Disease relevance of HUNK

• People who do not have P antigen, which is the cellular receptor for parvovirus B19, are naturally resistant to infection with this pathogen [1].
• We hypothesized that the rare persons with the p phenotype, whose erythrocytes do not have this receptor, would be naturally resistant to B19 infection, which causes erythema infectiosum [1].
• Treatment of parvovirus B19-associated polyarteritis nodosa with intravenous immune globulin [2].
• Parvovirus B19 as the cause of a syndrome resembling Lyme arthritis in adults [3].
• Capsids of the B19 parvovirus are composed of major (VP2; 58 kD) and minor (VP1; 83 kD) structural proteins [4].

Psychiatry related information on HUNK

• New LightCycler PCR for rapid and sensitive quantification of parvovirus B19 DNA guides therapeutic decision-making in relapsing infections [5].
• OBJECTIVES: to clarify the approximation of the frequency of B19-related nonimmune hydrops fetalis (NIHF), and to know the critical period during which maternal infection led to NIHF [6].
• Human parvovirus B19 antibodies in infantile autism [7].
• We describe a young man who had AIDS complicated by parvovirus B19 infection and RBC aplasia and who developed a painless, progressive dyspraxia of the left arm and an expressive dysphasia 4 weeks after commencing effective HAART [8].

High impact information on HUNK

• Expression of P antigen in parvovirus B19-infected bone marrow [9].
• Infectivity was measured by assays of erythroid progenitor cells, dot blot analysis, and in situ hybridization for B19 DNA, and an immunofluorescence assay for viral-capsid proteins [1].
• Resistance to parvovirus B19 infection due to lack of virus receptor (erythrocyte P antigen) [1].
• In vitro, bone marrow from donors with the p phenotype maintained normal erythropoiesis despite very high concentrations of virus, with no evidence of infection of erythroid progenitor cells by parvovirus B19 [1].
• Bone marrow from donors of known P antigen phenotype was inoculated with parvovirus B19 [1].

Chemical compound and disease context of HUNK

• Patients with parvovirus B19 infection had significantly lower bilirubin concentrations than age-matched patients with FH due to hepatitis A (nine) or other causes (nine) (poisoning with amanita excluded) [10].
• In contrast, primary human erythroid progenitor cells express high levels of both P antigen and alpha 5 beta 1 integrins and allow beta1 integrin-mediated entry of parvovirus B19 [11].
• The neurotransmitter 5-HT alters growth cone motility and neurite elongation in neuron B19, isolated from the buccal ganglion of Helisoma trivolvis (Haydon et al., 1984) [12].
• Acute parvovirus B19-induced pancytopenia in the setting of methotrexate therapy for rheumatoid arthritis [13].
• The immunohistological detection of parvovirus B19 in formalin-fixed, paraffin-embedded tissues has not previously been reported, and definitive diagnosis of infection in such specimens has relied on the use of specialized DNA hybridization and amplification techniques [14].

Biological context of HUNK

• We have isolated a 5.0-kb full-length cDNA clone that contains the 714-amino-acid open reading frame encoding Hunk [15].
• During fetal development and in the adult mouse, Hunk mRNA expression is developmentally regulated and tissue-specific [15].
• This culture system allowed study at a molecular level of events associated with the B19 life cycle [16].
• B19 parvovirus has been shown to persist in some immunocompromised patients, and treatment with specific antibodies can lead to decreased quantities of circulating virus and hematologic improvement [17].
• Distinctive neuron-specific (B5 versus B19) and state-specific (growing versus non-growing) differences in calcium homeostasis were observed in cultured identified Helisoma neurons [18].

Anatomical context of HUNK

• We previously identified a novel protein kinase, Hunk, by means of a degenerate PCR screen designed to isolate kinases expressed in the murine mammary gland [15].
• ACh release was reliably detected from neurites and growth cones of cholinergic neuron B5, but not neuron B19, as early as 3 s after contact with novel target neurons [19].
• However, an even higher proportion of the non-arthropathy controls were positive for B19 DNA in synovial membranes (13 [48%] of 27) [20].
• Parvovirus B19-infected erythroblasts in fetal cord blood [21].
• FINDINGS: All samples of synovial fluid, bone marrow, and blood were negative for B19 DNA [20].

Associations of HUNK with chemical compounds

• Analysis of this cDNA reveals that Hunk is most closely related to the SNF1 family of serine/threonine kinases and contains a newly described SNF1 homology domain [15].
• When applied simultaneously with serotonin, ACh prevents the inhibition of Helisoma neuron B19 neurite elongation that would occur in response to application of 5-HT alone [22].
• Acetylcholine-sensitive assay cells were micromanipulated into contact with B19 somata to assess its secretory state [23].
• Fura-2 studies revealed that A23187 induced a transient rise in intracellular calcium in growing neurons B5 but a sustained rise in growing neurons B19 [18].
• Photolysis of a calcium cage, DM-nitrophen, accelerated the frequency of synaptic currents in muscle-contacted, but not novel neuron-contacted, B19 somata [23].

Analytical, diagnostic and therapeutic context of HUNK

• Moreover, in situ hybridization analysis reveals that Hunk expression is restricted to subsets of cells within a variety of organs in the adult mouse [15].
• Replication of the B19 parvovirus in human bone marrow cell cultures [16].
• Serologic evidence of B19 infection was determined by using an enzyme-linked immunosorbent assay [24].
• Of the school and day-care personnel, 58% had evidence of previous B19 infection [24].
• Although human B19 parvovirus infection has been clearly associated with a number of distinct syndromes (including severe anemia, abortion, and arthritis), detailed knowledge of its pathogenesis has been hindered by the lack of a suitable animal model [25].

References