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12 HIV/AIDS, Page 1 of 2

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The period from 1994 to 1996 was in many ways a turning point for AIDS care in the western world, with significantly increased survival resulting. Treatment to prevent mother-to-child transmission; the introduction of a powerful class of antiretroviral drugs, the protease inhibitors; the recognition of continued high-level human immunodeficiency virus (HIV) replication throughout the course of the infection; the importance of the plasma viral load for prognosis; and the effectiveness of highly active antiretroviral therapy (HAART), which combined classes of antiretrovirals, all emerged during this time. There are two recognized variants of HIV: HIV-1 and HIV-2. Both belong to the lentivirus subgroup of retroviruses, which are, by definition, single-stranded RNA viruses that catalyze the production of a DNA strand complementary to their viral RNA. The target cells for infection with HIV are lymphocytes and macrophages. Central nervous system (CNS) disease clinically affected up to two-thirds of cases of AIDS presenting before treatment was available. In adults, cerebrovascular pathology has been described in 8 to 34% of autopsy series of AIDS cases. The diagnosis of the acute retroviral syndrome is established by the finding of viral RNA or p24 antigen in the blood in the absence of antibodies as tested for by enzyme-linked immunosorbent assay (ELISA) and Western blot. A wide range of infectious agents are associated with subacute or chronic meningitis in non-HIV-infected individuals. The laboratory evaluation of subacute or chronic meningitis is extensive and may prove to be frustrating in its failure to identify a causative agent.

Citation: Booss J, Esiri M. 2003. 12 HIV/AIDS, p 193-220. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch12
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Image of FIGURE 12.1

Sparse lymphocytic cuffing of meningeal veins overlying the cerebellum in a case of pre-AIDS HIV infection in a hemophiliac.

Citation: Booss J, Esiri M. 2003. 12 HIV/AIDS, p 193-220. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch12
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Image of FIGURE 12.2

An isolated multinucleated giant cell in white matter from a case of HIVE. Sparse HIV p24 antigen is visible at the periphery of the cytoplasm. Immunostain for p24 HIV core protein, counterstained with hematoxylin.

Citation: Booss J, Esiri M. 2003. 12 HIV/AIDS, p 193-220. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch12
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Image of FIGURE 12.3

Group of multinucleated cells of macrophage origin in the basal ganglia of a case of HIVE. Ricinus communis agglutinin I immunostain, counterstained with hematoxylin.

Citation: Booss J, Esiri M. 2003. 12 HIV/AIDS, p 193-220. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch12
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Image of FIGURE 12.4

Diffuse pallor of myelin staining of cerebral white matter in HIVE.

Citation: Booss J, Esiri M. 2003. 12 HIV/AIDS, p 193-220. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch12
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Image of FIGURE 12.5

Reactive microglia (a) and astrocytes (b) in HIVE, (a) Ricinus communis agglutinin I, (b) GFAP immunostain, both counterstained with hematoxylin.

Citation: Booss J, Esiri M. 2003. 12 HIV/AIDS, p 193-220. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch12
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Image of FIGURE 12.6

Focus of β-amyloid precursor-positive (damaged) axons in deep white matter from a case of HIVE. Counterstained with hematoxylin.

Citation: Booss J, Esiri M. 2003. 12 HIV/AIDS, p 193-220. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch12
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Image of FIGURE 12.7

The suggested pathogenic cascade leading to oligodendrocyte and myelin damage in the CNS in AIDS.

Citation: Booss J, Esiri M. 2003. 12 HIV/AIDS, p 193-220. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch12
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Image of FIGURE 12.8

MRI of HIV leukoencephalopathy. Axial FLAIR image shows symmetric hyperintense diffuse white matter lesions. (Courtesy of Judith Donovan Post, University of Miami School of Medicine.)

Citation: Booss J, Esiri M. 2003. 12 HIV/AIDS, p 193-220. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch12
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