Year : 2021 | Volume
: 63 | Issue : 1 | Page : 112--113
Susceptibility of clinically depressed patients to COVID-19: Is there a link?
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
Department of Pathology, D.Y. Patil Medical College, D. Y. Patil Education Society (Deemed University), Kolhapur, Maharashtra
|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;63:112-113
|How to cite this URL:|
Das A, Halder A, Patil RS, Harshe DG. Susceptibility of clinically depressed patients to COVID-19: Is there a link?. Indian J Psychiatry [serial online] 2021 [cited 2021 Apr 13 ];63:112-113
Available from: https://www.indianjpsychiatry.org/text.asp?2021/63/1/112/309494
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. 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. 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. 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.
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.
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. It is, therefore, plausible to conduct studies on the pathophysiology of patients with COVID-19 with a history of depression.
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Conflicts of interest
There are no conflicts of interest.
|1||WHO Coronavirus Disease (COVID-19) Dashboard. Available from: https://covid19.who.int/. [Last accessed on 2020 Jul 10].|
|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.|