Abstract
Human genomics is now, more than ever, poised to ask, and answer, challenging questions pertaining to the relationship between the inherent variability observed in populations and human diseases. Whether it is susceptibility or resistance, sensitivity to drugs or, indeed, differences in the host response to infection, it is evident that common genetic variants will emerge as a key component of a comprehensive understanding of many infectious diseases [1]. Traditionally, classical medical genetics has elucidated instances in which single, highly penetrant gene mutations have resulted in major defects in host defenses against infection. These rare instances of defects that result in immunodeficiency, which often segregate in families, have underscored key components of host defenses and have led to
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