Etiology of HIV-Associated Dementia

The etiologic agents of the neurological disease associated with pitying immunodeficiency virus and support are some(prenominal). Opportunistic infections- cryptococcus, toxoplasmosis, cytomegalo virus, are a few of the ingrained causes of neurologic disease in AIDS patients, notwithstanding bequeath not be the briny focus of this paper. The human immunodeficiency virus in itself is regard in much of the neurological manifestations of the disease, and it is the cause of the presence of the virus deep down the cardinal nervous dodging of rules which is of interest to me in this paper. \nWith the approach of more than(prenominal) consequenceive passing active antiretroviral therapy (HAART) and thus increase life span of muckle with AIDS, neurological disorders are bonnie a hot upshot in AIDS research. In the early(a) days of the epidemic, those infected with the virus could scarcely hold to live for a gyp time before develop the symptoms of broad blown AIDS , and decease ensued shortly afterwards. The progress make in discussion in the past two decades has protracted the lives of people with AIDS, to the point where diagnosing is no recollectiveer a sign of imminent enervation and wipeout, but rather an acknowledgment of a possible long road ahead with the assistance of drug cocktails. There is excessively a strong chance that the human immunodeficiency virus infected soul whitethorn develop human immunodeficiency virus associated frenzy after eld of living with the disease (1). \n\nhuman immunodeficiency virus associated monomania (HAD) is comprised of a spectrum of conditions from the wacky human immunodeficiency virus-1 repulse cognitive-motor disorder to stern and debilitating AIDS madness complex. Symptoms begin with motor slowing (2), and may progress to repelling red ink of cognitive function, loss of bladder and bowel chink, and paraparesis . A classification carcass has been formulate for HIV associated d ementia: \n\n re-create 0: Normal \n do 0.5: Subclinical or forked \nMinimal or obscure symptoms. \nMild (soft) neurological signs. \nNo impairment of acidulate or activities of daily living (ADL). \n symbolize 1: Mild \n unequivocal happy or motor impairment. \nAble to do on the whole but the most demanding work or ADL. \n fix up 2: Moderate \nCannot work or perform demanding ADL. \nCapable of self-care. \nAmbulatory, but may need a single prop. \nStage 3: Severe \nmajor(ip) intellectual disability, or \nCannot walk unassisted. \nStage 4: End-Stage \nNearly vegetative. \n3. \ndisease may government issue from the accept presence of the virus in the primeval nervous system, toxins released from the virus, the bodys immunologic responses, or any bit of other positionors. Studies live anchor that non physiological levels of cytokines in the genius may dumbfound an effect of enhancing comeback of HIV 3. Neurodegeneration is implicated in causing the manifestations of dem entia, even so the mechanism for neuronal death or malfunction is unknown as of yet. \n\nA riddle of HIV associated dementia was the fact that the human immunodeficiency virus does not seem to infect neurons. However, the virus has been base to infect astrocytes, a type of glial mobile ph atomic number 53 within the distrust. In 1998, researchers 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 keep group of HIV patients without dementia 4. This supports the idea that the astrocytes, which provide a major(ip) mechanism for removing glutamate from the learning ability, track down a role in dementia. Taken into context, the researchers postulated that the next metre in this research should be to determine the effect of the programmed cell death of the astrocytes on nerve cells. \n\nIt has been postulated t hat the exchange nervous system provides a sanctuary for the persistance and yield of HIV, main(a) of peripheral viral operation 5. Many drugs used for treatment of HIV are unable(p) to cross the demarcation promontory barrier, and thus virus is saved 6. The majority of research has support this idea, however a bod of studies have found that viral loads within the central nervous system may be scratched by antiretroviral therapy. Issues complicating this matter include a shortage of concrete education closely the mechanism for the viruss entrance past the blood- idea barrier and into the brain. It has been found that HIV can depart within monocytes (cells which differentiate into macrophages) trafficking into the central nervous system. In the by and by phase angles of AIDS, there is may be an influx of monocytes into the brain, triggered by the replication of HIV and the immune activating in the brain. The monocytes not only bring HIV into the brain done the blood brain barrier, but can similarly act as a reservior for further infection by the virus 7. \n\nThese pieces of research logic eachy present answers to some of the questions or so the etiology of HIV associated dementia. However, results generated through other research have presented at odds(p) information. This leads us the question of, which research presents us with the authorised answers? A lack of indicate of one straightforward causative mechanism implies a more complicated etiology and calls for go along multi-disciplinary research on these conditions. \n\ndeuce articles presented in Science clip last year represent the controversy 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 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 associat ed dementia may be controlled peripherally through HAART. She also states that proteinase inhibitors have led to a decrease 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 enamor HAART, HIV associated dementia ordain 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 of the antiretroviral drugs have great bother penetrating the blood brain barrier, and cannot get into the brain in significant enough levels to affect the viral loads there. Although it is heavy to assay the viral load in the brain duration a patient is living, post-mortem studies have supported the idea that the virus does appear to be defend while in the brain, and viral load levels differ from those of the periphery 6. They also state that it is a significant finding that HIV is indeed present in the brain very early in infection, and can return itself there, as a holy terror to neurological functioning at any time. \n\nPresently, we are go forth with more questions than answers on this topic. Is this because of the tangled nature of the nervous system? We are constantly left field with gaps in our companionship 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 medical challenges in novel history. They bring together the knowledge and research methods of neuroscientists, immunologists, virologists, and psychologists, among others, to attempt to maintain and piece together all of the elements of this disease 8. The common ending of all of their research is the growing of a functional working model for the development of remedy solutions to put an end to the slimy caused by the HIV virus. If you fatality to get a full essay, order it on our website:

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