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 Table of Contents    
LETTER TO THE EDITOR
Year : 2020  |  Volume : 52  |  Issue : 4  |  Page : 335-336
 

Human immunodeficiency virus, neuroinflammation, CD16+ pathobiological process, and haloperidol drug


1 Private Academic Consultant, Bangkok, Thailand
2 Department of Biological Science, Joseph Ayo Babalola University, Ikeji-Arakeji, Nigeria

Date of Submission21-Oct-2019
Date of Decision10-Jan-2020
Date of Acceptance18-Sep-2020
Date of Web Publication14-Oct-2020

Correspondence Address:
Dr. Beuy Joob
Private Academic Consultant, Bangkok
Thailand
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijp.IJP_688_19

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How to cite this article:
Joob B, Wiwanitkit V. Human immunodeficiency virus, neuroinflammation, CD16+ pathobiological process, and haloperidol drug. Indian J Pharmacol 2020;52:335-6

How to cite this URL:
Joob B, Wiwanitkit V. Human immunodeficiency virus, neuroinflammation, CD16+ pathobiological process, and haloperidol drug. Indian J Pharmacol [serial online] 2020 [cited 2023 Sep 28];52:335-6. Available from: https://www.ijp-online.com/text.asp?2020/52/4/335/298153




Sir,

Human immunodeficiency virus (HIV) is an important agent causing retrovirus infection. This infection results in immunodeficiency problem which can further lead to many clinical problems. HIV-associated neuroinflammation is an important neurological disorder that is due to the CD16+ monocyte transmigration across the blood–brain barrier.[1] To manage HIV-associated neuroinflammation, the present new focus is usually on CD16+ monocyte. The use of a therapeutic agent that can affect the CD16+ is expected to be a useful therapeutic approach. Here, the authors would like to discuss on the possible usefulness of haloperidol, a widely used antipsychotic drug.

Regarding the effect of haloperidol, it is accepted for usefulness in the management of neuropsychiatric problems such as delirium in HIV-infected patients.[2] Recently, haloperidol is also proposed as a possible inhibitor of HIV protease.[3] Here, the authors would like to discuss on another possible additional usefulness of haloperidol regarding CD16+ biological process in HIV-infected patients. Basically, haloperidol has anti-dopamine effect. Pathophysiologically, dopamine is reported for its association with CD16+ monocyte transmigration across the blood–brain barrier and the further consequent HIV-associated neuroinflammation.[4] Applying the standard common pathway mapping bioinformatics analysis, as used in the previous study,[4] the interrelationship among HIV infection and haloperidol neuroinflammation can be identified [Figure 1]. Hence, haloperidol that has actions against dopamine can further reduce the CD16+ monocyte transmigration across the blood–brain barrier and the further consequent HIV-associated neuroinflammation. Further study on the actual pharmacological effect of haloperidol in HIV patients is a very interesting research in clinical pharmacology.
Figure 1: The interrelationship among human immunodeficiency virus infection and haloperidol neuroinflammation

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Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

1.
Mattos JP, Rosso AL, Correa RB, Novis SA. Movement disorders in 28 HIV-infected patients. Arq Neuropsiquiatr 2002;60:525-30.  Back to cited text no. 1
    
2.
Breitbart W, Marotta R, Platt MM, Weisman H, Derevenco M, Grau C, et al. A double-blind trial of haloperidol, chlorpromazine, and lorazepam in the treatment of delirium in hospitalized AIDS patients. Am J Psychiatry 1996;153:231-7.  Back to cited text no. 2
    
3.
De Voss JJ, Sui Z, DeCamp DL, Salto R, Babé LM, Craik CS, et al. Haloperidol-based irreversible inhibitors of the HIV-1 and HIV-2 proteases. J Med Chem 1994;37:665-73.  Back to cited text no. 3
    
4.
Calderon TM, Williams DW, Lopez L, Eugenin EA, Cheney L, Gaskill PJ, et al. Dopamine increases CD14 CD16 monocyte transmigration across the blood brain Barrier: implications for substance abuse and HIV neuropathogenesis. J Neuroimmune Pharmacol 2017;12:353-70.  Back to cited text no. 4
    


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