Abstract
Identification of the genetic component of infectious disease susceptibility is an area of intense investigation, which, as presented in this chapter, can provide clues to fundamental questions about virus pathogenesis and the diversity, redundancy, and specialization of host mechanisms against infection. The chapter addresses some methodological approaches of the identification of susceptibility genes to virus infection. It talks about genetic control of virus entry into the host cell. Infection with mouse coronavirus has served as a model to understand the viral and immunological determinants of coronavirus disease, including severe acute respiratory syndrome. Parvovirus B19, a significant human pathogen that causes fetal loss and severe disease in immunocompro‐mised patients, is classified as an erythrovirus due to its ability to infect red blood cell precursors of the bone marrow. Noroviruses or Norwalk‐like viruses are the leading cause of viral acute gastroenteritis in humans. The chapter deals with genetic control of interferon (IFN)‐mediated immunity in viral infection. An important consequence of type I IFN secretion is the activation of natural killer (NK) cells, a central component of the innate response against virus infection. It also discusses major histocompatibility complex (MHC) I alleles and TCR repertoire which can influence CD81 t responses and outcomes after viral infection. Pathogens are considered one of the most powerful forces shaping the evolution of the human genome. Numerous studies have shown that genes or loci involved in host defense against infection present signs of positive or negative selection.