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BACKGROUND: Malaria in pregnant women continues to be a public health problem in India. The prevalence of malaria in pregnancy is particularly high in the tribal conflict areas of India such as Chhattisgarh. Pregnant women have less acquired immunity protecting them against malaria than non-pregnant women of child bearing age. The decreased immunity results in a much more severe presentation of malaria symptoms, and potential death of both mother and fetus during malaria in pregnancy. Recognizing the need for effective malaria interventions in pregnant women, global and national malaria prevention and treatment guidelines have been established. Practice of these guidelines has been found to be inadequate in the Asian Pacific Region. LITERATURE REVIEW FINDINGS: Qualitative studies on the knowledge, attitudes and practices of malaria interventions have demonstrated that meeting communities at their level of understanding is essential in circumventing malaria spread. In an effort to create a synergy between health care workers, national and global malaria control strategies and pregnant women, there is the need to identify pregnant women’s knowledge, attitudes and practices of malaria interventions. Currently, there is no data on the knowledge, attitudes and practices of pregnant women in the conflict districts of Chhattisgarh, India, where malaria prevalence and related symptoms have been identified to be significantly high. PROPOSED PROJECT: This study seeks to assess the knowledge, attitudes and practices of malaria prevention and treatment in pregnant women in the conflict areas of Chhattisgarh, India, using a cross-sectional qualitative research design. This study will highlight the understanding of malaria transmission, perceptions of cause, recognition of signs and symptoms, treatment-seeking behaviors, preventive measures and practices of pregnant women who visit the antenatal clinic and those who do not. CONCLUSION: If this study demonstrates knowledge and attitudes that favor customary or unproven methods of malaria interventions as shown in previous studies, then this may explain the present rate of MIP in these districts and hence the need for specific mediations for controlling and preventing malaria in this populace. SIGNIFICANCE: Findings from this study will help inform malaria education programs, health policies and practices that are tailored or targeted towards pregnant women in Chhattisgarh, India.

People of African ancestry (AA) are at greater risk of developing chronic kidney disease than those of non-AA. Much of this risk has been linked to specific genetic haplotypes on chromosome 22, near the genes APOL1, encoding apolipoprotein L1, and MYH9, encoding non-muscle myosin heavy chain IIA (NMHCIIA). The mechanisms by which the disease-associated chromosome 22 haplotypes promote kidney damage are unknown. Apolipoprotein L1 is a circulating protein with no known role in kidney function. However, the kidney disease-associated chromosome 22 haplotypes are protective against trypanosome infection, resulting in positive selective pressure for these haplotypes in western Africa, where trypanosome infection is endemic. In contrast, NMHCIIA may have an important role in glomerular function, and mutations in MYH9 are associated with glomerular disease, yet the disease-associated chromosome 22 haplotypes do not involve coding sequence variations in MYH9. With no clear disease-causing role for genes near the chromosome 22 risk locus, it is plausible that indirect mechanisms of gene regulation may be responsible for the increased disease risk. This study examines several potential pathways for kidney injury, including altered glomerular gene expression in carriers of chromosome 22 risk haplotypes, and the role of altered expression of MYH9 in podocyte cell biology and kidney disease. We found that carriers of chromosome 22 risk variants exhibited differential glomerular gene expression in pathways promoting kidney injury. We also found decreased glomerular NMHCIIA expression in human FSGS kidney biopsies, and altered cell structure and mechanical function when Myh9 is ablated in murine podocytes. Further, Myh9 podocyte deletion predisposed mice to glomerulopathy in response to injury by the DOCA-salt uninephrectomy model of hypertension. Taken together, these findings demonstrate direct and indirect effects of chromosome 22 risk variants on glomerular gene expression which promote kidney injury.