Human immunodeficiency virus syndrome

Human Immunodeficiency Virus. Human immunodeficiency vims (HIV) causes Acquired Immunodeficiency Syndrome (AIDS), which has no cure. HIV infects the cells of the human immune system, such as T-lymphocytes, monocytes, and macrophages. After a long period of latency and persistent infection, it results in the progressive decline of the immune system, and leads to full-blown AIDS, resulting in death. 

Wiley CA, Achim C (1994) Human immunodeficiency virus encephalitis is the pathological correlate of dementia in acquired immunodeficiency syndrome. Ann Neurol 36(4) 673-676 Wiley CA, Baldwin M, Achim CL (1996) Expression of HIV regulatory and structural mRNA in the central nervous system. Aids 10(8) 843-847... 

Wiley CA, MasUah E, Morey M, Lemere C, DeTeresa R, Grafe M, Hansen L, Terry R (1991) Neocorfical damage during HIV infection. Ann Neurol 29(6) 651-657 Wiley CA, Schrier RD, Nelson JA, Lampert PW, Oldstone MB (1986) Cellular localization of human immunodeficiency virus infection within the brains of acquired immune deficiency syndrome patients. Proc Natl Acad Sci USA 83(18) 7089-7093 Williams K, Westmoreland S, Greco J, Ratai E, Lentz M, Kim WK, Fuller RA, Kim JP, Autissier... 

Barohn RJ, Gronseth GS et al (1993) Peripheral nervous system involvement in a large cohort of human immunodeficiency virus-infected individuals. Arch Neurol 50(2) 167-171 Behar R, Wiley C et al (1987) Cytomegalovirus polyradiculoneuropathy in acquired immune deficiency syndrome. Neurology 37(4) 557-561... 

Blum AS, Dal Pan GJ et al (1996) Low-dose zalcitabine-related toxic neuropathy frequency, natural history, and risk factors. Neurology 46(4) 999-1003 Bradley WG, Verma A (1996) Painful vascuhtic neuropathy in HlV-1 infection relief of pain with prednisone therapy. Neurology 47(6) 1446-1451 Breen EC (2002) Pro- and anti-inflammatory cytokines in human immunodeficiency virus infection and acquired immunodeficiency syndrome. Pharmacol Ther 95(3) 295-304 Bremer J (1990) The role of carnitine in intracellular metabolism. J Clin Chem Clin Biochem 28(5) 297-301... 

Hoschele D (2006) Cell culture models for the investigation of NRTI-induced mitochondrial toxicity. Relevance for the prediction of clinical toxicity. Toxicol In Vitro 20(5) 535-546 Itescu S, Brancato LJ et al (1989) A sicca syndrome in HIV infection association with HLA-DR5 and CDS lymphocytosis. Lancet 2(8661) 466 68 Itescu S, Brancato LJ et al (1990) A diffuse infiltrative CDS lymphocytosis syndrome in human immunodeficiency virus (HIV) infection a host immune response associated with HLA-DR5. Ann Intern Med 112(1) 3-10... 

Pettersen JA, Jones G et al (2006) Sensory neuropathy in human immunodeficiency virus/acquired immunodeficiency syndrome patients protease inhibitor-mediated neurotoxicity. Ann Neurol... 

Puthanakit T, Oberdorfer P et al (2006) Immune reconstitution syndrome after highly active antiretroviral therapy in human immunodeficiency virus-infected thai children. Pediatr Infect Dis J... 

The human immunodeficiency virus (HIV lymphadenopathy-associated virus, LAV human T-cell lymphotrophic virus type 3, HTLV III) is responsible for acquired immune deficiency syndrome (AIDS see Chapter 3). Because of the hazard and difficulties of growing the virus outside humans, a different approach has to be examined for determining viral sensitivity to disinfectants. 

Infection with a human immunodeficiency virus (HIV-1 and HIV-2 see Chapter 3) can cause the destruction of the TH cell, which is the eritieal eell of the immune system. This leads to the condition known as acquired immune deficieney syndrome (AIDS). At present, it is still not known why, in some cases, infection with HIV leaves the immune system intact whereas in others it is irreversibly destroyed, giving rise to AIDS. 

The acquired immune deficiency syndrome (AIDS) was first recognized in 1981, and described in a cohort of young homosexual men with significant immune deficiency. Since then, human immunodeficiency virus type 1 (HIV-1) has been clearly identified as the major cause of AIDS.1 HIV-2 is much less prevalent than HIV-1, but also causes AIDS. HIV primarily targets CD4+ lymphocytes, which are critical to proper immune system function. If left untreated, patients experience a prolonged asymptomatic period followed by rapid, progressive immunodeficiency. Therefore, most complications experienced by patients with AIDS involve opportunistic infections and cancers. 

AIDS, acquired immune deficiency syndrome HIV, human immunodeficiency virus. (Adapted from the DHHS Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents, April 7, 2005.)... 

Neuropathy in human immunodeficiency virus infection has many causes. Multiple mechanisms cause neuropathy in patients with HIV. An immune-mediated, Guillain-Barre-like syndrome (see below) may occur at the time of HIV seroconversion. Later in the course of infection, patients may present with mononeuropathy multiplex, sometimes as a consequence of vasculitis associated with coinfection with hepatitis C. Distal sensory-autonomic axonal polyneuropathy may develop in patients with more advanced HIV, either as a consequence of high titers of HIV itself or of the neurotoxicity of antiretroviral drugs [18,19],... 

HIV, human immunodeficiency virus STD, sexually transmitted disease TSS, toxic shock syndrome UTI, urinary tract infection. 

Human Immunodeficiency Virus/Acquired Immune Deficiency Syndrome... 

AIDS, acquired immune deficiency syndrome HIV, human immunodeficiency virus PGL, persistent generalized lymphadenopathy. 

Acquired immune deficiency syndrome Human immunodeficiency virus... 

The human immunodeficiency virus began to spread among the homosexual population in the United States in the late 1970s, but it was not until 1981 that physicians in New York and at the Centers for Disease Control in Atlanta recognized the new clinical syndrome (acquired immunodeficiency syndrome), alerting the world to a new and fatal infection. 

In a biopsy of an AIDS patient s enlarged thymus (P4), the adipose involuted thymus, with persistence of many Hassall s corpuscles, was judged to be a large lymphoid follicular hyperplasia. This follicular hyperplasia was similar to that described for lymph nodes, spleen, and other lymphoid tissues at earlier stages of human immunodeficiency virus infection, before the development of acquired immune deficiency syndrome. Human immunodeficiency virus RNA and p 24 were detected in the hyperplastic germinal centers (lymphocytes and follicular dendritic infected cells) and also in many cells that may have been either lymphocytes or epithelial cells in the interfollicular areas. 

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