Abstract
For millennia, pathogens and human hosts have engaged in a perpetual struggle for supremacy. From the earliest recorded smallpox epidemics around 1350 B.C.E to the Black Death due to Yersinia pestis in the Middle Ages and continuing to modern times with HIV, there has been a continuous clash between pathogens and human hosts. But past pandemics are more than just ancient history—they are drivers of human genetic diversity and natural selection. Pathogens can dramatically decrease survival and reproductive potential, leading to selection for resistance alleles and elimination of susceptibility alleles. Despite this persistent struggle between host and pathogen, only in the past century have we developed an understanding of some of the human genetic differences that regulate infectious disease susceptibility and severity.
Highlights
The results unequivocally demonstrated that people with the sickle cell trait were less likely to be infected with malaria and developed less severe parasitemia
In the 1970s, Miller and colleagues made the association between resistance to P. vivax infection and high prevalence of Duffy blood group-negative individuals in areas lacking this species of malaria-associated parasites [4]
One reason may be the phenomenon of heterozygous advantage as is demonstrated by the sickle cell allele having the greatest fitness in heterozygotes due to their lack of sickle cell disease and protection against malaria
Summary
How Have Human Genetic Differences That Impact Infectious Diseases Been Discovered? With the advent of rapid, low-cost genotyping and next-generation sequencing techniques, genome-wide association studies (GWAS) have recently allowed for systematic identification of common genetic variants that impact infectious disease. In the 1970s, Miller and colleagues made the association between resistance to P. vivax infection and high prevalence of Duffy blood group-negative individuals in areas lacking this species of malaria-associated parasites [4].
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