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CUENCA SUBCUENCA MICROCUENCA AFLUENTES MICROCUENCAS

FIGURA 6 Brillo Solar

CUENCA SUBCUENCA MICROCUENCA AFLUENTES MICROCUENCAS

 

2.6Discussion      

This  work  has  applied  current  sequencing  technologies  and  genomics  to  investigate   genetic  diversity,  and  the  effect  of  immunity  and  antimalarial  drugs  selection  on  Malawi  P.   falciparum   genomes.   Studies   of   this   kind   have   successfully   identified   drug-­‐resistance   mechanisms   and   targets   of   naturally-­‐acquired   immunity   as   candidate   vaccine   targets   (Kidgell   et   al.   2006;   Mackinnon   and   Marsh   2010),   but   have   not   yet   been   conducted   in   Malawi  P.   falciparum   populations.   Here   examination   of   genetic   variation   is   provided   in   parasites   from   Chikwawa   district,   Malawi,   where   the   parasite   population   is   exposed   to   naturally-­‐acquired  immunity  and  was  recently  exposed  to  intense  pressure  from  IRS,  ITNs,   and   ACTs.   Previous   studies   have   shown   that   human   immune   pressure   produces   genomic   regions  with  high  levels  of  nucleotide  diversity,  while  antimalarial  drug  pressure  results  in   regions   with   low   diversity   and   extended   haplotypes   (Mu   et   al.   2007,   2010;   Sabeti   et   al.   2006;   Dharia   et   al.   2010;   Volkman   et   al.   2007).   This   work   has   used   population   genetics   metrics  exploiting  these  two  principles  to  detect  loci  under  balancing  and  positive  selection   in   a   Malawi   P.   falciparum   population.   This   population   was   also   compared   to   five   geographically   dispersed   others   using   FST   and   XP-­‐EHH   to   detect   regions   of   genetic   divergence  and  signatures  of  recent  selective  sweeps,  respectively.  In  particular,  searching   for  high-­‐scoring  SNP  clusters  gave  strong  indicators  of  positive  selection.    

Analysis   using   Tajima’s   D   identified   potential   genomic   regions   under   balancing   selection,  including  six  genes  encoding  merozoite  invasion  ligands:  msp3.8,  msp3,  dbl-­‐msp,   eba175,   ama1   and  surfin4.2.   These   antigens   are   exposed   to   the   immune   system   on   the   surface   of   merozoites   or   during   erythrocyte   invasion,   and   are   highly   polymorphic.   Thus,   balancing  selection  at  these  genes  maybe  mediated  by  host  immune  system  as  previously   reported  and  have  also  been  listed  as  possible  candidates  for  vaccines  in  previous  studies  

(Alexandre   et   al.   2011;   Baum   et   al.   2003;   Polley   and   Conway   2001;   Ochola   et   al.   2010;   Tetteh  et  al.  2009;  Mu  et  al.  2010;  Amambua-­‐Ngwa  et  al.  2012b).    

Positive  directional  selection  was  detected  in  genomic  regions  near  or  surrounding   drug   targets   (pfmdr1,  pfcrt,   pfdhps   and   gch1)   and   in   surface   antigens   such   as  trap,   ron2,   msp3.8,   ama1  and  msp7  genes   with   important   roles   in   invasion   of   host   cells   (Vulliez-­‐Le   Normand  et  al.  2012;  Tufet-­‐Bayona  et  al.  2009;  Ghosh  et  al.  2009).  Interestingly,  several  FST   test  results  reflect  parasite  adaptation  to  local  drug  selection.  First,  low  FST  values  in  pfcrt-­‐ K76T   between   Malawi   and   Kenya   may   reflect   the   withdrawal   of   CQ   in   these   regions   and   subsequent   disparity   in   the   reduction   in   the   prevalence   of   resistance   alleles   to   2-­‐4%   in   Malawi  and  60%  in  Kenya  (Nkhoma  et  al.  2007;  Mwai  et  al.  2009).  Second,  the  FST  values  in  

pfcrt-­‐K76T  between  Malawi  and  Burkina  Faso,  and  Malawi-­‐Mali  are  heterogeneous  and  may   suggest  varying  allele  frequencies  of  K76T  allele  between  Mali  and  Burkina  Faso.  Third,  high   FST  values  in  pfcrt-­‐K76T  between  Malawi  and  Cambodia,  and  Malawi-­‐Mali,  suggest  that  this   mutation  has  reached  fixation  in  Cambodia  and  Thailand;  indeed,  CQ  remains  the  first-­‐line   treatment  for  P.  vivax  malaria  in  these  two  countries  and  thus  may  continue  to  select  for   the  resistant  genotype  (Setthaudom  et  al.  2011).  Fourth,  fixation  of  pfdhps-­‐K540E  between   Malawi  and  Mali,  and  Malawi-­‐Burkina  Faso  may  reflect  the  use  of  SP  for  the  treatment  of   uncomplicated   malaria   and   as   intermittent   preventive   treatment   in   the   two   west-­‐African   countries,  where  the  pfdhps-­‐K540E  mutation  is  rare  (Pearce  et  al.  2009;  Somé  et  al.  2010;   Dicko   et   al.   2010).   High   prevalence   of  pfdhps-­‐K540E   and   A437G   is   consistent   with   90%   prevalence  of  quintuple  mutants  in  Malawi  (Nkhoma  et  al.  2007)  and  while  437G  is  found  all   over   Africa   the   540E   is   largely   absent   in   west   Africa   (Table   2.8).   Whilst,   FST   may   reflect   differences  in  allele  frequency  due  to  differential  selective  pressure,  they  may  also  reflect  

simply  random  genetic  drift.  FST  is  dependent  on  absolute  diversity,  where  regions  of  low   diversity  in  either  population  (or  both)  can  result  in  high  values,  even  if  those  regions  have   not  been  selected  differently.    

Positive  directional  selection  in  chromosome  12  containing  pfgch1  and  transcription   factors  is  also  particularly  interesting.  In  P.  vivax  it  is  thought  to  result  from  drug  selection   (Dharia  et  al.  2010).  Mutations  in  these  transcription  factors  are  thought  to  be  a  source  of   increased   genetic   variability   that   regulate   gene   expression   whose   products   may   include   drug-­‐resistance   genes   (Levine   and   Tjian   2003).   Increased   expression   levels   of  pvcrt   have   been   observed   in   CQ-­‐resistant   parasites   (Fernández-­‐Becerra   et   al.   2009),   and   higher   expression  levels  of  pvdhfr  occurred  in  P.  vivax  isolates  relative  to  P.  falciparum,  resulting  in   the  proposal  that  evolution  in  response  to  drug  and  immune  pressure  might  be  driven  by   genetic  changes  in  the  corresponding  transcription  factors  (Westenberger  et  al.  2010).    

In   conclusion,   this   chapter   describes   the   sequencing   of   93  P.   falciparum   clinical   isolates   sourced   from   uncomplicated   malaria   cases   in   Malawi   and   identification   of   loci   under  selection.  In  addition,  positive  selection  signals  are  identified  by  comparing  Malawi  to   five   other   dispersed  P.   falciparum   populations.   Further   work   could   evaluate   the   role   of   these  loci  in  malaria  intervention  strategies.  For  example,  the  genetic  variation  may  enable   monitoring  of  P.  falciparum  transmission  dynamics  as  the  epidemiology  of  malaria  changes   over  time  in  response  to  interventions  (Volkman  et  al.  2012).  In  particular,  by  using  XP-­‐EHH   and  FST  it  is  shown  that  selection  differences  between  geographically  dispersed  populations   reflect  the  history  of  antimalarial  drug  use  and  selection  at  any  given  time,  whereas  during   intense   drug   selection,   wild-­‐type   alleles   are   increasingly   replaced   by   mutant   alleles.   The   ability   to   use   this   strategy   to   monitor   local   adaptation   to   drug   pressure,   monitoring  

transmission,  and  inform  the  type  and  timing  of  interventions  is  appealing.  This  knowledge   will  now  be  used  in  Malawi  to  monitor  the  impact  of  ACTs,  ITNs  and  IRS  on  the  local  parasite   population  of  Chikwawa  district  over  three  malaria  seasons.  

                             

Chapter  3