Parvovirus B19

Last updated: September 12, 2024

Parvovirus B19

Block 2

Block 2

Pentose phosphate pathway
Diabetes mellitus
Disorders of carbohydrate metabolism: Pathology review
Amino acid metabolism
Disorders of amino acid metabolism: Pathology review
Dyslipidemias: Pathology review
Drug misuse, intoxication and withdrawal: Alcohol: Pathology review
Diabetes mellitus (Type 2): Clinical sciences
Fatty acid synthesis
Wernicke-Korsakoff syndrome
Alcohol-induced hepatitis: Clinical sciences
Diabetes mellitus: Clinical
Diabetes mellitus (Type 1): Clinical sciences
Fetal alcohol syndrome
Diabetes mellitus: Pathology review
Alcohol use disorder
Alcohol-associated liver disease
Enterococcus
Staphylococcus epidermidis
Mycobacterium tuberculosis (Tuberculosis)
Neisseria gonorrhoeae
Corynebacterium diphtheriae (Diphtheria)
Water-soluble vitamin deficiency and toxicity: B1-B7: Pathology review
Water-soluble vitamin deficiency and toxicity: B9, B12 and vitamin C: Pathology review
Vitamin D
Klebsiella pneumoniae
Vitamin B12 deficiency
Folate (Vitamin B9) deficiency
Streptococcus viridans
Clostridium perfringens
Chlamydia trachomatis
Staphylococcus saprophyticus
Staphylococcus aureus
Mycobacterium leprae
Clostridium botulinum (Botulism)
Bacillus anthracis (Anthrax)
Actinomyces israelii
Clostridium tetani (Tetanus)
Streptococcus agalactiae (Group B Strep)
Bacillus cereus (Food poisoning)
Listeria monocytogenes
Pseudomonas aeruginosa
Nocardia
Haemophilus influenzae
Neisseria meningitidis
Treponema pallidum (Syphilis)
Human papillomavirus
Herpes simplex virus
Neuraminidase inhibitors
Human herpesvirus 6 (Roseola)
Borrelia burgdorferi (Lyme disease)
Adenovirus
Yersinia pestis (Plague)
Rhinovirus
Rubella virus
Influenza virus
Mumps virus
Measles virus
Human herpesvirus 8 (Kaposi sarcoma)
Herpesvirus medications
Plasmodium species (Malaria)
Coxiella burnetii (Q fever)
Ehrlichia and Anaplasma
Bartonella henselae (Cat-scratch disease and Bacillary angiomatosis)
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Anthelmintic medications
Antimalarials
Trypanosoma cruzi (Chagas disease)
Francisella tularensis (Tularemia)
Candida
Anti-mite and louse medications
Miscellaneous antifungal medications
Azoles
Cytokines
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Hyper IgM syndrome
Leukocyte adhesion deficiency
Chronic granulomatous disease
X-linked agammaglobulinemia
Wound healing
Complement deficiency
Inflammation
Pulmonary corticosteroids and mast cell inhibitors
Selective immunoglobulin A deficiency
Necrosis and apoptosis
Ischemia
Wiskott-Aldrich syndrome
Immunodeficiencies: Clinical
Non-corticosteroid immunosuppressants and immunotherapies
Intrinsic hemolytic normocytic anemia: Pathology review
Heme synthesis disorders: Pathology review
Blood groups and transfusions
Macrocytic anemia: Pathology review
Cytomegalovirus infection after transplant (NORD)
Glucocorticoids
Blood products and transfusion: Clinical
Acute intermittent porphyria
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Aplastic anemia
Sideroblastic anemia
Microcytic anemia: Pathology review
Erythropoietin
Post-transplant lymphoproliferative disorders (NORD)
Platelet disorders: Pathology review
Thrombotic thrombocytopenic purpura
Neonatal jaundice: Clinical
Jaundice: Clinical
Mixed platelet and coagulation disorders: Pathology review
Von Willebrand disease
Immune thrombocytopenia
Hemolytic-uremic syndrome
Extrinsic hemolytic normocytic anemia: Pathology review
Jaundice
Iron deficiency anemia
Anemia: Clinical
Graft-versus-host disease
Iron deficiency anemia: Clinical sciences
Autoimmune hemolytic anemia
Severe chronic neutropenia (NORD)
Anemia of chronic disease: Year of the Zebra
Jaundice: Pathology review
Blood transfusion reactions and transplant rejection: Pathology review
Anemia of chronic disease
Non-hemolytic normocytic anemia: Pathology review
Antimetabolites: Sulfonamides and trimethoprim
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Fluoroquinolones
Protein synthesis inhibitors: Aminoglycosides
Nucleotide metabolism
Adenosine deaminase deficiency
Purine and pyrimidine synthesis and metabolism disorders: Pathology review
Gout
Gout and pseudogout: Pathology review
Lesch-Nyhan syndrome
Gout: Clinical sciences
Oncogenes and tumor suppressor genes
Anti-tumor antibiotics
Blood histology
DNA synthesis inhibitors: Metronidazole
Deep vein thrombosis
Disseminated intravascular coagulation
Factor V Leiden
Protein C deficiency
Protein S deficiency
Miscellaneous cell wall synthesis inhibitors
Miscellaneous protein synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Antithrombin III deficiency
Heparin-induced thrombocytopenia
Antiphospholipid syndrome
Hemophilia
Hemophilia: Year of the Zebra
Protease inhibitors
Nucleoside reverse transcriptase inhibitors (NRTIs)
Hepatitis medications
HIV and AIDS: Pathology review
Thrombosis syndromes (hypercoagulability): Pathology review
Mechanisms of antibiotic resistance
Coagulation disorders: Pathology review
Integrase and entry inhibitors
Leukemias: Pathology review
Myeloproliferative disorders: Pathology review
Lymphomas: Pathology review
Chronic leukemia
Acute leukemia
Non-Hodgkin lymphoma
Polycythemia vera (NORD)
Myelodysplastic syndromes
Hodgkin lymphoma
Essential thrombocythemia (NORD)
Waldenstrom macroglobulinemia
Multiple myeloma: Clinical sciences
Mastocytosis (NORD)
Plasma cell disorders: Pathology review
Plasma cell disorders: Clinical
Spleen histology
Myelofibrosis (NORD)
Lymphoma: Clinical
Varicella zoster virus
Coxsackievirus
Congenital TORCH infections: Pathology review
Streptococcus pyogenes (Group A Strep)
Lyme disease: Clinical sciences
Cortisol
Hematopoietic medications
Parvovirus B19
HIV (AIDS)
Zika virus

Transcript

Watch video only

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.