jules levin, NATAP: HIV/AIDS & neurologic disease EMERGENCY (045)

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jules-evin-ICAAC2007HIV/AIDS and neurologic disease — EMERGENCY

from Jules Levin
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By now it’s pretty clear aging with HIV and getting to over 55 yrs old is puting many patients at increased risk compared to HIV-negatives for frailty, increased neurologic disorders and cognitive impairment, kidney disease, CVD, and of course bone disease and fractures.
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Mortality will start to increase soon as a result of this development while we have been blindly rejoicing the success of HAART for years.
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BY devoting all our resources overseas we lost sight of these developments, and like turning an ocean liner around it is difficult now to get the NIH & NIAID to refocus effectively to address immediately tis time sensitive problem, if it’s not too late already.
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the fact is currently it’s estimated 20% with HIV in the USA are over 50 yrs old and by 2015 50% will be over 50. For the first time a significant portion of patients are reaching 65 yrs of age and facing increased HIV-related risk for vascular disease due to ARTs and HIV. Mitochondrial toxicity has been present for 20-30 years for many patients. Abnormal metabolics including lipoatropy are threatening to cause neurologic disorders for older patients. Frailty and gait disorders are emerging in older patients and in MACS. 60% of patients at 45 yrs old on average have osteopenia and 15% osteoporosis, isn’t that stunning.
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It is time not to say we are aware of this, as researchers are saying, but it is time to declare an EMERGENCY situation before it’s too late, it’s already very late to or too late for many patients to benefit from research in this area.
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What is the NIH thinking, where is leadership? Researchers, doctors, patients, and advocates should raise their cries for a declaration of emergency to address this NOW!
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Let me briefly mention HCV coinfection. 10 years ago I raised discussion about this problem that 30% had HCV in HIV, that 80% of IDUs had coinfection, that we were ignoring the needs crying out for greater attention. HCV became the leading cause for death and hospitalization besides AIDS. This problem persists, patients have been dying of end stage liver disease and the Federal government and advocates never launched a proper response.
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Will the same thing happen regarding aging?
We need a proportional response to the level of problem we face
“The results of this study extend previous observations indicating that current HAART regimens are inadequate to treat HIV-related NC”….“These findings indicate that patients with more severe memory impairment and executive dysfunction are more likely to remain neurocognitively impaired despite HAART”
Mechanisms of Neuronal Injury and Death in HIV-1 Associated Dementia – (10/24/08)
Infection with the human immunodeficiency virus-1 (HIV-1) and acquired immunodeficiency syndrome (AIDS) remain a persistent and even growing health problem worldwide. Besides its detrimental systemic effects on the immune system, HIV-1 seems to enter the brain very soon after peripheral infection and can induce severe and debilitating neurological problems that include behavioral abnormalities, motor dysfunction and frank dementia. Infected peripheral immune cells, in particular macrophages, appear to infiltrate the CNS and provoke a neuropathological response involving all cell types in the brain. Both viral and host factors, such as the viral strain and the response of the host’s immune system, strongly influence the course of HIV-1 disease. Moreover, HIV 1-dependent disease processes in the periphery have a substantial effect on the pathology developing in the central nervous system (CNS), although the brain eventually harbors a distinctive viral population of its own. In the CNS, HIV-1 also initiates activation of chemokine receptors, inflammatory mediators, extracellular matrix-degrading enzymes and glutamate receptor-mediated excitotoxicity, all of which can activate numerous downstream signaling pathways and disturb neuronal and glial function. Although there have been substantial improvements in the control of viral infection in the periphery, an effective therapy for HIV-1 associated dementia (HAD) is still not in sight. This article will review recently identified injurious mechanisms potentially contributing to neuronal death in association with HIV-1 disease and discuss recent and prospective approaches for therapy and prevention of HAD.
“Mood changes approaching the extent of disorders are one of many problems associated with HIV-1 disease”

“Neuronal death by apoptosis appears to be one of the hallmarks of neurodegenerative diseases including HAD”

“While HAART has tremendously improved the treatment of HIV-1 infection and disease in the periphery, an effective pharmacotherapy for HAD (HIV-associated dementia) is still not available.”
“HAART is unlikely to prevent the entry of HIV-1 into the CNS”

“Neuronal damage and loss has been observed in distinct brain regions, including frontal cortex”……”signs of neuronal death were not clearly associated with viral burden or a history of dementia”….”aging-associated amyloid accumulation with Alzheimer’s-like neuropathology”….. “Altogether, it seems that a vicious cycle of immune dysregulation, inflammation and BBB dysfunction is required on the side of the host to allow sufficient entry of infected or activated immune cells into the brain and to permit neuronal injury”
“These findings suggest that inflammatory cytokines, including TNF-aand IL-1beta, may have important regulatory roles in HIV-associated neuropathology”

The prevalence and incidence of neurocognitive impairment in the HAART era ACTG Research (08/30/07)
Even with HAART therapy, our data suggest that there is a significant subset of subjects on ALLRT who have mild-to-moderate neurocognitive impairment, and a subset that develop impairment after starting HAART. Additional studies are needed to understand the mechanisms behind neurocognitive impairment and to develop strategies to prevent and treat this condition.”

Neurologic Complications of HIV Disease and Their Treatment

The widespread use of ART has led to a decline in the more severe neurologic complications
of HIV, such as HAD, but people living with HIV continue to 
www.natap.org/2009/CROI/croi_185.htm

HIV-1 Infection Is Associated With an Earlier Occurrence of a 

“We examined whether the FRP was more likely to occur among individuals with comorbidities of cancers and neurological disorders, ascertained according to 
www.natap.org/2009/HIV/042009_12.htm

Neurological/Cognitive Impairment on HAART: 50% on HAART have 

Many factors likely contribute to ongoing neurologic complications despite the ability of current drugs to profoundly suppress viral replication. 
www.natap.org/2008/HIV/121008_01.htm

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