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| Credit CDC |
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Noroviruses - which are often mistakenly called `stomach flu’ - are single-stranded RNA viruses that (like influenza) are able to evolve rapidly. Victims usually experience nausea, frequent vomiting & diarrhea, and stomach pain – and may also suffer from headache, fever, and body aches.
While most people recover after 24-48 hours of misery, more than two hundred thousand people die each year from Norovirus infection (cite) around the world.Since 2002 GII.4 strains (genogroup II genotype 4) have caused the majority of outbreaks globally, and we typically see a new dominant norovirus strain emerge every few years.
In 2009, we saw the emergence of the New Orleans strain of GII.4, while in 2012, the Sydney strain appeared. Recently, non-GII.4 strains (i.e. GII.17 and GII.2), have emerged and replaced GII.4 strains in several Asian countries (cite CDC)
The `standard’ mode of norovirus transmission is considered to be the fecal-oral route, but limited airborne transmission is increasingly viewed as an important factor as well (see CID Study: Airborne Norovirus In Healthcare Facilities).
Not all norovirus strains are created equal, and some are more virulent than others. When a particularly `fit' and virulent strain emerges, we can see it spread rapidly around the globe as a pandemic strain.All of which brings us to a new Dispatch, published yesterday in the EID Journal, that describes the emergence of a new recombinant Norovirus strain (GII.P16-GII.2) with high infectivity and pandemic potential.
Volume 25, Number 1—January 2019
Dispatch
Higher Viral Load of Emerging Norovirus GII.P16-GII.2 than Pandemic GII.4 and Epidemic GII.17, Hong Kong, China
Sarah K.C. Cheung, Kirsty Kwok, Lin-Yao Zhang, Kirran N. Mohammad, Grace C.Y. Lui, Nelson Lee1, E. Anthony S. Nelson, Raymond W.M. Lai, Ting F. Leung, Paul K.S. Chan, and Martin Chi-Wai Chan
Abstract
We compared viral load of emerging recombinant norovirus GII.P16-GII.2 with those for pandemic GII.Pe-GII.4 and epidemic GII.P17-GII.17 genotypes among inpatients in Hong Kong. Viral load of GII.P16-GII.2 was higher than those for other genotypes in different age groups.
GII.P16-GII.2 is as replication competent as the pandemic genotype, explaining its high transmissibility and widespread circulation.
Norovirus, the leading cause of acute gastroenteritis, evolves through mutation and recombination (1). Noroviruses are named by dual nomenclature using the genotype of RNA-dependent RNA-polymerase (RdRp) and major capsid protein (VP1) (2).
Recently, 2 recombinant noroviruses carrying RdRp genotype GII.P16 with 2 other VP1 genotypes emerged and spread worldwide: GII.P16-GII.4 in the United States and Europe and GII.P16-GII.2 in Europe and Asia in 2016 (3–5). GII.P16 actively recombined with >8 capsid genotypes (6–8) and may have pandemic potential and lead to a change in norovirus epidemiology.
Phylogenetic and sequence analyses indicated that recent GII.P16-GII.2 had no remarkable change on capsid protein compared with earlier GII.2 strains, suggesting that factors other than immune escape or change in affinity for histo–blood group antigens (i.e., host susceptibility) may play a role in the recent reemergence (6).
We compared the viral load of norovirus GII.P16-GII.2 with pandemic GII.Pe-GII.4 and epidemic GII.P17-GII.17 in a cohort of hospitalized patients in Hong Kong over a 5-year period. Our findings may explain, at least in part, the high transmissibility and widespread circulation of GII.P16-GII.2.(SNIP)
Conclusions
We found that GII.P16-GII.2 shed in higher amounts than pandemic GII.Pe-GII.4 in different age groups. This new strain, which is as replication competent as pandemic GII.Pe-GII.4, may cause severe gastroenteritis and lead to poor clinical outcomes (13).
Our findings imply that the absence of prior exposure to this newly emerged strain may result in the delayed immune response and viral clearance in most populations. Immune naivety may be attributed to equally high viral loads of GII.P16-GII.2 and GII.Pe-GII.4 in children (1), providing a virologic explanation for the recent upsurge in the number of outbreaks caused by GII.P16-GII.2 in nursery schools, kindergartens, and elementary schools in Japan in the winter of 2016–17 (14).
That report found a higher reproductive number of GII.P16-GII.2 compared with the previous 4 seasons, during which other norovirus genotypes, such as GII.Pe-GII.4, predominated, a result consistent with our findings of prominent viral load of GII.P16-GII.2 in children.
Our findings agree with a previous phylogenetic analysis, which showed that the capsid of GII.P16-GII.2 was closely related to earlier GII.2 strains, when it was speculated that its recent emergence may be attributable to high replication efficiency (6). Furthermore, recombinants carrying GII.P16, including GII.P16-GII.4 and GII.P16-GII.2, have caused >60% of norovirus outbreaks in 2016 and 2017 in the United States (CaliciNet, https://www.cdc.gov/norovirus/reporting/calicinet/data.html).
We propose that this time, rather than acquiring a new capsid variant, a new polymerase variant GII.P16 may be affecting norovirus epidemiology worldwide. This emerging and actively recombining norovirus polymerase genotype GII.P16 is highly transmissible, with pandemic risk. The mechanism behind replication difference among norovirus genotypes needs to be further studied by a virus cultivation system such as human intestinal enteroids (15).
Our study has limitations. First, we did not evaluate the viral load of GII.P16-GII.4 because this recombinant was sporadically (n = 21; 1.7%) observed. Second, we did not perform multivariate analysis to control for other confounding factors such as time from symptom onset to sample collection (viral load decreases over time) because of incomplete information, which may have introduced bias.
In summary, our result show that the emerging recombinant norovirus GII.P16-GII.2 is as replication competent as pandemic genotypes, which explains its high transmissibility and widespread circulation. Norovirus GII.P16-GII.2 has pandemic potential.
Noroviruses are the bane of cruise ships, schools, and hospitals - anywhere large numbers of people congregate. While the illness usually runs its course in 1 to 3 (very long) days - among those who are aged or infirmed -the virus can take a heavy toll.
According to the CDC, in the United Sates each year the norovirus:
Globally, particularly in developing countries, Norovirus infections may claim 50,000 children's lives each year (cite).
- causes 19 to 21 million cases of acute gastroenteritis
- leads to 1.7 to 1.9 million outpatient visits and 400,000 emergency department visits, primarily in young children
- contributes to about 56,000 to 71,000 hospitalizations and 570 to 800 deaths, mostly among young children and the elderly.
One of the keys to prevention is good hand hygiene, unfortunately, unlike with many other bacteria and viruses, alcohol gel doesn’t do a particularly good job of killing the virus (see CMAJ: Hand Sanitizers May Be `Suboptimal’ For Preventing Norovirus).
The CDC offers this advice to help prevent the spread of this virus.
