Pathogenesis of Human Immunodeficiency Virus (HIV)

Pathogenesis of HIV
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Pathogenesis of HIV
Introduction
Pathogenesis of human immunodeficiency virus (HIV) refers to the process by which the lentivirus evolves from the HIV virion to the mature virion at the acquired immunodeficiency syndrome AIDS stage. The HIV virion at the entry phase is the infectious form of HIV outside the host cell, while the mature virions are the ones liberated into the host, where they affect other cells and structures. These points mark the phases from when a host is exposed to the virus to when it progresses to AIDS.
HIV Pathogenesis
To begin with, viral entry is the first stage of getting infected with HIV. During entry, the virus mainly targets the CD4+ T cells, where it begins its evolution process. The viral gp120 interacts with either CCR5 or CXCR4 to enable viral fusion with the cell membrane after binding to CD4 receptors on the surface of host cells (Kritzinger et al., 2020). If the virion fails to bind to the CD4 receptors and the co-receptor simultaneously, it cannot enter the host's cell. If successful, the viral core is discharged into the host cell at fusion or granted entry.
Secondly, once the virion enters the host cell, it releases its single-stranded RNA genome into double-stranded DNA through reverse transcriptase. Once the proviral DNA is formed here, it forms the integrase strand transfer. The viral integrase enzyme subsequently transports this viral DNA into the host cell's nucleus, where it combines with the cellular DNA or the host genome.
Subsequently, the host DNA undergoes several replications, which are usually error-prone, thus creating numerous copies with varying genomes. New viral RNA and proteins are produced at this viral replication and assembly stage, and integrated viral DNA is translated into RNA. These parts are subsequently put together at the cell membrane to create new virus particles known as immature viral polyproteins. The immature viral particles are discharged from the infected cell due to budding, obtaining their lipid envelope as they leave.
At this stage, mature virions are dispersed and spread throughout the host. A limited infection can result from the freshly created virus particles infecting surrounding target cells. HIV can, however, also get into the bloodstream and spread throughout the body. The formation of viral reservoirs in numerous tissues, including the brain, gut-associated lymphoid tissue, and systemic infection are caused by this spread.
Immune Reaction
Upon infection, the body responds by fighting the viral disease. First, it activates the innate immune response, where the natural killer cells, neutrophils, and macrophages attempt to identify and destroy contaminated cells (Salwe et al., 2019). However, with the mutations caused during its replication, it stymies immune responses. The body also uses the adaptive immune response, which the CD4+ T helper cells do. Unfortunately, HIV primarily targets and kills CD4+ T cells, depleting them, which also results in the development of the illness.
Immunodeficiency
CD4+ T cell depletion causes severe immune system deterioration, leaving the body more vulnerable to opportunistic infections and malignancies. In a...