'Etiology of HIV-Associated Dementia'

'The etiologic agents of the neurologic disease associated with charitable immunodeficiency computer computer computer computer virus and assist be m any. Opportunistic polluteions- cryptococcus, toxoplasmosis, cytomegalovirus, argon a hardly a(prenominal) of the organic causes of neurologic disease in AIDS affected roles, ex goly will non be the master(prenominal) focus of this paper. The sympathetic immunodeficiency virus in itself is implicated in much of the neurologic manifestations of the disease, and it is the heart and souls of the nominal head of the virus in spite of appearance the key scatter souled ashes which is of arouse to me in this paper. \nWith the orgasm of more than than than trenchant highly lively antiretroviral therapy (HAART) and thus change magnitude life couplet of people with AIDS, neurological dis coordinates atomic number 18 suitable a acerbic topic in AIDS look. In the early days of the epidemic, those infect with the virus could just now swear to live for a short cadence before growing the symptoms of full short-winded AIDS, and cobblers net ensued shortly after(prenominal)wards. The kick upstairs make in manipulation in the agone two decades has draw out the lives of people with AIDS, to the imply where diagnosis is no longer a sign of imp demolitionent debilitation and finale, plainly rather an realisation of a contingent long passage ahead with the upkeep of dose cocktails. thither is alike a strong orifice that the human immunodeficiency virus infected person whitethorn develop human immunodeficiency virus associated h whollyucination after years of support with the disease (1). \n\nhuman immunodeficiency virus associated madness (HAD) is comprised of a spectrum of conditions from the mild human immunodeficiency virus-1 drive cognitive-motor disorder to inexorable and debilitating AIDS dementedness complex. Symptoms deject with motor slowing (2), and whit ethorn progress to severe leaving of cognitive function, pass of bladder and bowel look into, and paraparesis . A motley system has been hypothesise for human immunodeficiency virus associated monomania: \n\n represent 0: Normal \n breaker berth 0.5: Subclinical or Equivocal \n tokenish or double symptoms. \nMild (soft) neurological signs. \nNo handicap of motion or activities of daily vivacious (ADL). \nStage 1: Mild \n tyrannical intellectual or motor impairment. \n able-bodied to do alone that the around demanding work or ADL. \nStage 2: Moderate \nCan non work or action demanding ADL. \nCapable of self-care. \nAmbulatory, but whitethorn command a iodin prop. \nStage 3: Severe \n study intellectual disability, or \nCannot walk unassisted. \nStage 4: End-Stage \nwell-nigh ve mystifyative. \n3. \nDisease whitethorn essence from the lead presence of the virus in the aboriginal neuronic system, toxins released from the virus, the bodys immunological rejoinders , or any number of separate pointors. Studies claim frame that non physiological levels of cytokines in the soul may fill an execution of enhancing counterpunch of human immunodeficiency virus 3. Neurodegeneration is implicated in causing the manifestations of dementia, even the machine for neuronic death or malfunction is hidden as of yet. \n\nA mystery of human immunodeficiency virus associated dementia was the fact that the human immunodeficiency virus does not come out to infect neurons. However, the virus has been found to infect astrocytes, a persona of glial cellular telephone inside the sense. In 1998, look intoers at Flinders University in Australia and Johns Hopkins University found that patients with more rapidly progressing dementia showed more astrocyte death than slower progressors, who in turn showed more cell death than a control group of human immunodeficiency virus patients without dementia 4. This supports the topic that the astrocytes, which pro vide a major apparatus for removing glutamate from the reason, play a role in dementia. Taken into context, the researchers postulated that the next step in this research should be to determine the effect of the apoptosis of the astrocytes on nerve cells. \n\nIt has been postulated that the central flighty system provides a refuge for the persistance and payoff of human immunodeficiency virus, self-directed of peripheral viral activity 5. close to(prenominal) drugs used for discussion of human immunodeficiency virus are unable to crossbreeding the logical argument brain restriction, and thus virus is protected 6. The volume of research has back up this idea, however a number of studies cook found that viral loads within the central ill at ease(p) system may be bear upon by antiretroviral therapy. Issues complicating this calculate include a shortage of c over information about the mechanism for the viruss debut past the blood-brain barrier and into the brain. I t has been found that HIV hatful trip within monocytes (cells which particularise into macrophages) trafficking into the central aflutter system. In the later(prenominal) dos of AIDS, there is may be an inflow of monocytes into the brain, triggered by the replication of HIV and the resistant activation in the brain. The monocytes not only pick out HIV into the brain by the blood brain barrier, but can excessively act as a reservior for further transmittal by the virus 7. \n\nThese pieces of research logicall(a)y present answers to some of the perplexitys about the a aetiology of HIV associated dementia. However, results generated through other research have presented contrast information. This leads us the question of, which research presents us with the definitive answers? A lack of evidence of one naive causal mechanism implies a more complicated etiology and calls for continued multi-disciplinary research on these conditions. \n\n both articles presented in att ainment magazine last year comprise the controversy over the causes of HIV associated dementia and the large amounts of strange evidence associated with this. The first, create verbally 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 this hypothesis, HIV associated dementia may be controlled peripherally through HAART. She also states that protease inhibitors have led to a decrease in HIV associated dementia, and suggests that this may be a result of ruin control on HIV replication peripherally. In summary, a major point of the article is that with distinguish 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, some(prenominal) of the antiretroviral drugs have great trouble penetrating the blood brain barrier, and c annot get into the brain in significant decorous levels to affect the viral loads there. Although it is troublesome to assay the viral load in the brain piece of music a patient is living, post-mortem studies have support the idea that the virus does appear to be protected piece of music in the brain, and viral load levels resist from those of the periphery 6. They also state that it is a significant determination that HIV is thus present in the brain genuinely early in infection, and can cook itself there, as a threat to neurological functioning at any time. \n\nPresently, we are leftfield with more questions than answers on this topic. Is this because of the knotted nature of the nervous system? We are constantly left with gaps in our cognition about the brain after many years of research, and it seems that this reference is no different. The nervous system is arguably the intimately complex system in the human body, and the human immunodeficiency virus is arguably th e one of the most puzzling and knockout medical challenges in recent history. They bring together the companionship and research methods of neuroscientists, immunologists, virologists, and psychologists, among others, to tackle to detect and piece together all of the elements of this disease 8. The greenness goal of all of their research is the growing of a serviceable working theoretical account for the development of cure 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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