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Gastroenteric viruses:

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Presentation on theme: "Gastroenteric viruses:"— Presentation transcript:

1 Gastroenteric viruses:
Current status Jim Gray Professor of Clinical Virology, UEA & Consultant Virologist, NNUH

2 Viruses infecting the gut
Viruses associated with gastroenteritis rotaviruses caliciviruses noroviruses sapoviruses astroviruses adenoviruses 40, 41 Rotaviruses Adenoviruses Sapoviruses Astroviruses Noroviruses

3 Viruses infecting the gut
Presumptive gastroenteric viruses Torovirus Coronavirus Parvovirus: Bocavirus Picobirnavirus Aichi virus Torovirus Parvovirus Kobuvirus Coronavirus

4 Noroviruses Family : Caliciviridae
Non-enveloped small round structured viruses (27-32 nm diameter) Genome: pos sense ssRNA ~ 7.5kb Endemic and epidemic in the community The most common cause of outbreaks of gastroenteritis

5 Clinical manifestations
Norovirus Clinical manifestations Infects enterocytes of the duodenum and jejunum resulting in malabsorption and increased secretion Nausea - 79% Vomiting - 69% Diarrhoea - 66% Fever - 37% Chills - 32% Abdominal cramps - 30% Myalgias -26% Headache - 22% Sore throat - 18% Incubation period: 10-50h Duration of symptoms: 24-48h Excrete >106 particles/g or ml Infectious dose: 10 virus particles

6 Seasonality

7 Age distribution of norovirus infection in cases of gastroenteritis and age-matched controls (IID study: Amar et al)

8 Temperature inactivation of norovirus

9 Phylogenetic grouping among noroviruses
Fort Lauderdale Saint Cloud Alphatron Fayetteville Snow Mountain Kashiwa47 Melksham Hillingdon Erfurt 546 290/White River Idaho Fall Girlington GGIII VA97207 Hawaii 314/S19/94 Amsterdam Wortley/90 M7 Jena 273/Gwyned Leeds GGIV Limburg Sw43 Seacroft Newbury Mexico CH126 Toronto GGII Bristol Lordsdale Blakemore Chiba Koblenz Winchester MNV-1 Thistle Malta GGV 318/S05/95 DSV GGI Musgrove Stavanger WhiteRose Southampton Norwalk KY89 Hesse Sindlesham

10 Mechanisms for generating genomic and antigenic diversity
Noroviruses Genetic recombination during dual infection of a single cell Accumulation of point mutations Rotaviruses Genetic reassortment during dual infection of a single cell Genome rearrangement

11 Inter- and Intra-seasonal diversity of NoV genotypes during 2003 to Early, mid and late season outbreaks characterised. Highlights the fitness of GII-4 to infect the human population against a background of herd immunity

12 GII-4 variants: September 2003 to September 2007

13 Calicivirus structure
Norovirus [Norwalk] Norovirus [Grimsby] Sapovirus Vesivirus (SMSV) Protruding domain

14 2002/03 epidemic Lack of short-term herd immunity to a new variant
Autumn Winter Spring Summer GII4 variant is selected, out of season outbreaks occur, becomes epidemic Normal winter season Narrowing diversity: GII4 predominates GII4 variants emerge Return to normal season, wide diversity at the beginning, narrowing as season progresses. Normal summer activity Lack of short-term herd immunity to a new variant Epidemic winter season Unusual summer activity 2002/03 epidemic

15 Structural changes on the P2 domain between GII-4 variants
Pre-2002 2002 epidemic Structural changes on the P2 domain between GII-4 variants Electrostatic surface Molecular surface Monoclonal antibodies raised against the pre-2002 GII-4 strains do not react with the 2002 GII-4 strain and vice versa. Pre-2002 2002


17 Outbreak tracking Gene encoding the P2 domain
Similarity among NoV GII-4 outbreaks reported between December/06 and September/07 from different regions of England and Wales. NE = North East, NW = North West, SW = South West. Gene encoding the P2 domain

18 Phylogenetic analysis of NNUH strains
revealed 8 genetic clusters of NoV were introduced into the hospital in the 2009/ 2010 NoV season

19 NNUH NoV Outbreaks, 2010 Sequencing the hypervariable region encoding the P2 domain revealed 8 distinct genetic clusters circulating or co-circulating in the hospital.

20 23d 20d 34d

21 Environmental NoV sampling
At the conclusion of the outbreak and after clinical cleaning Cleansers/ disinfectants Equipment Nurses station Bedside environment Furniture, fixtures and fittings

22 Environmental norovirus sampling
6 wards post-cleaning



25 Environmental contamination
Norovirus: Environmental contamination Two wards re-cleaned and re-sampled

26 Environmental monitoring: 2011
surveillance outbreak

27 Risk of norovirus spread within the hospital environment
Reduced risk of spread Increased risk of spread Virus variant/ mutant Projectile Ward closure vomiting Low infectious dose Risk of norovirus spread within the hospital environment Cohort nursing High attack rate Patients Adherence to hand washing Staff affected practices, soap and water Potential vaccines Reduced staffing Also consider: Bed occupancy rates Built environment Infection control procedures Admission Units Elbow/automatic Soft furnishings taps on contaminated handbasins Hand contact surfaces contaminated Single rooms Environment with en suite Unrestricted visiting/ admissions Surface finishes allowing decontamination Open wards

28 Keys to the success of gastroenteric viruses
Low infectious dose ~ virus particles Noroviruses 107 particles per gram/ml Rotaviruses 1011 particles per gram/ml Stability in the environment Norovirus survives up to 80oC Rotavirus survives in the environment for months Protected by the matrix – faeces and vomit, which also inactivate chlorine-based disinfectants Non-enveloped viruses – resistant to many disinfectants and alcohol Short term immunity ~ 6 months 16% of the population excrete NoV in the absence of symptoms 14% of the population excrete rotavirus in the absence of symptoms

29 Multiple routes of transmission - person to person contact, through
ingestion of contaminated water or food or by contact with contaminated environmental surfaces RNA genome replication results in the accumulation of point mutations Segmented rotavirus genome replication results in reassortment Dual infections can result in recombination or reassortment Rotaviruses are associated with zoonotic infection Hospital-acquired infections are predominantly associated with GII-4 There are multiple introductions into hospitals, of variants of GII-4, throughout the NoV season and many rotavirus strains co-circulate in the human population Antibody-escape mutants and rotavirus reassortants are selected and driven by herd immunity resulting in epidemics in an immunologically naive population

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