Immunoepidemiology of Human Immunodeficiency

Abstract

Acquired immunodeficiency syndrome (AIDS) was officially acknowledged as a new disease in 1981 by the US Center for Disease Control and Prevention (CDC). The etiologic agent of AIDS is a retrovirus – human immunodeficiency virus type 1 (HIV-1). In 1986, the isolation of another retrovirus, HIV-2, in AIDS patients in West Africa provided a clue to the origin of HIV-1. HIV-1 and HIV-2 infections in humans resulted from zoonotic transfers of simian immunodeficiency viruses (SIVs) infecting chimpanzees (SIVcpz) and sooty mangabeys (SIVsmm), respectively. For SIVcpz to adapt to its new human hosts, the viral matrix protein came under intense host-specific immune selection pressure that resulted in an amino acid substitution (Met to Arg or Lys) in the viral matrix protein (Gag-30). This chapter focuses on how host immune factors modify susceptibility to HIV-1 infection, progression and severity of HIV-1 disease, and the likelihood of transmission of HIV-1 to another person. Some of the factors are genes encoding a chemokine receptor (the C-C motif receptor 5 gene [CCR5]), chemokine ligands, human major histocompatibility complex (MHC) class I human leukocyte antigen (HLA), human β-defensins, and apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3 (APOBEC3). Despite scientific advancements in the field of HIV-1 research in the last three decades, the search for cure and preventative vaccines for HIV-1 continues to elude the scientific community. A better understanding of the interactions between HIV-1, host restriction factors, and immune responses might provide drug targets for cure and a framework for vaccine initiatives.