TY - JOUR
T1 - Proceedings from the NIMH symposium on “NeuroAIDS in Africa
T2 - neurological and neuropsychiatric complications of HIV”
AU - Buch, Shilpa
AU - Chivero, Ernest T.
AU - Hoare, Jackie
AU - Jumare, Jibreel
AU - Nakasujja, Noeline
AU - Mudenda, Victor
AU - Paul, Robert
AU - Kanmogne, Georgette D.
AU - Sacktor, Ned
AU - Wood, Charles
AU - Royal, Walter
AU - Joseph, Jeymohan
N1 - Funding Information:
The authors acknowledge funding from National Institutes of Health: MH094160 (to GDK); DA036157 (to SB).
Publisher Copyright:
© 2016, Journal of NeuroVirology, Inc.
PY - 2016/10/1
Y1 - 2016/10/1
N2 - Despite major advances in HIV-1 treatment, the prevalence of HIV-associated neurocognitive disorders (HAND) remains a problem, particularly as individuals on suppressive treatment continue to live longer. To facilitate discussion on emerging and future directions in HAND research, a meeting was held in Durban, South Africa in March 2015 as part of the Society of Neuroscientists of Africa (SONA) conference. The objective of the meeting was to assess the impact of HIV subtype diversity on HAND and immunological dysfunction. The meeting brought together international leaders in the area of neurological complications of HIV-1 infection with special focus on the African population. Research presentations indicated that HAND was highly prevalent and that inflammatory cytokines and immune-activation played important roles in progression of neurocognitive impairment. Furthermore, children on antiretroviral therapy were also at risk for developing neurocognitive impairment. With respect to the effect of HIV-1 subtype diversity, analyses of HIV-1 clade C infection among South Africans revealed that clade C infection induced cognitive impairment that was independent of the substitution in HIV-1 Trans-Activator of Transcription (Tat; C31S). At the cellular level, a Zambian study showed that clade C infection resulted in reduced brain cell death compared with clade B infection suggesting clade specific variations in mediating brain cell injury. Furthermore, ex vivo Tat protein from clade CRF02_AG, prevalent in West/ Central Africa, exhibited reduced disruption of brain endothelium compared with clade B Tat protein. Discussions shed light on future research directions aimed at understanding biomarkers and disease mechanisms critical for HAND.
AB - Despite major advances in HIV-1 treatment, the prevalence of HIV-associated neurocognitive disorders (HAND) remains a problem, particularly as individuals on suppressive treatment continue to live longer. To facilitate discussion on emerging and future directions in HAND research, a meeting was held in Durban, South Africa in March 2015 as part of the Society of Neuroscientists of Africa (SONA) conference. The objective of the meeting was to assess the impact of HIV subtype diversity on HAND and immunological dysfunction. The meeting brought together international leaders in the area of neurological complications of HIV-1 infection with special focus on the African population. Research presentations indicated that HAND was highly prevalent and that inflammatory cytokines and immune-activation played important roles in progression of neurocognitive impairment. Furthermore, children on antiretroviral therapy were also at risk for developing neurocognitive impairment. With respect to the effect of HIV-1 subtype diversity, analyses of HIV-1 clade C infection among South Africans revealed that clade C infection induced cognitive impairment that was independent of the substitution in HIV-1 Trans-Activator of Transcription (Tat; C31S). At the cellular level, a Zambian study showed that clade C infection resulted in reduced brain cell death compared with clade B infection suggesting clade specific variations in mediating brain cell injury. Furthermore, ex vivo Tat protein from clade CRF02_AG, prevalent in West/ Central Africa, exhibited reduced disruption of brain endothelium compared with clade B Tat protein. Discussions shed light on future research directions aimed at understanding biomarkers and disease mechanisms critical for HAND.
KW - HIV-associated neurocognitive disorders (HAND)
KW - Human immunodeficiency virus (HIV)
KW - NeuroAIDS
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U2 - 10.1007/s13365-016-0467-y
DO - 10.1007/s13365-016-0467-y
M3 - Article
C2 - 27473196
AN - SCOPUS:84980044692
SN - 1355-0284
VL - 22
SP - 699
EP - 702
JO - Journal of neurovirology
JF - Journal of neurovirology
IS - 5
ER -