Host immune components play both beneficial and pathogenic roles in human immunodeficiency virus type 1 (HIV-1) infection. During the initial stage of viral infection, a complex network of innate immune factors are activated. For instance, the immune cells express a number of inflammatory proteins including cytokines, chemokines, and antiviral restriction factors. These factors, specifically, interferons (IFNs) play a crucial role in antiviral defense system by modulating the downstream signaling events, by inducing maturation of dendritic cells (DCs), and by activation of macrophages, natural killer (NK) cells, and B and T cells. However, HIV-1 has evolved to utilize a number of strategies to overcome the antiviral effects of the host innate immune system. This review discusses the pathways and strategies utilized by HIV-1 to establish latent and persistent infection by defeating host’s innate defense system. 1. Introduction During the early phase of infection, hosts mount innate immune response that comprises defense mechanisms to protect the hosts from invading pathogens in an antigen independent manner. This immune response is the first and a rapid response launched against a variety of microorganisms. The innate immune system can distinguish between self and foreign proteins and responds accordingly. This nonspecific immune response is activated primarily by the structural motifs of invading pathogens. The major cell types that play key roles in innate immune response against invading pathogens include macrophages, dendritic cells, neutrophils, natural killer cells, mast cells, eosinophils, and basophils. Most of the innate effector cells produce inflammatory factors that function as chemical messengers. Among these molecules, IFNs are the most effective in elucidating antiviral immune responses [1]. Additionally, cytokines and chemokines also play important roles as chemoattractants controlling leukocytes trafficking. Innate immune response operates through the steps of recognition of the pathogen, signal transduction, and subsequent gene expression to produce the innate immune effector molecules. The first step is to recognize a pathogen as a foreign object and differentiate it from self-components. When pathogens breach physical barriers such as the skin or oral mucosa, they are recognized by pattern recognition receptors (PRRs) expressed either in the cytoplasm or on cell membranes. PRRs sense and interact with the structurally conserved motifs of proteins and nucleic acids unique to invading pathogens known as pathogen-associated molecular
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