Parvovirus B19 for the hematologist
Parvovirus B19 for the hematologist
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血液学家的细小病毒 B19
DOI：
10.1002/ajh.2830390209
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发表时间：
1992
影响因子：
12.8
通讯作者：
J. Harris
中科院分区：
文献类型：
--
作者：
J. Harris
In 1948, the conventional wisdom and teachings concerning the pathophysiology of so-called hemolytic crises (or hyperhemolytic crises) was most abruptly and effectively turned upside down by the young Norwegian hematologist Paul A. Owren. On the basis of observations begun in 1942 that have withstood the test of time, Owren concluded that the “crises are not due to increased hemolysis, but to a sudden cessation in formation of the new red cells because of acute aplastic crisis in the blood forming tissue of the bone marrow” [l]. Sequential hematologic, biochemical, and morphologic assessments of six patients with hereditary spherocytosis firmly established the aplastic nature of the events, but Owren very perceptively went further to suggest that “they can be produced by some extraneous reason, possibly infective.” Parvovirus B19 is now known to be the causative agent responsible for the great majority of aplastic crises encountered in diverse chronic hemolytic anemias, compensated hemolytic processes, and some additional unusual immunologic or hematopoietically unstable situations. This review places major emphasis on the frequent and infrequent hematologic changes that take place and the consequences of these changes when encountered in various clinical situations in which B 19 infection has occurred. Since there are no parvoviruses labeled B1 through B 18, the very designation B 19 indicates an unusual mode of discovery. While searching for a possible viral agent of hepatitis B in sera from asymptomatic blood donors, Cossart et al. [2] in 1975 encountered a parvovirus-like particle in a sample encoded B19 and found specific antibodies to the particle in some 30% of adults. Demonstrably not the etiologic agent for hepatitis B, it was at that time not known to be causative of any human disease. Since then it has been shown to be a heat-stable, single-stranded, small (15-28 nm) DNA virus; to be of a single antigenic type with two or three capsid proteins and one or more noncapsid proteins; to lack an envelope; to contain approximately 5,000 bases that have been cloned and sequenced; to replicate independently of a “helper” virus; and to have palindromic sequences at its genomic ends that allow the DNA to fold back in “flip flop” hairpin turns during replication so that by the
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细小病毒 B19 诱导的体外人类巨核细胞生成扰动。
影响因子：
20.3
作者：
Srivastava,A;Bruno,E;Briddell,R;Cooper,R;Srivastava,C;vanBesien,K;Hoffman,R
通讯作者：
Hoffman,R
宫内输血治疗继发于人细小病毒 B19 感染的非免疫性胎儿水肿。
影响因子：
9.8
作者：
Sahakian,V;Weiner,CP;Naides,SJ;Williamson,RA;Scharosch,LL
通讯作者：
Scharosch,LL
细小病毒：感染和关节病。
DOI：
--
发表时间：
1987
期刊：
Rheumatic diseases clinics of North America
影响因子：
--
作者：
Smith,CA;Woolf,AD;Lenci,M
通讯作者：
Lenci,M
甲氨蝶呤对急性淋巴细胞白血病骨髓移植后复发的影响。
DOI：
--
发表时间：
1989
期刊：
Lancet (London, England)
影响因子：
--
作者：
通讯作者：
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