Background The presence of a specific cellular receptor is thoughtto be necessary for susceptibility to viral infection. The erythrocyteP antigen is the cellular receptor for parvovirus B19. We hypothesizedthat the rare persons with the p phenotype, whose erythrocytesdo not have this receptor, would be naturally resistant to B19infection, which causes erythema infectiosum.
Methods Blood samples were collected from two populations incross-sectional studies. We determined the P antigen phenotypeof the red cells and tested plasma for anti-B19-specific antibodies.Bone marrow from donors of known P antigen phenotype was inoculatedwith parvovirus B19. Infectivity was measured by assays of erythroidprogenitor cells, dot blot analysis, and in situ hybridizationfor B19 DNA, and an immunofluorescence assay for viral-capsidproteins.
Results Of the 17 subjects with the p red-cell phenotype, whodid not have P antigen on their erythrocytes, none (0 of 11and 0 of 6) had serologic evidence of previous parvovirus B19infection. In contrast, the seropositivity rates in the twocontrol groups were 71 percent (53 of 75, P<0.001) and 47percent (32 of 68, P = 0.03). In vitro, bone marrow from donorswith the p phenotype maintained normal erythropoiesis despitevery high concentrations of virus, with no evidence of infectionof erythroid progenitor cells by parvovirus B19.
Conclusions People who do not have P antigen, which is the cellularreceptor for parvovirus B19, are naturally resistant to infectionwith this pathogen.
Source Information
From the Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, Md. (K.E.B., J.R.H., G.G., S.M.A., N.S.Y.); Mount Eaton Clinic, Mount Eaton, Ohio (E.D.L.); and the American Red Cross, Cleveland (P.M.).
Address reprint requests to Dr. Brown at Bldg. 10, Rm. 7C218, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892.
Kleinman, S. H., Glynn, S. A., Lee, T.-H., Tobler, L. H., Schlumpf, K. S., Todd, D. S., Qiao, H., Yu, M.-y. W., Busch, M. P., for the National Heart, Lung, and Blood Institute,
(2009). A linked donor-recipient study to evaluate parvovirus B19 transmission by blood component transfusion. Blood
114: 3677-3683
[Abstract][Full Text]
Rydell, G. E, Nilsson, J., Rodriguez-Diaz, J., Ruvoen-Clouet, N., Svensson, L., Le Pendu, J., Larson, G.
(2009). Human noroviruses recognize sialyl Lewis x neoglycoprotein. Glycobiology
19: 309-320
[Abstract][Full Text]
Pillet, S., Fichelson, S., Morinet, F., Young, N. S., Zhi, N., Wong, S.
(2008). Human B19 Erythrovirus In Vitro Replication: What's New?. J. Virol.
82: 8951-8953
[Full Text]
Lupescu, A., Bock, C.-T., Lang, P. A., Aberle, S., Kaiser, H., Kandolf, R., Lang, F.
(2006). Phospholipase A2 Activity-Dependent Stimulation of Ca2+ Entry by Human Parvovirus B19 Capsid Protein VP1. J. Virol.
80: 11370-11380
[Abstract][Full Text]
Stiehm, E. R.
(2006). Disease Versus Disease: How One Disease May Ameliorate Another. Pediatrics
117: 184-191
[Abstract][Full Text]
Corcoran, A., Doyle, S.
(2004). Advances in the biology, diagnosis and host-pathogen interactions of parvovirus B19. J Med Microbiol
53: 459-475
[Abstract][Full Text]
Young, N. S., Brown, K. E.
(2004). Parvovirus B19. NEJM
350: 586-597
[Full Text]
(2003). Acute severe anaemia in an elderly patient with hereditary sphaerocytosis. Postgrad. Med. J.
79: 246-247
[Full Text]
Hellberg, A., Poole, J., Olsson, M. L.
(2002). Molecular Basis of the Globoside-deficient Pk Blood Group Phenotype. IDENTIFICATION OF FOUR INACTIVATING MUTATIONS IN THE UDP-N-ACETYLGALACTOSAMINE: GLOBOTRIAOSYLCERAMIDE 3-beta -N-ACETYLGALACTOSAMINYLTRANSFERASE GENE. J. Biol. Chem.
277: 29455-29459
[Abstract][Full Text]
Heegaard, E. D., Brown, K. E.
(2002). Human Parvovirus B19. Clin. Microbiol. Rev.
15: 485-505
[Abstract][Full Text]
Chisaka, H., Morita, E., Murata, K., Ishii, N., Yaegashi, N., Okamura, K., Sugamura, K.
(2002). A transgenic mouse model for non-immune hydrops fetalis induced by the NS1 gene of human parvovirus B19. J. Gen. Virol.
83: 273-281
[Abstract][Full Text]
Blau, D. M., Turbide, C., Tremblay, M., Olson, M., Letourneau, S., Michaliszyn, E., Jothy, S., Holmes, K. V., Beauchemin, N.
(2001). Targeted Disruption of the Ceacam1 (MHVR) Gene Leads to Reduced Susceptibility of Mice to Mouse Hepatitis Virus Infection. J. Virol.
75: 8173-8186
[Abstract][Full Text]
Jordan, J. A., Huff, D., DeLoia, J. A.
(2001). Placental Cellular Immune Response in Women Infected with Human Parvovirus B19 during Pregnancy. CVI
8: 288-292
[Abstract][Full Text]
Kerr, J. R
(2000). Pathogenesis of human parvovirus B19 in rheumatic disease. Ann Rheum Dis
59: 672-683
[Full Text]
Jordan, J. A.
(2000). Comparison of a Baculovirus-Based VP2 Enzyme Immunoassay (EIA) to an Escherichia coli-Based VP1 EIA for Detection of Human Parvovirus B19 Immunoglobulin M and Immunoglobulin G in Sera of Pregnant Women. J. Clin. Microbiol.
38: 1472-1475
[Abstract][Full Text]
Schowengerdt, K. O., Ni, J., Denfield, S. W., Gajarski, R. J., Bowles, N. E., Rosenthal, G., Kearney, D. L., Price, J. K., Rogers, B. B., Schauer, G. M., Chinnock, R. E., Towbin, J. A.
(1997). Association of Parvovirus B19 Genome in Children With Myocarditis and Cardiac Allograft Rejection : Diagnosis Using the Polymerase Chain Reaction. Circulation
96: 3549-3554
[Abstract][Full Text]
Sedlik, C., Saron, M.-F., Sarraseca, J., Casal, I., Leclerc, C.
(1997). Recombinant parvovirus-like particles as an antigen carrier: A novel nonreplicative exogenous antigen to elicit protective antiviral cytotoxic T cells. Proc. Natl. Acad. Sci. USA
94: 7503-7508
[Abstract][Full Text]
Cohen, B.
(1995). Fortnightly Review: Parvovirus B19: an expanding spectrum of disease. BMJ
311: 1549-1552
[Abstract][Full Text]
Schachtner, S. K., Rome, J. J., Hoyt, R. F. Jr, Newman, K. D., Virmani, R., Dichek, D. A.
(1995). In Vivo Adenovirus-Mediated Gene Transfer Via the Pulmonary Artery of Rats. Circ. Res.
76: 701-709
[Abstract][Full Text]
Kerr, J. R., McQuaid, S., Coyle, P. V.
(1995). Expression of P Antigen in Parvovirus B19-Infected Bone Marrow. NEJM
332: 128-128
[Full Text]
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