently occur. Although most infections result in full recovery, severe outcomes, such as hospitalization and death, occur, particularly among children ages less than 5 years, adults ages greater than 65 years, and immunocompromised hosts.

Prevention and Treatment

There is no specific medicine to treat people with norovirus illness. The mainstay of treatment is correcting the dehydration caused by norovirus diarrhea and vomiting using either reduced-osmolality oral-rehydration solutions (ORS) or if the patient is unable to tolerate ORS, intravenous rehydration. Principles of norovirus outbreak prevention and control include hand hygiene, exclusion of ill persons, and environmental disinfection.

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References

1. Graaf M.de.; et al. Human norovirus transmission and evolution in a changing world. Nature Reviews Microbiology. 2016, 14(7): 421-433.
2. Graaf M.de.; et al. Capturing norovirus transmission. Current Opinion in Virology. 2017, 22: 64-70.

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