Day 2 :
Keynote Forum
Lynn Pulliam
Professor in Residence, Chief, Microbiology (VAMC) Laboratory Medicine and Medicine Clinical Laboratory,University of California, USA
• Outstanding Women in Neuroscience Lectureship, ISNV 2009
• President, International Society for Neurovirology – 2010-2012
Keynote: The evolution of the impact of peripheral immune activation on HIV cognitive impairment
Time : 09:30-10:00
Biography:
Lynn Pulliam received her PhD from the University of San Francisco Medical School in 1983. She is a Professor of Laboratory Medicine and Medicine at the University of California, San Francisco as well as Chief of Microbiology at the San Francisco Veterans Affairs Medical Center. She is the past President of the International Society for Neurovirology and serves on several editorial boards.
Abstract:
Human immunodeficiency virus (HIV) severely impacts the immune system causing phenotypic changes in peripheral cells altering both innate and adaptive immunity. In the acute phase, HIV attacks and kills CD4+T cells, followed by monocyte/macrophage (M/Mï¦) activation and an acute-phase inflammatory response. Approximately 30% of HIV-infected individuals develop an associated dementia caused by toxic soluble factors from activated M/Mï¦ï€ . With the introduction of antiretroviral therapy (ART), most infected individuals respond to therapy with a lowering of the viral load to undetectable and reconstitution to normal immune function. However, some individuals do not return to normal immune function and their M/Mï¦ continues to be activated. This continued peripheral monocyte immune activation, now chronic, continues to be associated with cognitive impairment as well as other co-morbidities. The factors responsible for this have changed as new biomarkers for milder cognitive impairment are evolving. Since the M/Mï¦ migrates to the brain, the activation state of this immune cell is critical. New mechanisms for cell-to-cell communication have been introduced. Exosomes are lipid vesicles normally secreted by a number of cells in the plasma and tissues but are increased and altered in pathological conditions. They can transport functional nucleic acids (mRNAs, miRNAs) and proteins into recipient neural cells. Monocyte-derived exosomes can enter neural cells and contribute to neural cell dysfunction by the transfer of dysregulated miRNAs. Activated monocyte-derived exosomes may contribute to the transfer of neurotoxic cargo from M/Mï¦ï€ to resident neural cells. Alternatively, miRNAs within exosomes may be exploited as a therapeutic target to diminish neural cell activation.
Keynote Forum
Sulie Chang
Seaton Hall University , USA
Keynote: HIV infection, NeuroHIV and Use of Addicitve Substances
Time : 10:00-10:30 am
Biography:
rnDr. Sulie L. Chang is the Director of the Institute of Neuroimmune Pharmacology and a Professor of Biological Sciences and Neuroscience at Seton Hall University in New Jersey. rnDr. Chang’s research is to sudy the interactions between various addictive substances including alcohol, morphine, as neuroHIV, and behavioral disorders caused by substance abuse, with the central hypothesis that neuroinflammation promotes substance abuse. Dr. Chang has been continuously funded by NIH since 1989. She has published over 100 articles in refereed journals with significant impact. Dr. Chang’s services to the scientific community include participation as a reviewer on more than 110 NIH Study Sections including as a member [2010-2014] and the Chairperson [2012-2014 of the Innate Immunity and Inflammation (III) Study Section. Dr. Chang has served on several editorial boards including the Journal of Neurovirology and Journal of Neuroimmune Pharmacology. rn
Abstract:
Abuse of addictive substances, including morphine, methamphetamine, and alcohol, is a key co-morbidity in human immunodeficiency virus-1 (HIV-1) infection. Use of various addictive substances hastens the progression of HIV-1 infection and HIV-associated neurocognitive disorders. Even with combination active anti-retroviral therapy (cART), HIV-1 viral proteins are still expressed in the body and eradication of the virus, particularly in the brain, the key reservoir organ, does not occur. Thus, the clinical challenge in the treatment of HIV infection is inflammation of the CNS and the subsequent neurological disorders. HIV-1-infected individuals reportedly use addictive substances more than the general public. There has recently been a shift from studying the detrimental impact of additive substances on HIV infection to investigation of whether HIV infection can lead to substance abuse. The HIV-1 transgenic (HIV-1Tg) rat mimiks HIV patients given cART. Even in the absence of infection, the presence of viral proteins in the HIV-1Tg rat causes immune deficiencies, neuroinflammation, and neurocognitive deficits similar to those seen in HIV-1-infected humans, such as a decline in cognitive abilities and decreased behavioral flexibility. We have demonstrated that HIV-1Tg rats are more prone to both behavioral sensitization and acute physiological effects (hyperthermia) of methamphetamine; they exhibit an increased sensitivity to morphine’s anti-nociceptive properties; and they have an increased sensitivity to the effects of binge consumption of ethanol. These studies suggest that HIV-1-induced neurological deficits and alterations in behavior associated with substance abuse and addiction may be a result of viral protein-induced neuroinflammation (partially supported by DA036175 and AA023172).