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Chapter 18 Lecture 7 (Replication of HIV (Attachment – HIV attaches to…
Chapter 18 Lecture 7
Replication of HIV
Attachment – HIV attaches to four kinds of cells: helper T cells; cells of the macrophage lineage, ; smooth muscle cells and dendritic cells
Entry- the cytoplasmic membrane forms a pocket and folds in to surround the virus, forming a vesicle
Uncoating the viral envelope fuses with the vesicle’s membrane and the intact capsid of HIV enters the cytosol
Synthesis of DNA- reverse transcriptase, making double- stranded DNA using viral ssRNA as a template
Integration- the DNA enters the nucleus and becomes part of the human DNA molecule- this is were it remains as part of the cell life (latency period)
Synthesis of RNA and polypeptides- an infected cell transcribes HIV genes to make messenger RNA and multiple copies of viral ssRNA that will act as a genomes for new viruses.
Release- then two molecules of genome RNA, and several other viral peptides bud or leave from the hosts cytoplasmic membrane
Assembly and maturation – HIV that buds from the cells is nonvirulent/(inability to damage or infect) because its capsid is not fully functional, and the reverse transcriptase is inactive. Protease will allow release of the reverse transcriptase and capsomeres. Protease only occurs after the viruses has budded from the cell , allows for full maturation and this is when HIV becomes active
Structure of HIV
Typical retrovirus in shape, components and size
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Gp41
Smaller glycoprotein that promotes fusion of the viral envelop to target cell (the membrane of the CD4+ cell)
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Epidemiology of AIDS
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HIV found in blood, semen, saliva, vaginal secretions, and breast milk can cause infections
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Origin of HIV
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Scientists have identified antibodies against HIV in human blood stores since 1959, but did not document first AIDS case until 1981
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Diagnosis, treatment, and prevention
Diagnosis
AIDS diagnosis is based on symptoms, low levels of CD4 lymphocytes, and presence of antibodies against HIV
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Long-term nonprogressors
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Possible reasons: defective virions, poor binding of HIV to cells, or well-developed immune systems
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