HIV and AIDS
The Centers for Disease Control and Prevention (CDC) first recognized human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS) in 1981. One of the most widely publicized diseases, AIDS is characterized by progressive immunodeficiency. Although it's characterized by progressive destruction of cell-mediated (I-cell) immunity, it also affects humoral immunity, and even autoimmunity because of the central role of CD4 + T cells in immune reactions. The resultant immunodeficiency makes the patient susceptible to opportunistic infections, unusual cancers, and other abnormalities that define AIDS.
A retrovirus - my, type I - is the primary etiologic agent. Transmission of HIV occurs by contact with infected blood or body fluids and is associated with identifiable high-risk behaviors. As a result, HIV incidence is disproportionately high in I. V. drug users, homosexual and bisexual men, neonates of HIV-infected women, recipients of contaminated blood or blood products (dramatically decreased since the mid-1980s), and heterosexual partners of people in the former groups. Because of similar routes of transmission, AIDS shares epidemiologic patterns with hepatitis B and sexually transmitted diseases. Thus, the number of women with HIV and AIDS is rising steadily, and HIV infection is now the third leading cause of death among women ages 25 to 44. HIV and AIDS also disproportionately affect minority women in the United States, making them the leading cause of death among Black women in this age group and Hispanic women in general. These two minority groups account for over 80% of women affected with HIV ANd AIDS in the United States. Also, because women in general have poorer access to or fail to use health care and social services, HIV-infected women are one third more likely to die sooner than HIV-infected men.
The natural history of AIDS infection begins with infection by the HIV retrovirus, which is detectable only by laboratory tests, and ends with the severely immunocompromised, terminal stage of this disease. Depending on individual variations and the presence of cofactors that influence progression, the time elapsed from acute HIV infection to the appearance of symptoms (mild to severe), to diagnosis of AIDS and, eventually, to death varies greatly. More recently, dramatic advances in antiretroviral therapy and treatment and prophylaxis of common opportunistic infections have delayed the natural progression of HIV infection and prolonged survival.
What causes HIV and AIDS ?
AIDS results from infection with HIV, which strikes cells bearing the CD4 antigen; the latter (normally a receptor for major histocompatibility complex molecules) serves as a receptor for the retrovirus and lets it enter the cell. HIV prefers to infect the CD4 + lymphocyte but may also infect other CD4 + antigen-bearing cells in the GI tract and uterine cervix as well as neuroglial cells. Mter invading a cell, the HIV replicates, leading to cell death, or becomes latent. HIV infection leads to profound pathology either directly,through destruction of CD4 + cells, other immune cells, and neuroglial cells, or indirectly, through the secondary effects of CD4 + T-cell dysfunction and resultant immunosuppression.The infection process takes three forms:
Signs and symptoms of HIV and AIDS
HIV infection manifests in many ways. after a high-risk exposure and inoculation, the infected person usually experiences a mononucleosis-like syndrome, which may be attributed to the flu or another virus. The patient then may remain asymptomatic for years. In this latent stage, the only sign of HIV infection is laboratory evidence of seroconversion. When symptoms appear, they may take many forms, such as persistent generalized adenopathy, nonspecific signs and symptoms (weight loss, fatigue, night sweats, and fevers), neurologic symptoms resulting from HIV encephalopathy, an opportunistic infection, or cancer.
In addition to the symptoms common to men and women, women also experience HIV-gynecologic problems, such as recurrent vaginal yeast infections, other vaginal infections, severe herpes simplex virus ulcers, idiopathic genital ulcers, human papillomavirus infections, pelvic inflammatory disease, and menstrual irregularities.
The clinical course of HIV and AIDS varies slightly in children. Apparently, incubation time is shorter, with a mean of 17 months. Signs and symptoms resemble those in adults, except for findings related to sexually transmitted disease. Children show virtually all of the opportunistic infections observed in adults, with a higher incidence of bacterial infections, including otitis media, pneumonias other than that caused by Pneumocystis carinii, sepsis, chronic salivary gland enlargement, and lymphoid interstitial pneumonia.
The CDC defines AIDS as an illness characterized by one or more "indicator" diseases that coexist with laboratory evidence of HIV infection and other possible causes of immunosuppression. The CDC's current AIDS surveillance case definition requires laboratory confirmation of HIV infection in people who have a CD4+ T-lymphocyte count of greater than 200 cells/ul or who have an associated clinical condition or disease.
The most commonly performed tests, antibody tests, indicate HIV infection indirectly by revealing HIV antibodies. The recommended protocol requires initial screening of individuals and blood products with an enzyme linked immunosorbent assay (EliS A). A positive EliSA should be repeated and then confirmed by an alternate method, usually the Western blot or an immunofluorescence assay. The radioimmunoprecipitation assay is considered more sensitive and specific than the Western blot. Because it requires radioactive materials, it's a poor choice for routine screening. In addition, antibody testing isn't reliable. Because people produce detectable levels of antibodies at different rates a "window" varying from a few weeks to as long as 3S months in one documented case - an HIV. infected person can test negative for HIV antibodies. Antibody tests are also unreliable in neonates because transferred maternal antibodies persist for 6 to 10 months; To overcome these problems, direct tests are used, including antigen tests, HIV cultures, nucleic acid probes of peripheral blood lymphocytes, and the polymerase chain reaction.
Additional tests to support an HIV diagnosis and help evaluate the severity of immunosuppression include CD4 + and CD8+ T-lymphocyte subset counts, erythrocyte sedimentation rate, complete blood cell count, serum beta2-microglobulin, p24 antigen, neopterin levels, and energy testing. Because many opportunistic infections in AIDS patients are reactivations of previous infections, patients are also tested for syphilis, hepatitis B, tuberculosis, toxoplasmosis and, in some areas, histoplasmosis.
Treatment of HIV and AIDS
To date, there's no known cure for AIDS; however, in 1998, the CDC recommended that all people who have symptomatic or HIV infection receive aggressive antiviral therapy. In July of 2003, the CDC revised its guidelines for initiating treatment of antiretroviral therapy. (See New guidelines for antiretroviral therapy.
Treatment for HIV infection can be divided into four categories: prevention and therapy for opportunistic infections and malignancies, antiretroviral treatment, and hematopoietic stimulating factors.
Nucleoside analogues (sometimes called reverse transcriptase inhibitors) have been the mainstay of AIDS therapy in recent years. These drugs, which include zidovudine (AZT), lamivudine, didanosine, stavudine, abacavir, and zaldtabine, interfere with viral reverse transcriptase, which impairs HIV's ability to turn its ribonucleic add into deoxyribonucleic add for insertion into the host cell.
Antiretroviral therapy typically begins when the patient's CD4+ T-cell count drops to less than 350/ul or when the patient develops an opportunistic infection. Most clinidans recommend starting the patient on a combination of these drugs in an attempt to gain the maximum benefit and inhibit the production of resistant mutant strains of HIV. The drug combinations and dosages are then altered, depending on the patient's response.
Increasingly, physicians are basing changes in therapy on the patient's viral load rather than on her CD4+T cell count. Because the CD4 + count is influenced by the total white blood cell count changes in the CD4 + count may have nothing to do with changes in the patient's HIV status. Many physicians recommend that a patient on antiretroviral therapy should have her viral load checked every 3 months.
Protease inhibitors. another class of antiretroviral agents, have greatly increased the life expectancy of AIDS patients. These drugs (which include ritonavir, indinavir, nelfinavir, and saquinavir) block the enzyme protease, which HIV needs to produce virions, the viral particles that spread the virus to other cells. The use of protease inhibitors dramatically reduces viral load - sometimes to undetectable levels - while producing a corresponding increase in the CD4 + T.cell COunt and, because they act at a different site than nucleoside analogues, protease inhibitors don't produce additional adverse effects when added to a patient's regimen.
After antiviral therapy is initiated, treatment should be aggressive. Initially, highly active antiviral therapy, consisting of a triple drug therapy regimen - a protease inhibitor and two non-nucleoside reverse transcriptase inhibitors - is recommended. In addition to these primary treatments,anti-infective's are used to combat opportunistic infections (or, with some patients, prophylactically to help resist opportunistic infections), and antineoplastic drugs are used to fight associated neoplasms. Supportive treatments help maintain nutritional status and relieve pain and other distressing physical and psychological symptoms.
Special considerations or prevention
Advise health care workers and the public to use precautions in all situations that risk exposure to blood, body fluids, and secretions. Diligently practicing standard precautions can prevent the inadvertent transmission of AIDS and other infectious diseases transmitted by similar routes.
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