Norovirus

Block 1.5 Digestion & Defence I

Block 1.5 Digestion & Defence I

Anatomy clinical correlates: Viscera of the neck
Anatomy of the salivary glands
Anatomy of the oral cavity
Anatomy of the pharynx and esophagus
Chewing and swallowing
Esophageal motility
Esophagus histology
Gastrointestinal system: Structure and function
Hunger and satiety
Anatomy of the abdominal viscera: Esophagus and stomach
Enteric nervous system
Gastric motility
Gastroesophageal reflux disease (GERD)
Gastrointestinal hormones
Gastrointestinal system anatomy and physiology
Stomach histology
Anatomy of the abdominal viscera: Liver, biliary ducts and gallbladder
Bile secretion and enterohepatic circulation
Biliary colic
Gallbladder histology
Liver anatomy and physiology
Liver histology
Chronic pancreatitis
Pancreas histology
Pancreatic secretion
Colon histology
Lactose intolerance
Vitamins and minerals
Carbohydrates and sugars
Fats and lipids
Proteins
Blood components
Inflammation
Introduction to the immune system
Wound healing
Complement system
Cytokines
Innate immune system
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
MHC class I and MHC class II molecules
T-cell activation
Vaccinations
Antibody classes
B- and T-cell memory
B-cell activation and differentiation
Giardia lamblia
Contracting the immune response and peripheral tolerance
Bacterial structure and functions
Cell wall synthesis inhibitors: Penicillins
Mechanisms of antibiotic resistance
Prebiotics and probiotics
Epstein-Barr virus (Infectious mononucleosis)
Hepatitis
Hepatitis B and Hepatitis D virus
Hepatitis A and Hepatitis E virus
Hepatitis C virus
Jaundice
Viral structure and functions
Bacillus cereus (Food poisoning)
Campylobacter jejuni
Diarrhea: Clinical
Escherichia coli
Vibrio cholerae (Cholera)
Appendicitis
Glycolysis
Citric acid cycle
Electron transport chain and oxidative phosphorylation
Pentose phosphate pathway
Gluconeogenesis
Fatty acid oxidation
Fatty acid synthesis
Protein structure and synthesis
Amino acid metabolism
Nitrogen and urea cycle
Nucleotide metabolism
Physiological changes during exercise
Ketone body metabolism
Glycogen metabolism
Metabolic acidosis
Approach to diarrhea (pediatrics): Clinical sciences
Rotavirus
Norovirus
Salmonella (non-typhoidal)
VDJ rearrangement

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You’ve probably had the stomach flu, at least once, right? Chances are, it was due to norovirus, which is one of the most common causes of viral gastroenteritis.

Sometimes it’s also called the Norwalk virus, after the town in Ohio where a big outbreak in 1968 allowed scientists to isolate the virus.

There are several genogroups of norovirus, but only groups I, II, and IV can cause disease in humans.

Norovirus is part of the caliciviridae family of viruses.

They are naked viruses surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces.

And they’re “naked” because the capsid isn’t covered by a lipid membrane.

They’re also single strand RNA viruses.

This means that their RNA is actually mRNA - and the host cell ribosomes use this mRNA to make only long polyprotein chain, which is then broken into smaller pieces by viral proteases.

This all happens in the cytoplasm of the host cell, since that’s where ribosomes are found, and results in several viral proteins.

The exact role of each specific viral protein is still a bit of a mystery, but we do know that they mainly affect the small intestine.

The small intestine has lots of tiny ridges and grooves, each of which projects little finger-like fibers called villi.

And in turn, each villus is covered in teeny tiny little microvilli. This is called the brush border.

All of this gives the small intestines plenty of surface area to absorb nutrients.

Norovirus blunts the villi and shortens microvilli, and this disrupts the ability of the brush border to absorb certain nutrients, specifically fat and a simple sugar called D-xylose.

It also lowers the activity of alkaline phosphatase and trehalase, which are digestive enzymes produced by brush border cells.

Under a microscope, intestinal cells infected by Norovirus have an intact mucosa and epithelium, but there are a lot of lymphocytes in the lamina propria layer of the mucosa.

Intercellular spaces are also larger, because tight junction proteins that keep the cells together are damaged.

Norovirus is very contagious and it’s primarily transmitted from person to person via the fecal-oral route.

In other words, you catch it by ingesting stool particles of someone who is sick.

This can happen if infected stool ends up in the water supply or on agricultural fields, if flies land on it, and transfer stool particles to other places, or by touching contaminated surfaces.

You can summarize it as the four Fs: fluids, fields, flies, and fingers.

Summary

Norovirus is a single-strand RNA virus of the calicivirus family, which is known to cause a very contagious form of gastroenteritis. It is transmitted via the fecal-oral route and droplets of vomit. Affected people commonly present with diarrhea, vomiting, and abdominal pain. Other symptoms may include fever, headache, and muscle aches.

Treatment focuses on supportive management, with the administration of oral rehydration solutions or IV fluids. Its spread can be limited by applying preventive measures, which are proper handwashing, sanitizing surfaces, and having effective water and sanitation systems.