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| LETTER TO EDITOR |
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| Year : 2020 | Volume
: 15
| Issue : 3 | Page : 517 |
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Human immunodeficiency virus-associated neuroinflammation and CD16+ pathobiological process in concurrent human immunodeficiency virus infection and parkinson disease
Beuy Joob1, Viroj Wiwantikit2
1 Medical Academic Center, Bangkok, Thailand
2 Dr. DY Patil University, Pune, Maharashtra, India
| Date of Submission | 18-Nov-2019 |
| Date of Decision | 15-Aug-2020 |
| Date of Acceptance | 30-Aug-2020 |
| Date of Web Publication | 1-Feb-2021 |
Correspondence Address:
Dr. Beuy Joob
Medical Academic Center, Bangkok
Thailand
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jdmimsu.jdmimsu_183_19
How to cite this article:
Joob B, Wiwantikit V. Human immunodeficiency virus-associated neuroinflammation and CD16+ pathobiological process in concurrent human immunodeficiency virus infection and parkinson disease. J Datta Meghe Inst Med Sci Univ 2020;15:517 |
How to cite this URL:
Joob B, Wiwantikit V. Human immunodeficiency virus-associated neuroinflammation and CD16+ pathobiological process in concurrent human immunodeficiency virus infection and parkinson disease. J Datta Meghe Inst Med Sci Univ [serial online] 2020 [cited 2021 Feb 25];15:517. Available from: http://www.journaldmims.com/text.asp?2020/15/3/517/308554 |
Sir,
The human immunodeficiency virus (HIV)-associated neuroinflammation is an important problem for HIV-infected patients. In a recent report by Moulignier et al.,[1] it was found that HIV infection in patients with underlying Parkinson disease could induce functional adaptation of dopaminergic neuron and resulted in reduced neuronal loss.[1] In fact, the interrelationship between HIV-associated neuroinflammation and Parkinson disease is interesting but not well clarified. Here, the authors tried to perform bioinformatics pathway analysis, based on pathway mapping technique as used in the previous study,[2] to identify the pathway linkage between HIV-associated neuroinflammation and Parkinson disease. From the available data in the database, an important pathogenesis mechanism of HIV-associated neuroinflammation is CD16+ monocyte transmigration across the blood–brain barrier.[3] This transmigration process is directly related to dopamine.[3] Increased dopamine results in an increased transmigration process and further results in increased HIV-associated neuroinflammation. In clinical practice, the movement disorders including to Parkinsonism More Details is detectable in HIV-infected patients.[3] In HIV-infected cases with underlying Parkinson disease, the underlying Parkinson disease-associated neurodegeneration can result in decreased dopamine level. This can further result in decreased CD16+ monocyte transmigration and decreased HIV-associated neuroinflammation. This identified biological process might explain the rarity of HIV-associated neuroinflammation among HIV-infected patients with underlying Parkinson disease.[1] This pathobiological process is similar to the observed biological process on CD16+ suppression effect of medial cannabis.[3]
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | Moulignier A, Gueguen A, Lescure FX, Ziegler M, Girard PM, Cardon B, et al. Does HIV infection alter Parkinson disease? J Acquir Immune Defic Syndr 2015;70:129-36.  |
| 2. | Joob B, Wiwanitkit V. Nitric oxide, liver fluke opisthorchis viverrini, thalassemia, deferiprone, and cholangiocarcinoma: A clinical interrelationship with reference to endemic area in Indochina. J Med Soc 2019;33:62-3. [Full text] |
| 3. | Mattos JP, Rosso AL, Correa RB, Novis SA. Movement disorders in 28 HIV-infected patients. Arq Neuropsiquiatr 2002;60:525-30. |
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