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Cd4 cell count at diagnosis of dementia appears to be increasing, from 70 cells/µl in 1992-1995 to clxx cells/µl in 1997. (12) pathogenesis of aids dementia complex the role of hiv-1 proliferation itself in the development of aids dementia complex (adc) is controversial. Although viral strains that are particularly efficient at replicating in brain macrophages may play a role in the pathogenesis of brain injury,(13,14) a heavy "viral burden" in brain has not been linked consistently with clinical aids dementia. (15) some investigators hold that increased hiv-1 proliferation in the brain is necessary for the development of adc. Others propose that a macrophage-initiated cascade of events can lead to brain dysfunction and clinical dementia, even in the absence of high viral load in the brain. Activated macrophages, whether infected with hiv or not, are capable of secreting potent neurotoxins, inducing pro-inflammatory cytokines, and generating oxygen free radicals that can damage cells and lead to neuronal dysfunction or death. (16-19) a particular subtype of monocyte/macrophages derived from the peripheral blood was found to be greatly increased among patients with aids dementia compared with both hiv-1-infected and -uninfected controls. Soluble factors from these macrophages were found to be highly neurotoxic--that is, they killed human brain cells in culture. (20) although the incidence of nearly all nervous system opportunistic infections has declined dramatically in the era of potent antiretroviral therapy, the impact on incidence and prevalence of hiv-associated cognitive impairment--including frank adc--has been low. The prevalence of adc in hiv-infected individuals with higher cd4 counts (200-350 cells/µl) actually appears to have increased since 1996. (12) pathologically, the prevalence of hiv-associated brain disease, or encephalopathy, is rising despite suppressive antiretroviral therapy. (21) poor penetration of the blood-brain barrier by many of the antiretroviral drugs, particularly the protease inhibitors, has been suggested as a reason for the persistence of adc. Unfortunately, there is currently no effective way to monitor successful suppression of cns hiv infection, making selection of a cns-penetrating antiretroviral regimen a matter of guesswork rather than clinical science. Patients with adc commonly have no detectable virus in csf. This does not exclude high viral burden in the brain, but rather emphasizes the limitations of csf as a "window on the central nervous system. classicmotocrossimages.com/mbs-uk-viagra-sales-yg/ cheapest viagra online cheapest canadian pharmacy for viagra buy cheap viagra cheap viagra online buy viagra online buy viagra buy generic viagra generic viagra cheap generic viagra " nonetheless, hiv-1-.
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