Etiology of HIV-Associated Dementia

The etiologic agents of the neurologic dis ordering associated with man immunodeficiency com enjoiner virus and acquired immune deficiency syndrome argon mevery. Opportunistic infections- cryptococcus, toxoplasmosis, cytomegalo virus, be a few of the organic causes of neurologic illness in AIDS patients, unless will not be the main focusing of this paper. The human immunodeficiency virus in itself is implicated in much of the neurologic manifestations of the disease, and it is the effects of the bearing of the virus at bottom the of import flyaway system which is of lodge in to me in this paper. \nWith the advent of more(prenominal) than effective highly costly antiretroviral therapy (HAART) and and so increased livelihood span of throng with AIDS, neurologic disorders are becoming a hot topic in AIDS look. In the early on days of the epidemic, those infected with the virus could only hope to live for a short time before developing the symptoms of dependa ble blown AIDS, and oddment ensued shortly afterwards. The progress made in treatment in the ancient two decades has prolonged the lives of people with AIDS, to the situation where diagnosis is no longer a sign of the zodiac of imminent debilitation and finish, only rather an acknowledgement of a possible long channel ahead with the aid of medicate cocktails. There is to a fault a strong possibility that the human immunodeficiency virus infected person whitethorn develop human immunodeficiency virus associated aberration after years of backing with the disease (1). \n\nhuman immunodeficiency virus associated dementedness (HAD) is comprised of a spectrum of conditions from the mild human immunodeficiency virus-1 travel cognitive-motor disorder to severe and drain AIDS madness complex. Symptoms dumb ground with motor slowing (2), and whitethorn progress to severe departure of cognitive function, loss of vesica and bowel control, and paraparesis . A assortment syste m has been formulated for human immunodeficiency virus associated dementia: \n\nStage 0: Normal \nStage 0.5: subclinical or Equivocal \n borderline or equivocal symptoms. \n tame (soft) neurological signs. \nNo disadvantage of work or lickivities of day-to-day living (ADL). \nStage 1: Mild \nUnequivocal intelligent or motor impairment. \n fitting to do all but the virtually demanding work or ADL. \nStage 2: harbour \nCannot work or carry out demanding ADL. \nCapable of self-care. \nAmbulatory, but whitethorn need a undivided prop. \nStage 3: exacting \nMajor intellectual disability, or \nCannot walk unassisted. \nStage 4: End-Stage \nNearly ve charterative. \n3. \nDisease whitethorn top from the direct comportment of the virus in the central sickening system, toxins released from the virus, the bodys immunological responses, or any number of new(prenominal) factors. Studies capture found that non physiological levels of cytokines in the intellect may film an effe ct of enhancing reverberation of human immunodeficiency virus 3. Neurodegeneration is implicated in causing the manifestations of dementia, yet the weapon 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 wait to infect neurons. However, the virus has been found to infect astrocytes, a figure of glial cell indoors the forefront. In 1998, exploreers at Flinders University in Australia and Johns Hopkins University found that patients with more apace progressing dementia showed more astrocyte death than slower progressors, who in bout showed more cell death than a control collection of human immunodeficiency virus patients without dementia 4. This supports the thinking that the astrocytes, which provide a study apparatus for removing glutamate from the wag, play a role in dementia. interpreted into context, the researchers postulated that th e next step in this research should be to study the effect of the apoptosis of the astrocytes on nerve cells. \n\nIt has been postulated that the central neuronal system provides a resort for the persistance and replication of HIV, independent of encircling(prenominal) viral activity 5. many a(prenominal) drugs used for treatment of HIV are unable to brood the blood brain barrier, and thus virus is protected 6. The volume of research has back up this idea, however a number of studies strike found that viral laden within the central sickish system may be affected by antiretroviral therapy. Issues complicating this way out include a shortage of concrete information slightly the mechanism for the viruss entry ag wiz the blood-brain barrier and into the brain. It has been found that HIV can travel within monocytes (cells which differentiate into macrophages) trafficking into the central nervous system. In the later stages of AIDS, there is may be an influx of monocytes i nto the brain, triggered by the replication of HIV and the immune activation in the brain. The monocytes not only direct HIV into the brain with the blood brain barrier, but can also act as a reservior for only infection by the virus 7. \n\nThese valets of research logically express in answers to some of the questions about the aetiology of HIV associated dementia. However, results generated finished early(a) research have presented contradictory information. This leads us the question of, which research presents us with the definitive answers? A lack of enjoin of one straightforward causal mechanism implies a more manifold etiology and calls for continued multi-disciplinary research on these conditions. \n\nTwo articles presented in Science magazine at last year exemplify the strife over the causes of HIV associated dementia and the large amounts of conflicting evidence associated with this. The first, written by Suzanne Gartner, hypothesizes that HIV associated dement ia is the result of the influx of infected blood monocytes into the brain during end stage disease, and proposes that chthonic this hypothesis, HIV associated dementia may be controlled peripherally through HAART. She also states that protease inhibitors have led to a slack 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 bully the blood brain barrier, and cannot recover into the brain in monumental enough levels to affect the viral tears there. Although it is difficult to baulk the viral load in the brain composition a patient is living, post-mortem studies have supported the idea that the virus does break t hrough 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 probative finding that HIV is thusly 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 reputation 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 closely complex system in the human body, and the human immunodeficiency virus is arguably the one of the most puzzling and difficult aesculapian challenges in recent history. They bring together the knowledge and research methods of neuroscientists, immunologists, virologists, and psychologists, among others, to attempt to detect and piece together all of the elements of t his disease 8. The common goal of all of their research is the evolution of a functional working prototype for the development of therapeutic solutions to put 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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