The etiologic agents of the neurologic ailment associated with adult male immunodeficiency virus and acquired immune deficiency syndrome be m any(prenominal). Opportunistic infections- cryptococcus, toxoplasmosis, cytomegalo virus, are a few of the organic causes of neurologic complaint in AIDS patients, and will non be the main commission of this paper. The human immunodeficiency virus in itself is implicated in much(prenominal) of the neurological manifestations of the disease, and it is the effects of the nominal head of the virus in spite of take careance the pro ensnare dying(p) system which is of quest to me in this paper. \nWith the advent of to a greater extent effective highly fighting(a) antiretroviral therapy (HAART) and at that placefore increased living(a) span of race with AIDS, neurological dis set outs are becoming a hot topic in AIDS question. In the archaean days of the epidemic, those infected with the virus could only hope to constitute for a short period before developing the symptoms of int execute blown AIDS, and stopping suggest ensued before long afterwards. The progress made in treatment in the ago two decades has prolonged the lives of people with AIDS, to the point where diagnosis is no longer a bulls eye of imminent debilitation and destruction, scarcely rather an acknowledgement of a possible long itinerary ahead with the aid of medicine cocktails. There is likewise a strong possibility that the human immunodeficiency virus infected person whitethorn develop human immunodeficiency virus associated madness after days of living with the disease (1). \n\nhuman immunodeficiency virus associated h solelyucination (HAD) is comprised of a spectrum of conditions from the mild human immunodeficiency virus-1 travel cognitive-motor disorder to severe and enfeeble AIDS hallucination complex. Symptoms lead off with motor slowing (2), and whitethorn progress to severe divergence of cognitive funct ion, loss of bladder and bowel control, and paraparesis . A classification system has been formulated for human immunodeficiency virus associated dementia: \n\nStage 0: Normal \nStage 0.5: subclinical or Equivocal \n tokenish or equivocal symptoms. \n soft (soft) neurological signs. \nNo harm of work or activities of free-and-easy living (ADL). \nStage 1: Mild \nUnequivocal expert or motor impairment. \n open to do all tho the some demanding work or ADL. \nStage 2: chairman \nCan non work or complete demanding ADL. \nCapable of self-care. \nAmbulatory, but whitethorn need a angiotensin-converting enzyme prop. \nStage 3: knockout \nMajor intellectual disability, or \nCannot walk unassisted. \nStage 4: End-Stage \nNearly ve gear upative. \n3. \nDisease whitethorn result from the direct posture of the virus in the fundamental ill at ease(p) system, toxins released from the virus, the bodys immunological responses, or any number of an early(a)(prenominal) factors. Studies guide found that non physiological levels of cytokines in the creative thinker may devote an effect of enhancing proceeds of human immunodeficiency virus 3. Neurodegeneration is implicated in causing the manifestations of dementia, yet the mechanics for neuronal death or malfunction is unknown as of yet. \n\nA mystery of human immunodeficiency virus associated dementia was the fact that the human immunodeficiency virus does not reckon to infect neurons. However, the virus has been found to infect astrocytes, a font of glial cell indoors the adept. In 1998, queryers at Flinders University in Australia and Johns Hopkins University found that patients with more than cursorily progressing dementia showed more astrocyte death than slower progressors, who in reverse showed more cell death than a control conference of human immunodeficiency virus patients without dementia 4. This supports the caprice that the astrocytes, which provide a study apparatus for removing glutama te from the head word, play a role in dementia. taken into context, the lookers postulated that the next step in this research should be to cast the effect of the apoptosis of the astrocytes on nerve cells. \n\nIt has been postulated that the central neuronal system provides a psychiatric hospital for the persistance and replication of HIV, independent of skirting(prenominal) viral activity 5. umpteen drugs used for treatment of HIV are unable to go bad the blood brain barrier, and thus virus is protected 6. The legal age of research has back up this idea, til now a number of studies claim found that viral tons within the central loathsome system may be affected by antiretroviral therapy. Issues complicating this motion include a shortage of concrete information just about the mechanism for the viruss entry historic the blood-brain barrier and into the brain. It has been found that HIV can travel within monocytes (cells which differentiate into macrophages) traff icking into the central nervous system. In the later stages of AIDS, there is may be an inflow of monocytes into the brain, triggered by the replication of HIV and the immune activation in the brain. The monocytes not only communicate HIV into the brain by with(predicate) the blood brain barrier, but can also act as a reservior for come along infection by the virus 7. \n\nThese spells of research logically pose answers to some of the questions about the etiology of HIV associated dementia. However, results generated through other research have presented counterpoint information. This leads us the question of, which research presents us with the definitive answers? A lack of severalise of peerless straightforward causal mechanism implies a more tangled etiology and calls for continued multi-disciplinary research on these conditions. \n\nTwo articles presented in Science magazine stomach year exemplify the rivalry over the causes of HIV associated dementia and the large a mounts of conflicting evidence associated with this. The first, written by Suzanne Gartner, hypothesizes that HIV associated dementia is the result of the influx of infected blood monocytes into the brain during end stage disease, and proposes that under(a) this hypothesis, HIV associated dementia may be controlled peripherally through HAART. She also states that protease inhibitors have led to a light in HIV associated dementia, and suggests that this may be a result of better control on HIV replication peripherally. In summary, a major point of the article is that with appropriate HAART, HIV associated dementia will not occur 7. \n\nIn a response to this article, Major and colleagues wrote that although HIV seems to be controlled peripherally by drug therapy, many of the antiretroviral drugs have great difficulty go in the blood brain barrier, and cannot puzzle into the brain in profound enough levels to affect the viral bear downs there. Although it is difficult to assay t he viral load in the brain composition a patient is living, post-mortem studies have supported the idea that the virus does appear to be protected while in the brain, and viral load levels differ from those of the periphery 6. They also state that it is a authoritative finding that HIV is so present in the brain very early in infection, and can establish itself there, as a threat to neurological functioning at any time. \n\nPresently, we are left with more questions than answers on this topic. Is this because of the elusive temperament of the nervous system? We are constantly left with gaps in our knowledge about the brain after many years of research, and it seems that this case is no different. The nervous system is arguably the most complex system in the human body, and the human immunodeficiency virus is arguably the one of the most puzzling and difficult health check challenges in recent history. They down together the knowledge and research methods of neuroscientists, im munologists, virologists, and psychologists, among others, to attempt to detect and piece together all of the elements of this disease 8. The common goal of all of their research is the evolution of a functional working exemplification for the development of therapeutic solutions to empower an end to the suffering caused by the HIV virus. If you want to get a full essay, order it on our website:
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