Viroj Wiwanitkit

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J Vect Borne Dis 43, December 2006, pp. 195–197Co-infection between tuberculosis and malaria : a consideration oninteraction of molecules and pathogenesisViroj WiwanitkitDepartment of Laboratory Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, ThailandKey words Function – malaria – tuberculosisHuman immunodeficiency virus (HIV) infection/acquired immunodeficiency syndrome (AIDS) andmalaria are counted as worst diseases for the follow-ing: (i) together cause 4 million deaths every year;and (ii) pregnant women are at high risk of develop-ing anaemia and infection of placenta1. Children bornto co-infected mother are in low birth weight. AIDSmay increase the risk of severe malaria and antima-larial drugs are less effective1. Virus that cause AIDSreplicate more readily. A common infection in apatient with AIDS is tuberculosis.Malaria and tuberculosis are endemic in many re-gions of the world, and co-infection with the twopathogens is common. The interaction between bothinfections within a co-infection episode is an interest-ing topic in infectious medicine. The public healthimportance of TB/malaria is highlighted in thispaper1–3. Page et al4 said that tuberculosis-inducedpotentiation of type 1 immune responses is associat-ed with protection against lethal murine malaria. Theprotective process is believed to relate to gammainterferon induction4. This induction of cellular im-mune responses is related to ATP-binding protein(ATPBP) of Plasmodium species5. Zheng et al6 foundthat heat shock protein 70 (HSP70) from Mycobac-terium tuberculosis was associated with the inductionof a strong humoral and cellular response directedagainst Plasmodium falciparum3.During the co-infection, the protective effect betweeneach other was noted and has been studied for a fewyears4–6. However, a study on the proteins’ expressionin an episode of co-infection is warranted. To studythe interaction between both infections, the new de-velopment in bioinformatics can be applied. Here, theauthor used a new gene ontology technology to pre-dict the molecular function of HSP70 and ATPBP inan episode of co-infection.The database PubMed was used for data mining of theamino acid sequence for HSP70 and ATPBP. Predic-tion of molecular function and biological process ofHSP70 and ATPBP was performed using a novel geneontology prediction tool, GoFigure7. GoFigure is acomputational algorithm tool which is recently devel-oped in gene ontology7.  The tool accepts an inputDNA or protein sequence, and uses BLAST to iden-tify homologous sequences in GO annotated databas-es7. The approach is to use a BLAST search to iden-tify homologues in public databases that have beenannotated with gene ontology terms7. These includeSwissProt, Flybase (Drosophila), the SaccharomycesGenome Database (SGD), Mouse Genome Informat-ics (MGI) and Wormbase (Nematode)7. The contentsof the results will show results for molecular functionas well as biological process of the studied protein7.The prediction of molecular function was presentedand compared.Sequence of LIPF in different Mycobacterium speciesfrom searching of the database, sequence of HSP70196 J  VECT  BORNE  DIS  43, DECEMBER 2006and ATPBP can be derived and used for further study.Using GoFigure server, the molecular functions inHSP70 and ATPBP were predicted and are present-ed in Figs. 1 and 2, respectively.New developments have forced a reevaluation of ourunderstanding on tropical infections. Both malariaand tuberculosis are important tropical infectiousdiseases. The co-occurrence between these two dis-eases can be expected8. A large proportion of peoplewith latent tuberculosis live in malaria-endemic ar-eas, so co-infection with these two organisms is likelyto be common9. Aberration in pathogenesis of infec-tion in an episode of malaria and tuberculosis co-occurrence is interesting and becomes a new focus intropical medicine. The aberration in immunologicalprocess is believed to be important part in the patho-genesis of co-infection4,6.In the present study two key documented moleculescorresponding to the pathogenesis of malaria-tuber-culosis co-infection were studied. The gene ontolo-gy technique that was used is a new concept and usedin some recent molecular biological studies10,11.Of interest, HSP70 and ATPBP share a commonmolecular function as ATP binding resulting frompurine nucleotide binding. Therefore, a competitiveantagonist effect between both molecules can beexpected. Indeed, in an animal model, co-infectedmice were less able to contain growth of M. tubercu-losis in lung, spleen and liver9. This finding can be agood explanation for the protective effect betweeneach other in malaria-tuberculosis co-infection. In-deed, the structural homology between both studiedmolecules was reported in a recent study by Garsia etal12. However, further experimental studies are need-ed before making a conclusion on this topic. Thefinding in this study not only supports the previousknowledge on malaria and tuberculosis but also givesFig. 1: Molecular function of HSP70 of M. tuberculosis Fig. 2: Molecular function of ATPBP of P. falciparumWIWANITKIT: CO-INFECTION BETWEEN TUBERCULOSIS AND MALARIA 197the new view on the pathogenesis of co-infection.References1. WHO document WHO/HTM/MAL/2005, 1105 (Annex3). Geneva: World Health Organization 2005.2. Hovette P, Ba K, Kraemer P, Chaudier B, Bahrouch L,Fourcade L. Does emergency tropical medicine exist? Thephysician’s point of view. Med Trop (Mars). 2002; 62:244–6.3. N’Gom PT, Jaffar S, Ricard D, Wilkins A, Ariyoshi K,Morgan G, Da Silva AP, Whittle HC. Immune stimulationby syphilis and malaria in HIV-2-infected and uninfectedvillagers in West Africa. Br J Biomed Sci 1997; 54:251–5.4. Page KR, Jedlicka AE, Fakheri B, Noland GS, KesavanAK, Scott AL, Kumar N, Manabe YC.  Mycobacterium-induced potentiation of type 1 immune responses andprotection against malaria are host specific. Infect Immun2005; 73: 8369–80.5. Riley EM, Williamson KC, Greenwood BM, Kaslow DC.Human immune recognition of recombinant proteinsrepresenting discrete domains of the Plasmodium falci-parum gamete surface protein, Pfs230. Parasite Immunol1995; 17: 11–9.6. Zheng C, Xie P, Chen Y. Immune response induced byrecombinant BCG expressing merozoite surface antigen 2from Plasmodium falciparum. Vaccine 2001; 20: 914–9.7. Khan S, Situ G, Decker K, Schmidt CJ. GoFigure: automat-ed gene ontology annotation. Bioinformatics 2003; 19:2484–5.8. Kustner HG. Trends in four major communicable diseases.S Afr Med J 1979; 55: 460–73.9. Scott CP, Kumar N, Bishai WR, Manabe YC. Short report:modulation of Mycobacterium tuberculosis infection byPlasmodium in the murine model. Am J Trop Med Hyg2004; 70(2):144–8.10. Wiwanitkit V. Interaction between BRCA1 and humanpapilloma virus E7: an ontology study. Arch GynecolObstet 2006; 274: 146–9.11. Tsai JR, Chong IW, Chen CC, Lin SR, Sheu CC, HwangJJ. Mitogen-activated protein kinase pathway was signi-ficantly activated in human bronchial epithelial cells bynicotine. DNA Cell Biol 2006; 25: 312–22.12. Garsia RJ, Hellqvist L, Booth RJ, Radford AJ, BrittonWJ, Astbury L, Trent RJ, Basten A.  Homology of the 70-kilodalton antigens from Mycobacterium leprae andMycobacterium bovis with the Mycobacterium tuber-culosis 71-kilodalton antigen and with the conserved heatshock protein 70 of eucaryotes. Infect Immun 1989; 57:204–12.Corresponding author: Dr. Viroj Wiwanikit, Department of Laboratory Medicine, Faculty of Medicine, ChulalongkornUniversity, Bangkok–10330, Thailand.E-mail: wviroj@yahoo.com; wviroj@pioneer.netserv.chula.ac.thReceived: 26 April 2006 Accepted in revised form: 22 August 2006

Co-infection between tuberculosis and malaria : a consideration on interaction of molecules and pathogenesis

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