Human immunodeficiency virus (HIV), a member the the retrovirus family, is the causative certified dealer of acquired immunodeficiency syndrome (AIDS). HIV invades assorted immune cell (e.g., CD4+ T cells and monocytes) leading to a decrease in CD4+ T cabinet numbers below the crucial level, and loss that cell-mediated immune − therefore, the human body becomes progressively an ext susceptible come opportunistic infections and also cancer.
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HIV invasion of immune cells
HIV infects T cells via high-affinity interaction in between the virion envelope glycoprotein (gp120) and also the CD4 molecule. The infection of T cell is aided by the T-cell co-receptor called CXCR4 while HIV infects monocytes by interacting with CCR5 co-receptor (Figure 1). As portrayed in Figure 2, after gp120 binds to CD4 top top the T cell (1). Nucleocapsids containing viral genome and also enzymes start the target cabinet (2). Following the relax of famous genome and enzymes indigenous the main point protein, viral turning back transcriptase catalyses reverse warrior of ssRNA to kind RNA-DNA hybrids (3). To yield HIV dsDNA the viral RNA template is partially degraded through ribonuclease H and the second DNA strand is synthesized (4). The viral dsDNA is translocated right into the nucleus and integrated right into the hold genome by the viral integrase enzyme (5). Transcription components transcribe the proviral DNA into genomic ssRNA (6), which is exported to cytoplasm (7). In the cytoplasm, host-cell ribosome catalyse synthesis of viral precursor proteins (8). The viral precursor proteins are cleaved into viral protein by famous proteases (9). HIV ssRNA and proteins assemble beneath the host-cell plasma membrane (10) forming virion sprout from it (11). Maturation occurs either in the forming buds or after budding from the hold cell (12). Throughout maturation, HIV proteases cleave the poly-proteins into individual useful HIV proteins. The mature virions are able come infect an additional host cell.
Innate immune solution to HIV
Innate immune cells (e.g., dendritic cells and natural killer cells) space the first line that defence i beg your pardon HIV encounters top top entry to the body.
Macrophages. Tissue macrophages are among the target cells because that HIV. This macrophages harbour the virus and also are recognized to it is in the source of famous proteins. However, the infected macrophages are presented to lose their capability to ingest and kill international microbes and present antigen to T cells. This can have a major contribution in overall immune dysfunction brought about by HIV infection.
Dendritic cell (DCs). DCs are huge cells with dendritic cytoplasmic extensions. This cells existing processed antigens to T lymphocytes in lymph nodes. Epidermal DCs, expressing CD1a and Birbeck granules, are probably among the very first immune cell to combat HIV at the mucosal surfaces. These cells deliver HIV indigenous the site of epidemic to lymphoid tissue. The follicular DCs, found in lymphoid tissue, space also key antigen-presenting cells that trap and present antigens on your cell surfaces. In the lymph node follicles, DCs administer signals for the activation of B lymphocytes.
Natural killer (NK) cells. NK cells have lytic activity against cells that have diminished expression the major histocompatibility facility (MHC) I antigens. Due to the fact that the presence of MHC course I is required for peptide presentation to T cabinet receptors, NK cells are crucial line that defence once HIV escapes the to move immune response. NK cells proliferate in solution to type 1 interferon secreted by DCs. These stimulated NK cells release cytokines such together interferon γ (IFN-γ), tumour necrosis element α (TNF-α), and also chemokines come activate T-cell proliferation (cellular immune response). NK cells also inhibit viral replication by publication IFN-γ.
Adaptive immune an answer to HIV
Cellular immune an answer to HIV. The moving immune an answer is induced top top the entrance of HIV right into the target cell (e.g., T cells) and also synthesis of viral proteins (Figure 1). MHC class I ~ above the cabinet surface displays the intracellularly degraded HIV peptide fragments for acknowledgment by T-cell receptor (TCR) on CD8+ T cell (Figure 3). CD8+ T cell lyse HIV infected cells and secrete cytokines, i.e. Interferon-γ (IFN-γ), tumor necrosis aspect α (TNF-α), and chemokines, i.e. MIP-1 α, MIP β and RANTES, that inhibit virus replication and also block viral entry into CD4+ T cells. Development of CD8+ T cells is an essential for regulate of HIV replication. This results in declining viraemia after major infection. In the early stages of infection, CD4+ T cells shed their proliferative capacity and also therefore their contribution to viral manage is minor. However, during chronic infection CD4+T cells are present and also secrete interleukin-2 (IL-2) or cytokines, such together IFN-γ, to control viraemia.
Humoral solution to HIV. The humoral immune solution occurs later on in infection; therefore, the level that antibodies throughout the acute epidemic is very low. Non-neutralising antibodies to structural proteins (i.e. P17 and also P24) are an initial to appear and generally execute not persist. Later on neutralising antibodies certain to proteins, involved in the entrance of the virus into the cells, will be generated. This antibodies are particular to: (1) the variable an ar of gp120 (V3); (2) CD4 binding sites and chemokine receptors (i.e., CXCR4 and also CCR5); (3) the transmembrane protein gp41. Potent neutralizing antibodies have been displayed to play a significant role in managing HIV epidemic in a couple of symptom-free HIV+ people who preserve high level that CD4+ T cells and also low famous load.
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cellular & humoral immune responses to HIV
There are miscellaneous reasons which can add to the failure of the immune device to regulate HIV infection and also prevent AIDS development. Through infecting CD4+ T cells, HIV is able to replicate primarily in caused T cells and also paralyse one of the main contents of adaptive immune system. HIV can also establish latent infection in CD4+ T cells and also remain invisible to CD8+ T cells and therefore replication can take place later in the infection and generate new virions. Antigenic mutation within the T-cell epitopes can impact the binding volume of MHC molecules to the viral peptides, bring about the inability of the TCRs to recognise the MHC-peptide complex. Finally, HIV is able come hide from anti-HIV antibodies by expressing non-immunogenic glycans on vital antibody epitopes.