This chapter gives a detailed account of the clinical manifestations of AIDS. It begins with a discussion of the difference between being exposed to HIV and being infected and points out that even individuals who are infected may show no clinical symptoms for many years. The importance of being tested using the HIV antibody test immediately after potential exposure to HIV and then six months later to determine whether infection has occurred is emphasized.
The clinical progression of HIV infection is then described in detail. The initial or acute phase of HIV infection occurs in the first few weeks or months following infection and the symptoms that may occur are described. These include a mononucleosis-like disease that may present as swollen glands, sore throat and fever or symptoms of brain infection leading to headaches and impairment of brain function. Following the acute phase is the asymptomatic phase that is variable in length but typically lasts as long as ten years during which time patients appear well. Importantly, the conclusions of recent clinical studies indicating that at a cellular level, HIV infection is active during the asymptomatic phase are included. The rapid turnover of helper T cells and virus leading to a balance between the immune system and HIV infection during these years is described. Finally, the symptomatic phase of HIV infection, which occurs when the virus finally overwhelms the immune system and helper T cells drop to low levels, is described. This phase is subdivided into three periods: initial symptoms that include generalized swollen glands (lymphadenopathy); early immune failure typified by conditions such as thrush or shingles; and finally full-blown AIDS, when the infected individual becomes susceptible to a wide range of opportunistic diseases. The next section is a comprehensive, well-illustrated description of individual bacterial, viral, and fungal opportunistic diseases associated with AIDS, including pneumocystis pneumonia, toxoplasmosis, tuberculosis, and cryptosporidium gastroenteritis as well as other AIDS-related conditions such as Kaposi’s sarcoma, lymphoma, dementia and, for women, cervical cancer.
Then, there is an up-to-date discussion of antiviral drug treatment in AIDS that includes the three major classes of drugs: reverse transcriptase nucleoside inhibitors, non-nucleoside inhibitors, and protease inhibitors including AZT treatment for women and the development of drug-resistant HIV.
Finally, there is an excellent discussion of the advantages, limitations, and uncertainties of triple combination therapies. These new triple combination therapies that usually include a protease inhibitor have dramatically reduced the rate of AIDS-related deaths since their introduction in 1996. Viral loads are reduced to undetectable levels in some individuals and the incidence of opportunistic infections is significantly reduced.
However, as is pointed out by the authors, triple combination therapies are not effective in all people because of drug resistant strains of virus. The treatment schedules are difficult to comply with because of the number of pills that have to be taken at different times throughout the day, and the treatment costs of about $15,000 annually are a burden in developed countries and prohibitive in developing countries. The greatest uncertainty is how long these therapies will be effective.
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