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Goth's Medical pharmacology¿¡¼­ chapter 60. antiviral agentÀÇ AZT¿¡ °üÇÑ ºÎºÐÀÌ´Ù.
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The advent of AIDS causedby human immunodeficiency virus(HIV) has spurred development of a wide variety of antiviral components. Trial with 3'-azido-3'deoxythymidine showed efficacy for AIDS victims with Pneumocytis carini pneumonia(PCP) or for HIV-positive patients with an absolute helper/inducer(CD4+,T4+) T-cell count of less than 200/mm (adult or children) Although commonly referred to in the United States as AZT, the compound has been renamed zidovudine(Retrovir). It is available as 100mg capsules, a syrup with 50mg/5ml, and for IV infusion(10mg/ml)
The drug interrupts elongation of DNA chains, making it impossible for the virus to complete DNA synthesys and reproduce. In doses of at least 200mg every 4 hours, patients with low CD4+ lymphocyte counts dah fewer infectious complecations than untreated controls, had a trasient rise in circulationg T4-lymphocytes, and could manifest delayed hypersensitivity. Recently, dasage of 100mg 5 times daily significantly reduced the time to onset of PCP in those asynptomatic HIV-positive patients with CD4+ lymphocyte counts <500/mm. serious side effects, such as sever anemia necessitating transfusions, headache, myalgias, and gastrointestinal intolerance, have been observed. The drug may also crcinogenic. Many other agents, including dideoxyinosone(ddI, didanosone, Vidox), dideoxycytidine(ddC), and soluble CD4+, are under investigation.

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±×¸®°í antiviral agent ¿£ Aciclovir¶û Interferon°è¿­ÀÇ ¾à¹°ÀÌ Àִµ¥ °¢°¢ÀÇ Pharmacokinetics¿¡
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´ÙÀ½Àº HIVÀÇ pathogenesis´Ù.
Microbiology¿¡¼­ ij°£´ÜÇÏ°í ½±°Ô ¼³¸íµÈ ºÎºÐÀÌ´Ï±î ³Ê°°Àº ijÂîÁúÀÌÇÑÅÙ Á¦°ÝÀÏ°Í °°±¸³ª.
ÀÌÁ¤µµ ¿µ¾îµµ ¾ÈµÇ¸é Á¢½Ë¹°Àº ³»°¡ ÁÙÅ×´Ï ³Ê´Â ÄÚ¸¦ ¹Ú°Å¶ó DZ

The main determinant in both pathogenesis and the disease caused by HIV is the tropism of this virus for CD4-expressiing cells, namely the helper and delayed-type hypersensitivity T cells, together with macrophages and some brain cells.

The interactions between
HIV and the immune system are now known to be cignificnatly more dynamic than scientists first thought. It was originally belived that after infecting CD4 cells the virus replicated and then established latency. Activation of the infected CD4 Tcell at a later date, for example by contact with a foreign antigen, was then belived to result in viral killing of the cel. Recent evidence indicated that HIV replicates prodigiously and destroys many cells of the immune system everyday. However, this growth is countered, usually for many years, by a vigorous host-defence response that prevents the virus from multiplying out of control. Desruction of CD4+ cell is achieved in several ways, including cytotoxic T-cell Lysis, NK cells, and antibody dependent cellular cytotoxicity. Ultimately, however, the balance of power shifts so that HIV gains the upper hand, resulting in the severe immunodeficiency characteristic of full blwn AIDS.
The CD4 T cells are central to the initiation of an immune response. They relapse lymphokines required for the activation of macrophages, other T cells, B cells, and NK cells. When the number of  these cells is reduced substatiallly by HIV infection, antigen-specific immune response, especially cellular response, are in capacitated and humoral response uncontrolled.
The abilities of HIV to disable the immune system and alter its antigenicity by repreated mutation allow the virus to escape compete immune clearance and prevent disease rsolution.
HIV infection also has effects onthe nervous system. It is present in the brain, mainly in macrophages but also in macroglial, oligodedroglial, and capillary endothelial cells. Most AIDS patients develop neurological disease ajd it has been suggested that macrophages carry the virus into brain.

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µðÁö±â ½ÈÀ¸¸é ÀÏ´ÜCell biology(õÆäÀÌÁöÂë µÈ´Ù) °øºÎÇÏ°í
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