Treatment and Prevention of HIV Disease

The Revised Authoritative Guide To Vaccine Legal Exemptions

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In terms of prevention, some efforts have shown singular success (e.g., the virtual elimination of medical transmission in industrialized countries by ensuring the safety of blood supplies and use of universal precautions during medical treatments). On the other hand, the modification of sexual and drug use practices has been more difficult. Some successes have been achieved in selected high-risk groups (e.g., homosexual/bisexual men and some injection drug users participating in needle exchange programs). On a worldwide level, anti-AIDS campaigns have often been limited by political, cultural, socioeconomic, and education factors.

Progress toward developing a vaccine that might prevent the establishment of infection in the first place has been slow because of the great genetic diversity of HIV and its tendency toward rapid mutation. Several vaccines are in the process of being tested, but it remains to be seen whether such vaccines, usually based on the subtype B2 of HIV-1, will be useful in areas of the world where other subtypes predominate.

Considerable progress has been made in the development of antiretroviral medications that interfere at various stages of HIV replication. The earliest example was zidovudine [azidothymidine (AZT)], which interferes with HIV's ability to utilize reverse transcriptase (RT) to form viral DNA. There are now multiple examples of RT drugs of the nucleoside type, of which AZT is an example. Other types of RT inhibitors, termed nonnucleoside RT, have also been developed. Recently, drugs that interfere with another critical step in viral assembly, the protease inhibitors, have become available. The use of combination therapies that interfere at different stages of viral replication has proved effective in lowering plasma viral load to undetectable levels in many individuals that are treated. However, these drug combinations often have very significant undesirable and toxic side effects that may limit their tolerability; additionally, HIV's ability to rapidly mutate can eventually produce quasispecies that are resistant to various drug combinations. It is uncertain whether combination therapies can be effective in controlling viral replication on an indefinite basis. For a list of currently available drugs, see Table II. The U.S. federal guidelines for use of these drugs are shown in Table III.

Figure 1 Stages of HIV replication. (a) HIV virion attaching to host cell. A segment of HIV envelope protein gp120 attaches to host cell CD4 receptor. Further process of attachment will involve linkage to a second host cell site, a chemokine coreceptor either of the CXCR4 (lymphocyte) or CCR5 (macrophage, dendritic cell) type. (b) After fusing with host cell wall, the uncoated HIV enters host cell cytoplasm. (c) Using its RNA template, HIV utilizes the viral enzyme reverse transcriptase to manufacture viral DNA within the host cell. This viral DNA ultimately enters the host cell nucleus and becomes integrated into host cell's DNA. (d) The viral DNA that is integrated into host cell's DNA directs formation of a viral RNA transcript, which leads to formation of viral RNA and genomic RNA. Through a translation process viral proteins are formed. (e) Viral constituents are assembled, virus particle buds off from host cell, and viral proteins are clipped into functional units by the viral protease enzyme.

Figure 1 Stages of HIV replication. (a) HIV virion attaching to host cell. A segment of HIV envelope protein gp120 attaches to host cell CD4 receptor. Further process of attachment will involve linkage to a second host cell site, a chemokine coreceptor either of the CXCR4 (lymphocyte) or CCR5 (macrophage, dendritic cell) type. (b) After fusing with host cell wall, the uncoated HIV enters host cell cytoplasm. (c) Using its RNA template, HIV utilizes the viral enzyme reverse transcriptase to manufacture viral DNA within the host cell. This viral DNA ultimately enters the host cell nucleus and becomes integrated into host cell's DNA. (d) The viral DNA that is integrated into host cell's DNA directs formation of a viral RNA transcript, which leads to formation of viral RNA and genomic RNA. Through a translation process viral proteins are formed. (e) Viral constituents are assembled, virus particle buds off from host cell, and viral proteins are clipped into functional units by the viral protease enzyme.

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