acquired immune deficiency syndrome (redirected from Reading , Writing, and Aids)

acquired immune deficiency syndrome [ə′kwīrd ə¦myün də¦fish·ən·sē ′sin‚drōm]

(medicine)

A disease that is caused by the human immunodeficiency virus (HIV) and compromises the competency of the immune system; characterized by persistent lymphadenopathy and opportunistic infections such asPneumocystis cariniipneumonia, cytomegalovirus, disseminated histoplasmosis, candidiasis, isosporiasis, and malignancies such as Kaposi's sarcoma. Abbreviated AIDS.

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Acquired immune deficiency syndrome (AIDS)

A viral disease of humans caused by the human immunodeficiency virus (HIV), which attacks and compromises the body's immune system. Individuals infected with HIV proceed through a spectrum of stages that ultimately lead to the critical end point, acquired immune deficiency syndrome. The disease is characterized by a profound progressive irreversible depletion of T-helper-inducer lymphocytes (CD4+ lymphocytes), which leads to the onset of multiple and recurrent opportunistic infections by other viruses, fungi, bacteria, and protozoa, as well as various tumors (Kaposi's sarcoma, lymphomas). HIV infection is transmitted by sexual intercourse (heterosexual and homosexual), by blood and blood products, and perinatally from infected mother to child (prepartum, intrapartum, and postpartum via breast milk).

Since retroviruses such as HIV-1 integrate their genetic material into that of the host cell, infection is generally lifelong and cannot be eliminated easily. Therefore, medical efforts have been directed toward preventing the spread of virus from infected individuals. See Retrovirus

Approximately 50–70% of individuals with HIV infection experience an acute mononucleosis-like syndrome approximately 3–6 weeks following primary infection. In the acute HIV syndrome, symptoms include fever, pharyngitis, lymphadenopathy, headache, arthralgias, myalgias, lethargy, anorexia, nausea, and erythematous maculopapular rash. These symptoms usually persist for 1–2 weeks and gradually subside as an immune response to HIV is generated.

Although the length of time from initial infection to development of the clinical disease varies greatly from individual to individual, a median time of approximately 10 years has been documented for homosexual or bisexual men, depending somewhat on the mode of infection. Intravenous drug users experience a more aggressive course than homosexual men and hemophiliacs because their immune systems have already been compromised.

As HIV replication continues, the immunologic function of the HIV-infected individual declines throughout the period of clinical latency. At some point during that decline (usually after the CD4+ lymphocyte count has fallen below 500 cells per microliter), the individual begins to develop signs and symptoms of clinical illness, and sometimes may demonstrate generalized symptoms of lymphadenopathy, oral lesions, herpes zoster, and thrombocytopenia.

Secondary opportunistic infections are a late complication of HIV infection, usually occurring in individuals with less than 200 CD4+ lymphocytes per microliter. They are characteristically caused by opportunistic organisms such as Pneumocystis carinii and cytomegalovirus that do not ordinarily cause disease in individuals with a normally functioning immune system. However, the spectrum of serious secondary infections that may be associated with HIV infection also includes common bacterial pathogens, such as Streptococcus pneumoniae. Secondary opportunistic infections are the leading cause of morbidity and mortality in persons with HIV infection. Tuberculosis has also become a major problem for HIV-infected individuals. Therefore, HIV-infected individuals are administered protective vaccines (pneumococcal) as well as prophylactic regimens for the prevention of infections with P. carinii, Mycobacterium tuberculosis, and M. avium complex. See Opportunistic infections, Pneumococcus, Streptococcus, Tuberculosis

Antiretroviral treatment with deoxyribonucleic acid (DNA) precursor analogs—for example, azidothymidine (AZT), dideoxyinosine (ddI), and dideoxycytidine (ddC)—has been shown to inhibit HIV infection by misincorporating the DNA precursor analogs into viral DNA by the viral DNA polymerase. Nevertheless, these agents are not curative and do not completely eradicate the HIV infection.