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| Year : 2021
| Volume
: 63 | Issue : 1 | Page
: 112-113 |
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| Susceptibility of clinically depressed patients to COVID-19: Is there a link? |
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Abhishek Das1, Ankit Halder2, Rajendra S Patil1, Devavrat G Harshe2
1 Department of Pathology, D.Y. Patil Medical College, D. Y. Patil Education Society (Deemed University), Kolhapur, Maharashtra, India
2 Department of Psychiatry, D.Y. Patil Medical College, D. Y. Patil Education Society (Deemed University), Kolhapur, Maharashtra, India
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| Date of Submission | 11-Jul-2020 |
| Date of Decision | 11-Jul-2020 |
| Date of Acceptance | 30-Aug-2020 |
| Date of Web Publication | 15-Feb-2021 |
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How to cite this article:
Das A, Halder A, Patil RS, Harshe DG. Susceptibility of clinically depressed patients to COVID-19: Is there a link?. Indian J Psychiatry 2021;63:112-3 |
Sir,
The novel coronavirus disease (COVID-19, previously known as 2019-nCoV), first reported in Wuhan, China, in December 2019, has affected 216 countries/territories worldwide. The total number of cases amount to 12.96 million across the globe, and 0.9 million in India as of mid-July 2020.[1] It is an acute respiratory disease, and the case fatality has been reported as 3%. Severe infection causes alveolar damage and progressive respiratory failure, leading to death. Furthermore, the severity or fatality is more in older population, who have comorbidities and weaker immune functions.[2] It is plausible to correlate further that clinical depression and the subsequent low immunity can act as risk factors for prognosis, predicting the severity of COVID-19 cases.
Patients with clinical depression have lower immunity than those of healthy controls.[3] An association between declining immunologic responses and fewer circulating CD4+ T-cells in the elderly with depression has been suggested. There is also reduction in natural killer cell cytotoxic responses of lymphocyte proliferation, which is a result of mitogen activation and suppression of delayed hypersensitivity reaction in individuals with clinical depression. Patients with COVID-19 also displayed a rise in the production of pro-inflammatory cytokines with low lymphocyte proliferation. There is an abnormal regulation of the hypothalamus–pituitary–adrenal axis, sympathetic–adrenal–medullary axis, and hypothalamopituitary ovarian axis in patients with clinical depression.[4]
Patients with COVID-19 present with the symptoms of lymphopenia, particularly the reduction of peripheral blood T-cell number, and increased plasma concentrations of pro-inflammatory cytokines, including interleukin (IL)-6, IL-10, granulocyte monocyte-colony stimulating factor (GM-CSF), monocyte chemoattractant protein 1, macrophage inflammatory protein 1α, and tumor necrosis factor-α. Presence of checkpoint receptors, Tm3+PD-1+ subsets in CD4+ and CD8+ T-cells, indicated their exhaustion. GM-CSF has been reported to be produced in response to viral infections in CD8+ T-lymphocytes. Severe acute respiratory syndrome-coronavirus-2 infects epithelial cells of the lungs and produces IL-8 in addition to IL-6 in severely affected patients. IL-8 is a chemoattractant for neutrophils and T-cells. Infiltration of many inflammatory cells has been observed in the lungs of severely affected patients, comprising both innate and adaptive cells. Patients with COVID-19 who were severely affected showed CD8+ cytotoxic T-cells derived from CD4+ T-cells, which not only neutralize the virus but also cause lung injury. Circulating monocytes are induced by GM-CSF released by these T-cells. Surface markers of inflammatory monocyte subsets such as CD14+ and CD16+ which rarely exist in healthy people have also been reported in significantly higher concentrations in severe COVID-19 cases. These monocyte subsets also show high expression of IL-6, which is likely to accelerate the systemic inflammatory response. Overactivation of T-cells, manifested Th17 rise, and high cytotoxicity of CD8+ T-cells are also known to account for severe immune injury in these patients.[5]
Following the outbreak of COVID-19, there have been multiple reports on how COVID-19 can lead to depression in patients and people of other classes of society. However, the fact that patients with clinical depression have a compromised immune system and this can act as a comorbidity which helps in accelerating COVID-19 infection and hence its progression remains to be elucidated.[6] It is, therefore, plausible to conduct studies on the pathophysiology of patients with COVID-19 with a history of depression.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
 References | |  |
| 1. | |
| 2. | Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020;395:497-506.  |
| 3. | Andersson NW, Goodwin RD, Okkels N, Gustafsson LN, Taha F, Cole SW, et al. Depression and the risk of severe infections: Prospective analyses on a nationwide representative sample. Int J Epidemiol 2016;45:131-9. |
| 4. | Herbert TB, Cohen S. Depression and immunity: A meta-analytic review. Psychol Bull 1993;113:472-86. |
| 5. | Azkur AK, Akdis M, Azkur D, Sokolowska M, van de Veen W, Brüggen MC, et al. Immune response to SARS-CoV-2 and mechanisms of immunopathological changes in COVID-19. Allergy 2020;75:1564-81. |
| 6. | Fu R, Zhang Y. Case report of a patient with suspected COVID-19 with depression and fever in an epidemic stress environment. Gen Psychiatr 2020;33:e100218. |
Correspondence Address:
Abhishek Das
Department of Pathology, D.Y. Patil Medical College, D. Y. Patil Education Society (Deemed University), Kolhapur, Maharashtra
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/psychiatry.IndianJPsychiatry_850_20
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