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Rather, the transmission rate needs to be pushed down so that each malaria infection is passed on to less than one new person and the disease gradually dies out.
Longitudinal models showed the same results, with p-values<0.0001 at all post-immunization time points for each malaria vaccine dose group compared to rabies vaccine.
For each malaria infection, the locus with the highest number of alleles was considered as a proxy for the multiplicity of infection (MOI), representing the minimal number of parasite haplotypes in the sample.
However, removing 28 days person-time at risk after each malaria episode increased the duration of protection following IPTi by just one more week and there was no evidence of any protection after week seven post IPTi.
A period of 28 days after each malaria episode was deducted from the person time at risk, since individuals were assumed not to be at risk of malaria during this period.
For each malaria phenotype, we first performed statistical analyses of the data using multivariate regression analysis to take into account non-genetic factors such as age, year of study and transmission intensity (see Materials and Methods).
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Data for each malaria-related phenotype were first analysed using multivariate regression analysis according to the distribution of the data.
In addition, 200 µL of whole blood was collected from each malaria-negative patient and used for DNA extraction with a QIAamp kit (QIAGEN, Hilden, Germany).
In contrast, a significant difference was found in the distribution of P. falciparum, P. vivax, and P. malariae obtained during the 3 periods in each malaria-endemic area (p<0.05 for all pairwise comparisons), and P. ovale was not detected in samples obtained during 1996 but comprised 1.41% and 0.21% of samples obtained during 2006 2007 and 2008 2009, respectively (Table 3).
Each year, malaria kills more than 800,000 people annually, of which 91% of them reside in Africa and 85% of them are under five children [2].
Each year, malaria kills 1 to 2 million human beings.
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