PMID- 18824049
OWN - NLM
STAT- MEDLINE
DCOM- 20090311
LR  - 20081208
IS  - 0198-8859 (Print)
IS  - 0198-8859 (Linking)
VI  - 69
IP  - 12
DP  - 2008 Dec
TI  - Evolution and selection of human leukocyte antigen alleles by Plasmodium 
      falciparum infection.
PG  - 856-60
LID - 10.1016/j.humimm.2008.08.294 [doi]
AB  - Infection by Plasmodium falciparum malaria was one of the major driving forces 
      for the selection of various genes, some of which might be involved in protection 
      against this infection. The human leukocyte antigen (HLA) system is a highly 
      polymorphic supergene complex with extensive diversity across different 
      populations. In areas traditionally endemic for malaria for centuries, there 
      seems to be some selection of certain HLA alleles that may somehow be involved in 
      protection against the infection. One of the major conundrums is the lack of 
      homogeneity in the HLA alleles selected by P. falciparum across different 
      populations. Various factors like microheterogeneity in parasite species, genetic 
      drift in parasitic antigens, varying intensities of transmission, different 
      polymorphisms of red cell antigens, and diversity in the HLA system have exerted 
      selection pressure, which probably determined the emergence of different dominant 
      HLA antigens in different endemic populations. The complex life cycle of P. 
      falciparum, with different antigens becoming important at different phases of the 
      cycle and invasion of different tissues causing different clinical manifestations 
      of the same disease, is also another significant factor contributing to a 
      selection pattern. Evolutionary selection pressure probably selected different 
      HLA antigens for modulations of different components of the disease as well as 
      the severity of the disease. A coevolution, where the parasite polymorphisms meet 
      the host heterogeneity, is likely to have occurred, resulting in the selection of 
      a few HLA antigens associated with P. falciparum infection. Data might have been 
      overwhelmed by the noise of additional selection pressure exerted by other 
      infectious agents prevalent in endemic areas of P. falciparum malaria.
FAU - Ghosh, Kanjaksha
AU  - Ghosh K
AD  - National Institute of Immunohaematology, KEM Hospital, Mumbai, India. 
      kanjakshaghosh@yahoo.com
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20080925
PL  - United States
TA  - Hum Immunol
JT  - Human immunology
JID - 8010936
RN  - 0 (Antibodies, Protozoan)
RN  - 0 (HLA Antigens)
RN  - 0 (Protozoan Proteins)
RN  - 145112-81-8 (glutamate-rich protein, Plasmodium)
SB  - IM
MH  - Africa, Western
MH  - Animals
MH  - Antibodies, Protozoan/*immunology
MH  - Evolution, Molecular
MH  - Gene Frequency
MH  - Genetic Predisposition to Disease
MH  - HLA Antigens/genetics/immunology
MH  - Host-Parasite Interactions/genetics/immunology
MH  - Humans
MH  - Immunity, Innate
MH  - India
MH  - Malaria, Falciparum/epidemiology/genetics/*immunology
MH  - Plasmodium falciparum/*immunology/pathogenicity
MH  - Polymorphism, Genetic
MH  - Population Groups
MH  - Prevalence
MH  - Protozoan Proteins/*immunology
MH  - Severity of Illness Index
MH  - Thailand
MH  - Vietnam
MH  - Virulence
RF  - 35
EDAT- 2008/10/01 09:00
MHDA- 2009/03/12 09:00
CRDT- 2008/10/01 09:00
PHST- 2008/03/07 00:00 [received]
PHST- 2008/08/05 00:00 [revised]
PHST- 2008/08/15 00:00 [accepted]
PHST- 2008/10/01 09:00 [pubmed]
PHST- 2009/03/12 09:00 [medline]
PHST- 2008/10/01 09:00 [entrez]
AID - S0198-8859(08)00449-7 [pii]
AID - 10.1016/j.humimm.2008.08.294 [doi]
PST - ppublish
SO  - Hum Immunol. 2008 Dec;69(12):856-60. doi: 10.1016/j.humimm.2008.08.294. Epub 2008 
      Sep 25.