|LETTER TO THE EDITOR
|Year : 2020 | Volume
| Issue : 4 | Page : 335-336
Human immunodeficiency virus, neuroinflammation, CD16+ pathobiological process, and haloperidol drug
Beuy Joob1, Viroj Wiwanitkit2
1 Private Academic Consultant, Bangkok, Thailand
2 Department of Biological Science, Joseph Ayo Babalola University, Ikeji-Arakeji, Nigeria
|Date of Submission||21-Oct-2019|
|Date of Decision||10-Jan-2020|
|Date of Acceptance||18-Sep-2020|
|Date of Web Publication||14-Oct-2020|
Dr. Beuy Joob
Private Academic Consultant, Bangkok
Source of Support: None, Conflict of Interest: None
|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 Jun 5];52:335-6. Available from: https://www.ijp-online.com/text.asp?2020/52/4/335/298153
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. 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. Recently, haloperidol is also proposed as a possible inhibitor of HIV protease. 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. Applying the standard common pathway mapping bioinformatics analysis, as used in the previous study, 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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Conflicts of interest
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