Parvovirus B19

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Parvovirus B19

NBME

NBME

Amino acid metabolism
Nitrogen and urea cycle
Citric acid cycle
Electron transport chain and oxidative phosphorylation
Gluconeogenesis
Glycogen metabolism
Glycolysis
Pentose phosphate pathway
Physiological changes during exercise
Cholesterol metabolism
Fatty acid oxidation
Fatty acid synthesis
Ketone body metabolism
Alkaptonuria
Cystinuria (NORD)
Hartnup disease
Homocystinuria
Maple syrup urine disease
Ornithine transcarbamylase deficiency
Phenylketonuria (NORD)
Essential fructosuria
Galactosemia
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Hereditary fructose intolerance
Lactose intolerance
Pyruvate dehydrogenase deficiency
Abetalipoproteinemia
Familial hypercholesterolemia
Hyperlipidemia
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Glycogen storage disease type I
Glycogen storage disease type II (NORD)
Glycogen storage disease type III
Glycogen storage disease type IV
Glycogen storage disease type V
Mucopolysaccharide storage disease type 1 (Hurler syndrome) (NORD)
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Fabry disease (NORD)
Gaucher disease (NORD)
Krabbe disease
Leukodystrophy
Metachromatic leukodystrophy (NORD)
Niemann-Pick disease type C
Niemann-Pick disease types A and B (NORD)
Tay-Sachs disease (NORD)
Cystinosis
Disorders of amino acid metabolism: Pathology review
Disorders of carbohydrate metabolism: Pathology review
Disorders of fatty acid metabolism: Pathology review
Dyslipidemias: Pathology review
Glycogen storage disorders: Pathology review
Lysosomal storage disorders: Pathology review
Carbohydrates and sugars
Fats and lipids
Proteins
Excess Vitamin A
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Vitamin D deficiency
Vitamin K deficiency
Kwashiorkor
Marasmus
Iodine deficiency
Zinc deficiency
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Folate (Vitamin B9) deficiency
Niacin (Vitamin B3) deficiency
Vitamin B12 deficiency
Vitamin C deficiency
Wernicke-Korsakoff syndrome
Fat-soluble vitamin deficiency and toxicity: Pathology review
Water-soluble vitamin deficiency and toxicity: B1-B7: Pathology review
Zinc deficiency and protein-energy malnutrition: Pathology review
Cell membrane
Cell signaling pathways
Cell-cell junctions
Cellular structure and function
Cytoskeleton and intracellular motility
Endocytosis and exocytosis
Extracellular matrix
Nernst equation
Osmosis
Resting membrane potential
Selective permeability of the cell membrane
Alport syndrome
Ehlers-Danlos syndrome
Marfan syndrome
Osteogenesis imperfecta
Primary ciliary dyskinesia
Adrenoleukodystrophy (NORD)
Zellweger spectrum disorders (NORD)
Cytoskeleton and elastin disorders: Pathology review
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DNA cloning
ELISA (Enzyme-linked immunosorbent assay)
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Polymerase chain reaction (PCR) and reverse-transcriptase PCR (RT-PCR)
Amino acids and protein folding
Cell cycle
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DNA mutations
DNA replication
DNA structure
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Gene regulation
Lac operon
Mitosis and meiosis
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Protein structure and synthesis
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Adenosine deaminase deficiency
Lesch-Nyhan syndrome
Orotic aciduria
Bloom syndrome
Fanconi anemia
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Xeroderma pigmentosum
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Purine and pyrimidine synthesis and metabolism disorders: Pathology review
Human development days 1-4
Human development days 4-7
Human development week 2
Human development week 3
Development of the digestive system and body cavities
Development of the fetal membranes
Development of the placenta
Development of the umbilical cord
Development of twins
Hedgehog signaling pathway
Ectoderm
Endoderm
Mesoderm
Development of the cardiovascular system
Fetal circulation
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Development of the eye
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Pharyngeal arches, pouches, and clefts
Development of the gastrointestinal system
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Development of the axial skeleton
Development of the limbs
Development of the muscular system
Development of the nervous system
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Evolution and natural selection
Hardy-Weinberg equilibrium
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Achondroplasia
Alagille syndrome (NORD)
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Parvovirus B19
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Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Cell wall synthesis inhibitors: Cephalosporins
Cell wall synthesis inhibitors: Penicillins
DNA synthesis inhibitors: Fluoroquinolones
DNA synthesis inhibitors: Metronidazole
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Introduction to pharmacology
Enzyme function
Drug administration and dosing regimens
Pharmacodynamics: Agonist, partial agonist and antagonist
Pharmacodynamics: Desensitization and tolerance
Pharmacodynamics: Drug-receptor interactions
Pharmacokinetics: Drug absorption and distribution
Pharmacokinetics: Drug elimination and clearance
Pharmacokinetics: Drug metabolism
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
Adrenergic antagonists: Presynaptic
Adrenergic receptors
Cholinergic receptors
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Muscarinic antagonists
Sympatholytics: Alpha-2 agonists
Sympathomimetics: Direct agonists
Selective serotonin reuptake inhibitors
Atypical antidepressants
Monoamine oxidase inhibitors
Serotonin and norepinephrine reuptake inhibitors
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Atypical antipsychotics
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Anticonvulsants and anxiolytics: Barbiturates
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Lithium
Nonbenzodiazepine anticonvulsants
Psychomotor stimulants
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Lipid-lowering medications: Fibrates
Lipid-lowering medications: Statins
Miscellaneous lipid-lowering medications
Positive inotropic medications
Adrenal hormone synthesis inhibitors
Mineralocorticoids and mineralocorticoid antagonists
Hypoglycemics: Insulin secretagogues
Insulins
Miscellaneous hypoglycemics
Hyperthyroidism medications
Hypothyroidism medications

Transcript

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Parvovirus B19 is the smallest known DNA animal virus, coming in at an itty bitty 18 to 28 nanometers in diameter.

In comparison, the average size of a single human red blood cell is a whopping 7200 nanometers!

While it’s mostly known for causing fifth disease, or “slapped cheek syndrome,” in children, parvovirus B19 can also affect adults and it can cause serious illness in individuals with pre-existing conditions like sickle-cell anemia and HIV.

Parvovirus B19 is part of the parvoviridae family.

It’s a single-stranded DNA virus surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces.

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

Parvovirus B19 is primarily transmitted by respiratory droplets when someone coughs or sneezes.

You can also catch it via an infected blood transfusion and a pregnant female can also transmit it through the placenta to her unborn child.

Now, although the virus first enters cells of the respiratory tract by binding to receptors on host cells, it doesn’t replicate in them.

Instead it keeps travelling through cells and into the circulatory system until it reaches bone marrow, where red blood cells are made, a process called erythropoiesis.

Once there, parvovirus B19 uses receptor-mediated endocytosis to enter erythroid progenitor cells, also called proerythroblasts, the early cells that eventually become red blood cells.

It then uses these cells’ DNA replication machinery in the nucleus to replicate its DNA and assemble new copies of the virus.

Why not simply replicate in cells of the respiratory system?

Well it turns out that Parvovirus B19 needs two things: it prefers to bind to a specific receptor, the P antigen, which is found in large numbers on proerythroblasts’ cell membrane and it needs cells that pass through the S phase of the cell cycle, which is the phase where cell DNA is replicated.

Since the body is constantly producing new red blood cells, there are always proerythroblasts going through the S phase at any given time.

As the virus replicates and matures, it produces a protein called non-structural protein 1 or NS1, which is toxic to human cells and causes apoptosis, or cell death.

This means that erythropoiesis breaks down, and fewer new red blood cells go into circulation as a result of parvovirus B19 infection.

But thankfully this is only temporary.

When the cell dies, it bursts open, releasing copies of the virus into the blood, also called viremia.

Our immune system detects the virus and starts producing specific immunoglobulin M and immunoglobulin G antibodies to fight the infection by forming immune complexes with the parvovirus B19 antigen.

For individuals with a functioning immune system, this typically happens between 10 and 14 days after first becoming infected with the virus.

Parvovirus B19 is most common in young children and those who live or work with them, like parents, siblings, and daycare workers.

Fetuses are at risk of parvovirus B19 if their pregnant mother has never had the virus in the past.

Immunocompromised individuals are also particularly at risk of chronic parvovirus B19 infection, since their immune system cannot mount an appropriate response to the virus.

The incubation period for parvovirus B19 - basically the period before viremia starts - is between 4 and 14 days, after which symptoms develop.

Flu-like symptoms - like a mild fever, headache, and aching muscles - are most common during viremia.

Once the immune response begins and the viremia ends, these symptoms go away and some individuals will then develop a rash and/or joint pain.

The rash appears as uniform redness of the cheeks, but not the area around the mouth, giving the classic fifth disease “slapped cheek” appearance.

A lace-like rash might also appear on the trunk and the limbs.

Joint pain and inflammation, or arthralgia and arthritis, linked to parvovirus B19 infection usually affects the small joints of the hands, wrists, feet, and knees, and are often symmetrical, meaning that the same joints on both sides of the body will be affected.

Children tend to get the rash whereas adults are more likely to develop joint pain, but it’s not exclusive to either group.

There are a few complications caused by parvovirus B19 infection.

The decreased red blood cell production can cause transient aplastic crisis in individuals who have underlying conditions like sickle cell anemia, hereditary spherocytosis, and thalassemia.

Key Takeaways

Parvovirus B19 is a single-strand DNA virus of the parvoviridae family, which is commonly known for causing diseases in the pediatric population, though it can also affect adults.

Parvovirus B19 is primarily spread by infected respiratory droplets and causes the Fifth disease or "slapped cheek syndrome" in children, characterized by a distinctive red rash on the cheeks. It can also cause redness and joint pain (arthritis) in adults. Parvovirus B19 can also affect the bone marrow, resulting in anemia secondary to decreased erythropoiesis. Anemia can even be worse in patients with pre-existing bone marrow stress, for example, sickle cell anemia or hereditary spherocytosis which can lead to an aplastic crisis.

Treatment for parvovirus B19 varies according to the symptoms, and can involve blood transfusion for transient aplastic crisis and hydrops fetalis and immune globulin intravenous therapy for chronic infections.