|
|
 Previous Article | Table of Contents | Next Article 
Blood, Vol. 93 No. 9 (May 1), 1999:
pp. 3116-3119
Impairment of Plasmodium falciparum Growth in Thalassemic Red
Blood Cells: Further Evidence by Using Biotin Labeling and Flow
Cytometry
Kovit Pattanapanyasat,
Kosol Yongvanitchit,
Pongsri Tongtawe,
Kalaya Tachavanich,
Wanchai Wanachiwanawin,
Suthat Fucharoen, and
Douglas S. Walsh
From the Center of Excellence for Flow Cytometry, Office for Research
and Development; the Department of Pediatrics, the Department of
Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University,
Bangkok, Thailand; the Department of Immunology and Medicine, US Army
Medical Component, Armed Forces Research Institute of Medical Sciences
(AFRIMS), Bangkok, Thailand.
Certain red blood cell (RBC) disorders, including thalassemia, have
been associated with an innate protection against malaria infection.
However, many in vitro correlative studies have been inconclusive. To
better understand the relationship between human RBCs with thalassemia
hemoglobinopathies and susceptibility to in vitro infection, we used an
in vitro coculture system that involved biotin labeling and flow
cytometry to study the ability of normal and variant RBC populations in
supporting the growth of Plasmodium falciparum malaria
parasites. Results showed that both normal and thalassemic RBCs were
susceptible to P falciparum invasion, but the parasite
multiplication rates were significantly reduced in the thalassemic RBC
populations. The growth inhibition was especially marked in RBCs from
 -thalassemia patients (both -thalassemia1/-thalassemia2 and
-thalassemia1 heterozygote). Our observations support
the contention that thalassemia confers protection against malaria and
may explain why it is more prevalent in malaria endemic areas.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
C.-A. Lobo
Babesia divergens and Plasmodium falciparum Use Common Receptors, Glycophorins A and B, To Invade the Human Red Blood Cell
Infect. Immun.,
January 1, 2005;
73(1):
649 - 651.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Ayi, F. Turrini, A. Piga, and P. Arese
Enhanced phagocytosis of ring-parasitized mutant erythrocytes: a common mechanism that may explain protection against falciparum malaria in sickle trait and beta-thalassemia trait
Blood,
November 15, 2004;
104(10):
3364 - 3371.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. P. Mockenhaupt, S. Ehrhardt, S. Gellert, R. N. Otchwemah, E. Dietz, S. D. Anemana, and U. Bienzle
{alpha}+-thalassemia protects African children from severe malaria
Blood,
October 1, 2004;
104(7):
2003 - 2006.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. PATTANAPANYASAT, D. S. WALSH, K. YONGVANITCHIT, N. PIYAWATTHANASAKUL, W. WANACHIWANAWIN, and H. K. WEBSTER
ROBUST IN VITRO REPLICATION OF PLASMODIUM FALCIPARUM IN GLYCOSYL-PHOSPHATIDYLINOSITOL-ANCHORED MEMBRANE GLYCOPROTEIN-DEFICIENT RED BLOOD CELLS
Am J Trop Med Hyg,
October 1, 2003;
69(4):
360 - 365.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Chotivanich, R. Udomsangpetch, K. Pattanapanyasat, W. Chierakul, J. Simpson, S. Looareesuwan, and N. White
Hemoglobin E: a balanced polymorphism protective against high parasitemias and thus severe P falciparum malaria
Blood,
July 30, 2002;
100(4):
1172 - 1176.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
