PubMed · 985684
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Y Carcassonne, J A Gastaut. 1976-06-12. Pancytopenia and scleroderma.. https://doi.org/10.1136/bmj.1.6023.1446
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A-2 plaque virus (A2 virus) was originally isolated from the icteric-phase sera of US servicemen with viral hepatitis in the 1960s, but apart from a preliminary characterization little is known about the agent. We have now successfully cloned and sequenced the complete viral genome. A2 viral RNA consists of 7312 nucleotides, excluding the 62 nucleotide poly(A) tract at the 3' end, with one large open reading frame. Although clearly a member of the Picornaviridae, there is low homology to the available sequences, suggesting it is only loosely related to the classic rhino/enterovirus genus. In addition, there was no reactivity with group specific monoclonal antibody blends against polioviruses, enteroviruses 70 and 71, coxsackievirus B, and echoviruses. Two tamarins were inoculated with A2 virus to study viral pathogenesis. Both animals that received A2 virus became transiently viremic 1 week after the infection, as determined by RT-PCR, and they developed an antibody response to A2 virus. However, no physical signs or biochemical abnormalities, including elevated liver transaminases, were observed. In addition, no liver samples from patients with fulminant hepatitis (n = 7) or controls (n = 7) were positive for A2 viral RNA nor was anti-A2 neutralizing antibody detected in sera from hepatitis patients (n = 14), healthy laboratory donors (n = 14), or US blood donors (n = 33); however, most sera contained antibodies reactive with A2 virus proteins. These results suggest that A2 virus is a new member of the Picornaviridae but that its pathogenicity in nonhuman primates and association with human disease still need to be determined.
We utilize a model of platelet concentration kinetics and bone marrow production based on three terms (a constant loss term, a random loss term and a higher order loss term) to compare a hypoplastic bone marrow patient and a patient with Idiopathic Thrombocytopenic Purpura (ITP) for the same platelet concentration. We compare this model to published data and show that in many ITP patients there is an overall decrease in platelet production. However, for almost all cases of ITP there is an increase in peripheral platelet destruction, even in those cases where total bone marrow production is less than that in a normal individual or is severely depressed. We are able to graphically depict the variable contributions of decreased production and increased peripheral destruction in patients with ITP and hence give insight into their relative contributions in a given patient. We apply a unique feature of our model, the newly postulated destruction term proportional to the platelet concentration squared (the higher order loss term), to explain cases of antibody negative ITP. Application of our model to data on patients splenectomized as treatment for ITP shows promise in predicting which patients are likely to respond.