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21.Electron
microscopy has demonstrated the completion of the budding phase. The intact virus is
released from the cell. The viral envelope can be clearly seen.
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22.The
electron micrograph demonstrates the release of several viruses from one host cell. These
viruses can then bind to and infect other uninfected cells which express CD4.
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23.Antibodies
directed against antigens on pathogens, such as HIV, are released from plasma cells. Each
plasma cell synthesises antibodies which recognise a specific antigen on the pathogen,
e.g. the HIV gp 120 protein.
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24.The
rate of viral replication in productively infected CD4 cells is extremely high (one
billion viral particles are produced every day). The immune system attempts to control the
infection by producing vast numbers of cells, such as |
T helper cells. The battle between
the viral infection and the cells of the immune system continues throughout the course of
the infection. Eventually the virus' ability to damage the immune system exceeds the
body's capacity to fight HIV.
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25.During
the course of HIV infection, quantities of virus are trapped in the germinal centres of
the lymph nodes by the follicular dendritic cell network. As uninfected helper T cells
pass through the lymph nodes, they become infected with HIV.
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26.During
the later stages of HIV disease, the follicular dendritic cell network begins to break
apart. This releases increasing amounts of the virus into the
bloodstream.
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27.Scanning
electron microscopy has visualised HIV and the cells of the immune system. Many viral
particles bud from the surface of an infected CD4 cell. Measuring the amount of virus in
the plasma enables physicians to detect the levels
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of a patient's viral
load.
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28.HIV
infects the vulnerable CD4 cells and replicates at a high rate within these cells. As the
number of infected cells increases, the destruction of the immune system progresses.
Controlling HIV disease is only possible by
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potent combination therapy. In the absence of
such therapy, the 'fittest' strain of HIV (red), known as the wild type, dominates the
viral population.
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29.In the presence of inadequate therapy, such as monotherapy or partially
suppressive therapy, resistant viral strains (green, purple) develop. The rapid
replication of HIV and its high mutation rate mean that mutant strains with different
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attributes, e.g. drug resistance, emerge very quickly. Drug resistance may develop within
few weeks or several months. If a drug resistant viral strain develops in the presence of
inadequate therapy, it will have a growth advantage over the other strains and quickly
become one of the dominant strains in the population. Rapid 'outgrowth' of the resistant
strain leads to drug failure.
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30.The
main components involved in viral replication are two copies of HIV genomic RNA, transfer
RNA and the protease, integrase and reverse transcriptase enzymes. Protease is the target
of protease inhibitor drugs and reverse
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transcriptase is the target of reverse
transcriptase inhibitor agents.
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