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LETTER TO THE EDITOR |
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| Year : 2008 | Volume
: 14
| Issue : 2 | Page : 70 |
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Falciparum malaria selected while HIV-1 slaughtered
Kanjaksha Ghosh, Shrimati Shetty, Leenam Mota
Department of Haemostasis, National Institute of Immunohaematology (ICMR), 13th Floor, KEM Hospital, Parel, Mumbai, India
Correspondence Address:
Kanjaksha Ghosh
Institute of Immunohaematology (ICMR), 13th Floor, KEM Hospital, Parel, Mumbai
India
DOI: 10.4103/0971-6866.44109 PMID: 20300298
How to cite this article:
Ghosh K, Shetty S, Mota L. Falciparum malaria selected while HIV-1 slaughtered. Indian J Hum Genet 2008;14:70 |
Sir,
Human leukocyte antigen (HLA) is one of the most polymorphic systems known to man and its direct involvement in immune response is well known. It is generally accepted that two major infections, i.e. falciparum malaria and tuberculosis, exerted extreme selective pressure to fashion our genome as we see it today. Of the two, falciparum malaria is more important in tropical and sub tropical areas where the disease has been endemic for centuries.
The development of HLA polymorphism and resistance to malaria make interesting reading. [1],[2] In different populations, different HLA polymorphisms were linked to resistance to malaria. However HLA B35 came up as one of the alleles in several population groups where falciparum malaria is endemic. [3],[4] In India, HLA B35 is a common allele with 12-36% frequency among various populations and caste groups exposed for centuries to falciparum malaria. A study also has shown that HLA B35 can present HIV1 Gag protein (aa20-50 RPGGKKRYMIKHLVWASRELERFALNPGL) to generate cytotoxic T lymphocytes. [5] Simultaneously several studies from all over the world have shown that HLA B35 is associated with faster disease progression in HIV1 infection. [6]
Falciparum malaria, by way of positive selection, has given human beings an Achilles heel in the form of HLA B35 through which the HIV arrow is now passing. The study of HLA in human population gives us an unusual insight i.e. malaria selected HLA B35 positive population, only for it to be slaughtered by HIV1 infection in future. Nature is blind and unforgiving in driving evolution!
 References | |  |
| 1. | Hill AV, Elvin J, Willis AC, Aidoo M, Allsopp CE, Gotch FM, et al. Molecular analysis of the association of HLA-B53 and resistance to severe malaria. Nature 1992;360:434-9.  [PUBMED] [FULLTEXT] |
| 2. | Hill AV. Malaria resistance genes: A natural selection. Trans R Soc Trop Med Hyg 1992;86:225-32. [PUBMED] |
| 3. | Shankarkumar U, Devaraj JP, Ghosh K, Karnad D, Anand K, Mohanty D. HLA associations in P. falciparum malaria patients from Mumbai, western India. Indian J Malariol 2002;39:76-82. |
| 4. | Contu L, Carcassi C, Orru S, Mulargia M, Arras M, Boero R, et al. HLA-B35 frequency variations correlate with malaria infection in Sardinia. Tissue Antigens 1998;52:452-61. |
| 5. | Thakar MR, Bhonge LS, Lakhashe SK, Shankarkumar U, Sane SS, Kulkarni SS, et al. Cytolytic T lymphocytes (CTLs) from HIV-1 subtype C-infected Indian patients recognize CTL epitopes from a conserved immunodominant region of HIV-1 Gag and Nef.J Infect Dis 2005;192:749-59. [PUBMED] [FULLTEXT] |
| 6. | Gao X, Nelson GW, Karacki P, Martin MP, Phair J, Kaslow R, et al. Effect of a single amino acid change in MHC class I molecules on the rate of progression to AIDS. N Engl J Med 2001;344:1668-75. [PUBMED] [FULLTEXT] |
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