Noroviruses are a genetically diverse group of single stranded RNA, non-enveloped viruses belonging to the Caliciviridae family. Each virion contains a single-stranded RNA molecule in a round to hexagonal capsid, with icosahedral symmetry. The norovirus genus contains more than 40 different strains that are divided into 5 genogroups (I – IV) based on sequence similarity. The majority of infections in humans are cause by genogroups I and II. Norovirus was first recognized as a cause of gastroenteritis in 1968, when it was detected in stool samples collected from infected elementary school students and contacts during an outbreak in Norwalk, Ohio. Currently, Norovirus is considered the most common cause of epidemic nonbacterial gastroenteritis in the world.
Norovirus infection is usually self-limiting and characterized by nausea, vomiting, diarrhea, and abdominal pain. General lethargy, weakness, muscle aches, and low-grade fever may also occur. Noroviruses are transmitted person to person via direct contact, exposure to aerosols, or fecal–oral routes. The virus is extremely stable in the environment and highly resistant to extreme temperature and chemical disinfection. Moreover, noroviruses are highly contagious, with infection requiring fewer than 10 virions3,4. Incubation occurs for 1 to 2 days, and symptoms typically last 1 to 3 days (or longer in immunocompromised individuals). Shedding occurs for up to 3 weeks following infection. Risk factors include age, compromised immune status, and exposure to group settings. Outbreaks have been reported in health care facilities, schools, cruise ships, and military barracks. Viral transmission occurs year-round, with a higher incidence of disease in winter months in temperate climates.
NOROVIRUS IN TRANSPLANT PATIENTS
Norovirus infection can cause severe disease with significant morbidity and mortality after transplantation, in both SOT and HSCT (before and after engraftment). Due to the similar and nonspecific features of norovirus gastroenteritis and gut GVHD, differentiation requires laboratory testing. Misdiagnosis of norovirus as GVHD may lead to inappropriate augmentation with immunosuppressants, which has been shown to significantly worsen symptoms and adversely affect outcome1. Conversely, a reduction in immunosuppression may be critical to resolving infection1. Thus, norovirus should always be considered in the differential diagnosis of gut GVHD or graft rejection2. This allows for early diagnosis in these vulnerable patients and prevents escalation of immunosuppression for wrongly suspected GVHD or graft rejection2.
Real-time RT-PCR has become the method of choice to detect norovirus infection due to its superior sensitivity and specificity over electron microscopy and standard ELISA assays. However, designing an assay that accounts for all pathogenic strains in groups I and II is challenging due to a high level of genetic diversity. Viracor Eurofins' assay utilizes a multiple primer and probe target design to ensure comprehensive detection of norovirus groups I and II. Monitoring sequence repositories for new strains and refining our assay when necessary ensures we provide the most accurate detection possible.
Symptoms of norovirus infection are usually self-limited and resolve spontaneously within 24 to 48 hours. Oral fluid and electrolyte replacement is generally adequate for the treatment of norovirus infections. In the immunocompromised population, proper immunomodulation may be necessary to mitigate the effects of infection.
1. Kaufman SS, Chatterjee NK, Fuschino ME, et al. Calicivirus enteritis in an intestinal transplant recipient. Am J Transplant. 2003;3(6):764-8.
2. Roddie C, Paul JP, Benjamin R, et al. Allogeneic hematopoietic stem cell transplantation and norovirus gastroenteritis: a previously unrecognized cause of morbidity. Clin Infect Dis. 2009;49(7):1061-8.
3. Caul EO. Small round structured viruses: airborne transmission and hospital control. Lancet.1994;343(8908):1240-42.
4. Hutson AM, Atmar RL, Estes MK. Norovirus disease: changing epidemiology and host susceptibility factors. Trends Microbiol. 2004:12(6):279-87