Two types of viruses have been examined for their role in the etiology of bone marow failure in animals and man. The first, the Parvoviridae, are the smallest DNA containing animal viruses. The B19 human parvovirus causes selective erythroid aplasia in individuals with underlying hemolysis. Feline panleukopenia virus is a common agent of cat disease and capable of causing a true pancytopenia and bone marrow aplasia. The human parvovirus was discovered only 10 years ago and a major stumbling block to its investigation has been an adequate in vitro cell culture system. Using suspension cultures of erythroid bone marrow cells from patients with sickle cell disease, we have achieved the first propagation of the B19 agent. This virus is highly selective for erythroid in comparison to myeloid progenitor cells. Events associated with the replication, transcription, and protein production of this virus have been elucidated in detail. The feline virus, in contrast, is less selective in vitro, with a strong inhibitory action on the proliferation of both erythroid and myeloid cells. This virus can also be propagated in suspension cultures of cat bone marrow. Studies of the cat retrovirus, feline leukemia virus, have shown that its effect on in vitro colony formation by cat cells is minimal. In animal studies, feline leukemia virus had marginal effects on hematopoiesis. Extensive studies of human patients of a possible role for a retrovirus in human aplastic anemia had failed to reveal consistent reverse transcriptase activity or retroviral particles by electron microscopy.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Intramural Research (Z01)
Project #
1Z01HL002319-03
Application #
3966621
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
3
Fiscal Year
1986
Total Cost
Indirect Cost
Name
U.S. National Heart Lung and Blood Inst
Department
Type
DUNS #
City
State
Country
United States
Zip Code
Wong, Susan; Brown, Kevin E (2006) Development of an improved method of detection of infectious parvovirus B19. J Clin Virol 35:407-13
Lu, Jun; Zhi, Ning; Wong, Susan et al. (2006) Activation of synoviocytes by the secreted phospholipase A2 motif in the VP1-unique region of parvovirus B19 minor capsid protein. J Infect Dis 193:582-90
Gergely Jr, Peter; Pullmann, Rudolf; Stancato, Christina et al. (2005) Increased prevalence of transfusion-transmitted virus and cross-reactivity with immunodominant epitopes of the HRES-1/p28 endogenous retroviral autoantigen in patients with systemic lupus erythematosus. Clin Immunol 116:124-34
Prikhod'ko, Grigori G; Vasilyeva, Irina; Reyes, Herbert et al. (2005) Evaluation of a new LightCycler reverse transcription-polymerase chain reaction infectivity assay for detection of human parvovirus B19 in dry-heat inactivation studies. Transfusion 45:1011-9
Mamyrova, Gulnara; Rider, Lisa G; Haagenson, Laura et al. (2005) Parvovirus B19 and onset of juvenile dermatomyositis. JAMA 294:2170-1
Brown, K E (2004) Variants of B19. Dev Biol (Basel) 118:71-7
Brown, Kevin E (2004) Detection and quantitation of parvovirus B19. J Clin Virol 31:1-4
Vashisht, Kapil; Faaberg, Kay S; Aber, Amanda L et al. (2004) Splice junction map of simian parvovirus transcripts. J Virol 78:10911-9
Liu, Zhengwen; Qiu, Jianming; Cheng, Fang et al. (2004) Comparison of the transcription profile of simian parvovirus with that of the human erythrovirus B19 reveals a number of unique features. J Virol 78:12929-39
Zhi, Ning; Zadori, Zoltan; Brown, Kevin E et al. (2004) Construction and sequencing of an infectious clone of the human parvovirus B19. Virology 318:142-52

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