Parvovirus Flashcards
B19 structure & classification
Family: Parvoviridae
Subfamily: parvovirinae
Eight genera, of which five include human pathogens: Erythroparvovirus (B19), Dependoparvovirus (adeno-associated viruses), Protoparvovirus (human bufavirus), Bocaparvovirus (Human bocaviruses), and Tetraparvovirus (Human parvovirus 4) along with Aveparvovirus, Copiparvovirus, and Amdoparvovirus
There are three genotypes within the Erythroparvovirus genus. Parvovirus B19 is the predominant parvovirus pathogen in humans and the prototype genotype 1 strain. Genotype 2 is comprised of A6 and LaLi, while genotype 3 includes V9 and V9-related isolates
NON enveloped ssDNA
Encodes 2 structural proteins - VP1 & VP2, 3 non-structural proteins - biggest is NS1
B19 receptor & tropism
Receptor: P blood group antigen, also known as globoside, which is found in high concentrations on red blood cells and their precursors
Tropism: Productive infections occur only in CD36 human erythroid progenitor cells. To date, erythroid precursor cells of the colony and burst forming units (E-CFU and E-BFU) are the only cells known to support a fully productive infection with parvovirus B19
B19 viral replication location
NUCLEUS
B19 IgM & IgG timing
Parvovirus B19-specific IgM antibodies to both VP1 and VP2 proteins develop soon after infection, can be detected at days 10 through 12, and can persist for up to five months;
specific IgG antibodies to the viral capsid proteins are detectable about 15 days postinfection and persist long term
B19 rash pathogenesis
Although the pathogenesis of rash and arthropathy associated with parvovirus B19 infection is not clear, both symptoms generally coincide with measurable serum antibody production and are thus presumed to be at least partially immune mediated. The role of serum antibodies in rash development is also suggested by the appearance of rash after IVIG administration to immunodeficient patients with chronic infection
Direct viral effects may also be involved in the pathogenesis of these symptoms. Parvovirus B19 DNA and antigen have been detected in a skin biopsy specimen from a patient with erythema infectiosum, suggesting that direct infection of epidermal cells may also contribute to rash development
B19 clinical syndromes - 5 types
●Fifth disease/erythema infectiosum in children
●Arthropathy
●Transient aplastic crisis in those with chronic hemolytic disorders
●Fetal infection leading to non-immune hydrops fetalis, intrauterine fetal death, miscarriage, or cardiomyopathy
●Pure red blood cell aplasia in immunocompromised individuals
B19 diagnostics
Serology is the mainstay.
Because the nonhematologic manifestations of parvovirus B19 infection are thought to be mediated by the immune response, antibodies are typically detectable at the time these symptoms appear.
Parvovirus B19-specific IgM antibodies to both VP1 and VP2 proteins develop soon after infection, can be detected at days 10 through 12 of exposure, and can persist for up to five months; specific IgG antibodies to the viral capsid proteins are detectable about 15 days 15 days postinfection and persist long term.
Detection of parvovirus B19 DNA using polymerase chain reaction (PCR) is generally not useful for the diagnosis of acute infection in immunocompetent hosts without aplasia. By the time symptoms arise, viremia has generally resolved, so a negative PCR test does not rule out acute parvovirus B19 infection. Furthermore, low levels of parvovirus B19 DNA may be present in serum and other body fluids or tissues for months to years following infection, even in healthy patients, so detectable DNA by PCR does not necessarily indicate acute infection. Thus, serology remains the diagnostic method of choice in such patients.
Most of these oligonucleotides were designed to detect genotype 1 DNA, but not genotypes 2 or 3, which can lead to failure in detecting non-genotype 1 erythrovirus infections [4,5,92,93]. Some PCR assays can quantitate parvovirus B19 DNA for all three genotypes [94]. To ensure that the parvovirus B19-specific NAAT being used in the lab can detect all three genotypes, the World Health Organization (WHO) International Reference Panel can be included as part of the testing
B19 therapeutics
In patients with solid organ transplant or other non-HIV causes of immunosuppression, we suggest 400 mg/kg/day of IVIG for five consecutive days, along with reducing or minimizing immunosuppressive therapy, if possible
For patients with refractory anemia despite IVIG, foscarnet may be an option, although evidence is scarce.
NO VACCINES
B19 infectious period
10 days before to day of onset of rash
B19 incubation
4-21 days
