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Table of Contents
Year : 2022  |  Volume : 1  |  Issue : 2  |  Page : 76-81

Coronavirus disease 2019 and Mycobacterium tuberculosis reactivation and coinfections: A review of the literature

1 Pediatric Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2 Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
3 Mycobacteriology Research Center (MRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran

Date of Submission01-Feb-2022
Date of Acceptance02-May-2022
Date of Web Publication15-Jun-2022

Correspondence Address:
Dr. Zahra Daneshmandi
Pediatric Allergists/Immunologists Pediatric Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran; Mailing Address: Masih Daneshvari Hospital, Darabad Avenue, Shahid Bahonar roundabout, Tehran
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpdtsm.jpdtsm_6_22

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The emergence of coronavirus disease 2019, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), greatly affects the health systems and socioeconomic parameters. Post pandemic, the SARS-CoV-2 might activate dormant bacterial infections like Mycobacterium tuberculosis in the long term. The mechanism of tuberculosis (TB) reactivation is still not clear, but it is thought that in healthy individuals, a strong immune response can form granulomatous lesion and prevents the development of active TB, while, in patients with dysregulated immune systems, TB reactivation occurs. Here, we reviewed the current knowledge about the interactions between SARS-CoV-2 and TB as an unwavering health hazard.

Keywords: Coinfection, coronavirus, immunologic pathways, interaction, pandemic, severe acute respiratory syndrome coronavirus 2

How to cite this article:
Daneshmandi Z, Pourdowlat G, Rekabi M, Honarpisheh P, Mirzendedel M, Sadati E, Ghaffaripour HA, Hasanzad M, Mahdaviani SA, Velayati AA. Coronavirus disease 2019 and Mycobacterium tuberculosis reactivation and coinfections: A review of the literature. J Prev Diagn Treat Strategies Med 2022;1:76-81

How to cite this URL:
Daneshmandi Z, Pourdowlat G, Rekabi M, Honarpisheh P, Mirzendedel M, Sadati E, Ghaffaripour HA, Hasanzad M, Mahdaviani SA, Velayati AA. Coronavirus disease 2019 and Mycobacterium tuberculosis reactivation and coinfections: A review of the literature. J Prev Diagn Treat Strategies Med [serial online] 2022 [cited 2023 Feb 8];1:76-81. Available from: http://www.jpdtsm.com/text.asp?2022/1/2/76/347550

  Introduction Top

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-mediated coronavirus disease 2019 (COVID-19) pandemic indicates the ability of an emerging virus to jeopardize health systems and greatly affect socioeconomic parameters.[1] In the long term, the SARS-CoV-2 might activate dormant bacterial infections, and Mycobacterium tuberculosis (Mtb), the biggest chronic infectious killer, is one of the key bacterial infections affected by viral pandemics.[1]

Tuberculosis (TB) history is very old. No part of the world has been spared from the impact of TB, and this problem is more important in developing countries with overcrowding, undernutrition, and poverty.[2] TB was considered a manageable disease with the development of treatment and vaccinations, but unfortunately, global emergencies including human immunodeficiency virus (HIV) outbreak and increase in multidrug-resistant patients were responsible for relapse of the disease.[3]

The mechanism of TB reactivation is still not clear, but it is thought that in healthy individuals, a strong immune response can form granulomatous lesion and prevents the development of active TB, while, in patients with dysregulated immune systems, TB reactivation occurs.[4] The reactivation of dormant bacterial infection is also known to be due to viral infection and related transient immune suppression.[5],[6],[7],[8],[9] In 1918, the Spanish flu pandemic, in 2009 the influenza A (H1N1) pandemic, and interestingly, SARS-CoV-1 and Middle East respiratory syndrome coronavirus pandemics led to the rise of pulmonary TB incidence.[10],[11],[12],[13],[14]

In addition, in this pandemic, administrative measures to contain SARS-CoV-2 have simultaneously led to a break in the chain of TB management and led to a regression in the milestones achieved in the battle against TB. Hence, all attempts to restrict TB were strongly influenced by the SARS-CoV-2 pandemic.[2],[15] Extended treatment regimens and poor outcomes with drug resistance resulting from therapy discontinuation are significant problems posed by the COVID-19 pandemic.[16],[17]

With a better understanding of two disease interactions, we can better equip ourselves to develop a more sophisticated and robust strategy to tilt the balance against TB. In this study, we aim to review the interactions between SARS-CoV-2 and TB as an unwavering health hazard and to discuss how the COVID-19 can reactivate TB.

  Coronavirus Disease 2019 and Tuberculosis Interactions Top

Shared biological pathways show a similarity between COVID-19 and TB pathways and identify common genes, highlighting shared molecular determinants between COVID-19 and TB disease. These common biological pathways including antigen presentation,[18],[19] membrane trafficking,[20],[21] reactive oxygen species/reactive nitrogen species production,[22],[23] activation of complement,[24],[25] cytokine production,[26],[27] and platelet activation signify activation of innate immune responses directed against both Mtb and SARS-CoV-2.[28],[29]

In healthy individuals and the TB granuloma, cytokine-mediated communication between innate and adaptive immune systems is required to mount protective anti-mycobacterial responses. The cytokines most commonly associated with protection are interferon-γ (IFN-γ) and tumor necrosis factor-alpha (TNF-α) (Th1 cytokines).[30],[31],[32] Both of them are released by Mtb-specific T-cells and cause macrophage activation and bactericidal activity. The roles of Th2 cytokines such as interleukin-4 (IL-4) and IL-10 are more controversial but correlated with diminished protection against TB and poor prognosis like downregulating monocyte and macrophage costimulatory molecules and impairing CD4+ and CD8+ T-cell-mediated cytotoxicity in TB patients.[30] The available data support that the balance of pro-inflammatory and anti-inflammatory factors in the granuloma may play a major role in the control of infection.[30]

In patients with critical COVID-19, there are an imbalance and high systemic levels of interleukins (IL-2, IL-6, and IL-10), IFN-γ-inducible protein 10, monocyte chemoattractant protein 1, granulocyte-macrophage colony-stimulating factor, and TNF-α along with lymphopenia. Besides, elevated immune cell infiltrations in the lungs lead to severe inflammation, cellular immune response failure, and the onset of a cytokine storm.[33] Some inflammatory cytokines, such as IL-6, IL-1β, and IFN-γ, can activate the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) JAK/STAT pathway and induce the NF-kB signaling.[26],[33],[34] Subsequent nuclear translocation of NF-KB and p38 phosphorylation is responsible for the induction of inflammatory cytokines and chemokines that leads to cytokine storm. Therefore, this pathway has been considered a possible therapeutic target for severe COVID-19 cases.[33] Besides, transcriptome analysis has shown that induction of the activator protein 1 pathway is crucial and in relation to milder inflammation throughout COVID-19 disease, as it connects the mitogen-activated protein kinase pathway with T-cell function.[33] This imbalance is maybe one of the reasons for TB reactivation.[33]

One of the cytokines that play an important key role in the body's inflammatory responses is TNF-α, and five TNF-α antagonists are currently used in the clinical fields and recently in COVID-19 disease.[35],[36] Infliximab as a TNF-α antagonist has been discussed in many randomized clinical trials. It was first reported with a fourfold risk of developing TB infection, and then further studies reported the same result.[35] In an animal study with TNF-deficient mice, which were unable to control mycobacterial infection, although no bacilli were detected after 4-week and 8-week periods of rifampicin and isoniazid therapy, the TNF-deficient mice reactivated faster than the control group. In contrast, extensive treatment for 12 weeks had eliminated all viable bacilli.[37]

Khayat et al. suggest that the CD4 + T-cell depletion related to COVID-19 is also implicated within the progression of latent TB infection (LTBI) to active TB and also the presentation of TB in these patients may additionally be atypical.[38] Chen et al. also found that the amount of CD4+ and CD8+ T-cells was markedly reduced in severe cases with reduced IFN-γ production.[39]

In a meta-analysis performed by Sheerin et al., overlapping of the gene, cell, and system levels between TB and COVID-19 was recognized for the first time. They concluded that patients diagnosed with SARS-Cov-2 should be followed up for the presentation of TB.[40] In their study, the most convincing overlaps reside in the circulating innate immune cells; which monocytes and macrophages as fundamental innate immune cells have a broad range of protective functions in front of different microbial factors.[41],[42] Alongside their advantageous activities, they exert undesirable results on the host in some of the viral infections such as COVID-19 through increasing the inflammatory cytokines, extreme interaction with adaptive immune cells, and their products that finally lead to serious tissue damage and enhancement of clinical presentation of the disease.[42] An important factor in the prognosis of COVID-19 is the activated state of circulating monocytes with a particular phenotype.[41] Similar monocyte phenotypes have been demonstrated during TB infection, and the presence of these monocytes in the precoinfection cycle of SARS-CoV-2 may be detrimental to the activation of important adaptive antiviral immune responses[43] Conversely, population of adaptive immune cells enriched in milder COVID-19 cases was associated with lower risk scores in activated TB (aTB). Functional CD4+ and CD8+ T-cell impairment may be aggravated by the presence of exhausted T-cell phenotypes indicative of chronic Mtb infection which show reduced ability to produce effector cytokines.[44],[45]

Some animal studies also confirm the reactivation of TB following COVID-19. An animal study, employing a mouse model, showed the rapid formation of pulmonary TB lesions that were because of the influenza A pandemic.[46] Another mouse model of influenza A virus and Mtb coinfection led to enhanced Mtb growth by a type I IFN signaling pathway.[47] Another mouse coronavirus model demonstrated the ability to reactivate dormant TB from CD271 + mesenchymal stem cells (MSCs) through the altruistic stem cell-based defense.[48] The CD271+ BM-MSCs (CD271 + BM-MSCs) are the potential niche for dormant Mtb in both mice and humans.[48]

Hence, based on the literature, many potential mechanisms like lymphopenia, including the depletion of TH4 cells,[49] T-cell exhaustion because of long-term antigen stimulation,[50] and cytokine storm, could lead to impaired immune regulation and play a role in TB reactivation [Figure 1].[51]
Figure 1: Potential mechanisms which could lead to immune dysregulation and play a role in tuberculosis reactivation

Click here to view

  Risk Factors for Coronavirus Disease 2019 and Tuberculosis Interactions Top

TB and COVID-19 are infectious diseases that primarily involve the lungs and spread via droplet and aerosol, and overcrowding promotes them.[2],[52],[53] Older people, malnourished, diabetics, or people with other chronic illnesses or immune deficiencies are more likely to get these infections.[5],[54] One infection may increase the chance of the other, probably due to the weakening of the host immune system.[6],[7]

In the literature conducted by Ai et al., several high-risk factors for TB reactivation, such as HIV coinfection, organ transplantation, TNF-α blockers, silicosis, close contact exposure, or chronic renal failure requiring dialysis, have been identified.[35] A recent study of COVID-19 patients conducted by Sy et al. found that having concurrent active TB or in the past was associated with a 2.17-fold increase in the risk of death;[55] they reported many risk factors for TB reactivation, including being born in an endemic country for TB, diabetes mellitus, using corticosteroids in the intensive care unit, acute kidney injury, and using hemodialysis for more than 1 month.[55]

  The Role of Drugs in Tuberculosis Reactivation Top

Acquiring COVID-19, as well as using corticosteroids to manage it, may also carry the risk of exogenous or reactivation of old endogenous TB infection. Likewise, people with active TB or structural lung disease are at a higher risk for developing COVID-19.[40],[56],[57],[58] Both SARS-CoV-2 and the steroid use induce profound lymphopenia which could predispose patients to TB reactivation as a consequence of a transient suppression of cellular immunity and/or increase the risk of progressive primary TB infection by reducing the pool of memory T-cells.[59] One study showed that COVID-19 did not induce a concomitant activation of TB-specific CD4+ T-cells, which means that acute SARS-CoV-2 infection may not immediately result in progression of latent TB to subclinical or active TB disease.[59] They also found a significant reduction in the frequency of TB-specific CD4+ T-cells in COVID-19 patients compared with healthy participants. This decline in TB-specific CD4+ T-cells could affect the ability of the host to control latent or new Mtb infection.[59]

There have been many other case reports of steroid-related TB reactivation, including treatments for autoimmune diseases,[60] anaphylactic reactions,[61] or nonmedical abuse.[62]

The biological drugs also increase the risk of TB reactivation by suppression of cell-mediated immunity and IFN-γ production. In Garg and Lee study, although the patient received high-dose steroids and tocilizumab, the effect of COVID-19 on the immune system could also have contributed.[63]

  Coronavirus Disease 2019 and Tuberculosis Coinfection Top

During the COVID-19 pandemic, several respiratory coinfections, including bacterial and fungal pathogens, were reported, and about 50% of the patients who died from COVID-19 had secondary respiratory infections.[64],[65],[66]

Evidence suggests that both COVID-19 and TB have a lethal synergistic relationship, because of boosting detrimental effects of each other, disrupting existing health-care models, and also contributing to more severe clinical evolution.[67] The coinfection in macrophages plays a crucial role in pathogenesis by increasing the production of pro- and anti-inflammatory cytokines. Severe infection of type II pneumocytes with SARS-CoV-2 can disrupt cell regeneration and eventually lead to lung damage.[68],[69]

The Th1 immune response against TB is characterized by the predominance of specific phagocytes and CD4+ T-lymphocytes; however, the defenses against SARS-CoV-2 also depend on specialized lymphocytes.[70] At first, the TB/COVID-19 coinfection should delay or jeopardize the response against SARS-CoV-2, while successive inflammatory stimuli over time would result in generalized exhaustion of T-cells. Both in TB and COVID-19, lymphocytes act as immune mediators, orchestrating the release of cytokines and chemokines at the infectious site; lymphopenia resulting from coinfection directly affects this regulation of the immune response against pathogens.[70] The main consequence observed from lymphopenia is the exacerbated cytokine expression, mainly pro-inflammatory. These expressed cytokines may also have side effects that increased IFN-γ-stimulated angiotensin-converting enzyme 2 receptor expression at the cell surface is one of them. IL-4 and IL-13 are associated with immunological damage and a worse prognosis for TB and COVID-19.[70] The immune dysregulation due to lymphopenia is also associated with a significant neutrophil infiltration into the lungs that is associated with the exacerbation of inflammation.[70] The relationship between the lymphocyte counts and neutrophils has already been identified as a possible risk marker for both diseases.[70]

  Conclusions Top

There is not enough data regarding TB reactivation during COVID-19 disease and further studies are needed to understand the effects of COVID-19 on the immune system and the possibilities of opportunistic infections activation. In summary, many potential mechanisms could lead to immune dysregulation and play a role in TB reactivation. Thus, in TB-endemic regions, because of a significant proportion of the LTBI population, the COVID-19 pandemic may lead to a spike in the incidence of active TB. Early diagnosis of patients with TB and subsequent follow-up is essential to help control the spread of TB. Furthermore, toward a greater understanding of the pathophysiology of COVID-19 and of how COVID-19 reactivates TB, more research should be directed.

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Conflicts of interest

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  References Top

Pathak L, Gayan S, Pal B, Talukdar J, Bhuyan S, Sandhya S, et al. Coronavirus activates a stem cell-mediated defense mechanism that reactivates dormant tuberculosis: implications in COVID-19 pandemic. bioRxiv 2020;2020.05.06.077883.  Back to cited text no. 1
Kant S, Tyagi R. The impact of COVID-19 on tuberculosis: challenges and opportunities. Ther Adv Infect Dis SAGE Publications; 2021;8:20499361211016972.   Back to cited text no. 2
Sullivan JT, Young EF, McCann JR, Braunstein M. The Mycobacterium tuberculosis SecA2 system subverts phagosome maturation to promote growth in macrophages. Infect Immun 2012;80:996-1006.  Back to cited text no. 3
Flynn JL, Chan J. Tuberculosis: Latency and reactivation. Infect Immun Am Soc Microbiol 2001;69:4195-201.  Back to cited text no. 4
Mendenhall E, Kohrt BA, Norris SA, Ndetei D, Prabhakaran D. Non-communicable disease syndemics: Poverty, depression, and diabetes among low-income populations. Lancet 2017;389:951-63.  Back to cited text no. 5
Zenaro E, Donini M, Dusi S. Induction of Th1/Th17 immune response by Mycobacterium tuberculosis: Role of dectin-1, Mannose Receptor, and DC-SIGN. J Leukoc Biol 2009;86:1393-401.  Back to cited text no. 6
Zhou Y, Fu B, Zheng X, Wang D, Zhao C, Sun R, et al. Aberrant pathogenic GM-CSF+ T cells and inflammatory CD14+ CD16+ monocytes in severe pulmonary syndrome patients of a new coronavirus. BioRxiv Cold Spring Harbor Laboratory; 2020.  Back to cited text no. 7
Harding E. WHO global progress report on tuberculosis elimination. Lancet Respir Med 2020;8:19.  Back to cited text no. 8
Wong CY, Wong KY, Law TS, Shum TT, Li YK, Pang WK. Tuberculosis in a SARS outbreak. J Chin Med Assoc 2004;67:579-82.  Back to cited text no. 9
Mamelund SE, Dimka J. Tuberculosis as a risk factor for 1918 influenza pandemic outcomes. Trop Med Infect Dis 2019;4:74.  Back to cited text no. 10
Oei W, Nishiura H. The relationship between tuberculosis and influenza death during the influenza (H1N1) pandemic from 1918-19. Comput Math Methods Med 2012;2012:124861.  Back to cited text no. 11
Park Y, Chin BS, Han SH, Yun Y, Kim YJ, Choi JY, et al. Pandemic influenza (H1N1) and Mycobacterium tuberculosis co-infection. Tuberc Respir Dis (Seoul) 2014;76:84-7.  Back to cited text no. 12
Low JG, Lee CC, Leo YS, Guek-Hong Low J, Lee CC, Leo YS. Severe acute respiratory syndrome and pulmonary tuberculosis. Clin Infect Dis 2004;38:e123-5.  Back to cited text no. 13
Alfaraj SH, Al-Tawfiq JA, Altuwaijri TA, Memish ZA. Middle east respiratory syndrome coronavirus and pulmonary tuberculosis coinfection: Implications for infection control. Intervirology 2017;60:53-5.  Back to cited text no. 14
Togun T, Kampmann B, Stoker NG, Lipman M. Anticipating the impact of the COVID-19 pandemic on TB patients and TB control programmes. Ann Clin Microbiol Antimicrob 2020;19:21.  Back to cited text no. 15
Crisan-Dabija R, Grigorescu C, Pavel C-A, Artene B, Popa IV, Cernomaz A, et al. Tuberculosis and COVID-19: Lessons from the Past Viral Outbreaks and Possible Future Outcomes. Can Respir J Hindawi; 2020;2020:1401053.   Back to cited text no. 16
Amimo F, Lambert B, Magit A. What does the COVID-19 pandemic mean for HIV, tuberculosis, and malaria control? Trop Med Health 2020;48:32.  Back to cited text no. 17
Matzaraki V, Kumar V, Wijmenga C, Zhernakova A. The MHC locus and genetic susceptibility to autoimmune and infectious diseases. Genome Biol 2017;18:76.  Back to cited text no. 18
Wilk AJ, Rustagi A, Zhao NQ, Roque J, Martínez-Colón GJ, McKechnie JL, et al. A single-cell atlas of the peripheral immune response in patients with severe COVID-19. Nat Med 2020;26:1070-6.  Back to cited text no. 19
Bayati A, Kumar R, Francis V, McPherson PS. SARS-CoV-2 uses clathrin-mediated endocytosis to gain access into cells. biorxiv Cold Spring Harbor Laboratory; 2020.  Back to cited text no. 20
Schnettger L, Rodgers A, Repnik U, Lai RP, Pei G, Verdoes M, et al. A Rab20-dependent membrane trafficking pathway controls m. Tuberculosis replication by regulating phagosome spaciousness and integrity. Cell Host Microbe 2017;21:619-28.e5.  Back to cited text no. 21
Laforge M, Elbim C, Frère C, Hémadi M, Massaad C, Nuss P, et al. Tissue damage from neutrophil-induced oxidative stress in COVID-19. Nat Rev Immunol 2020;20:515-6.  Back to cited text no. 22
Franchini AM, Hunt D, Melendez JA, Drake JR. FcγR-driven release of IL-6 by macrophages requires NOX2-dependent production of reactive oxygen species. J Biol Chem ASBMB 2013;288:25098-108.  Back to cited text no. 23
Esmail H, Lai RP, Lesosky M, Wilkinson KA, Graham CM, Horswell S, et al. Complement pathway gene activation and rising circulating immune complexes characterize early disease in HIV-associated tuberculosis. Proc Natl Acad Sci U S A 2018;115:E964-73.  Back to cited text no. 24
Java A, Apicelli AJ, Liszewski MK, Coler-Reilly A, Atkinson JP, Kim AH, et al. The complement system in COVID-19: Friend and foe? JCI Insight 2020;5e140711.  Back to cited text no. 25
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.  Back to cited text no. 26
Kaufmann SH. Protection against tuberculosis: Cytokines, T cells, and macrophages. Ann Rheum Dis 2002;61 Suppl 2:i54-8.  Back to cited text no. 27
Hottz ED, Azevedo-Quintanilha IG, Palhinha L, Teixeira L, Barreto EA, Pão CR, et al. Platelet activation and platelet-monocyte aggregate formation trigger tissue factor expression in patients with severe COVID-19. Blood 2020;136:1330-41.  Back to cited text no. 28
Fox KA, Kirwan DE, Whittington AM, Krishnan N, Robertson BD, Gilman RH, et al. Platelets regulate pulmonary inflammation and tissue destruction in tuberculosis. Am J Respir Crit Care Med 2018;198:245-55.  Back to cited text no. 29
Mattila JT, Diedrich CR, Lin PL, Phuah J, Flynn JL. Simian immunodeficiency virus-induced changes in T cell cytokine responses in cynomolgus macaques with latent Mycobacterium tuberculosis infection are associated with timing of reactivation. J Immunol 2011;186:3527-37.  Back to cited text no. 30
Wang W, Ye L, Ye L, Li B, Gao B, Zeng Y, et al. Up-regulation of IL-6 and TNF-α induced by SARS-coronavirus spike protein in murine macrophages via NF-κB pathway. Virus Res 2007;128:1-8.  Back to cited text no. 31
Lee AJ, Ashkar AA. The dual nature of type I and type II interferons. Front Immunol 2018;9:2061.  Back to cited text no. 32
Gopalaswamy R, Subbian S. Corticosteroids for COVID-19 therapy: Potential implications on tuberculosis. Int J Mol Sci 2021;22:3773.  Back to cited text no. 33
Borekci S, Karakas FG, Sirekbasan S, Kubat B, Karaali R, Can G, et al. The Relationship between Pre-Pandemic Interferon Gamma Release Assay Test Results and COVID-19 Infection: Potential Prognostic Value of Indeterminate IFN-γ Release Assay Results. Detolla L, ed. Can J Infect Dis Med Microbiol Hindawi; 2021;2021:1989277.  Back to cited text no. 34
Ai JW, Ruan QL, Liu QH, Zhang WH. Updates on the risk factors for latent tuberculosis reactivation and their managements. Emerg Microbes Infect 2016;5:e10.  Back to cited text no. 35
Robinson PC, Liew DFL, Liew JW, Monaco C, Richards D, Shivakumar S, et al. The Potential for Repurposing Anti-TNF as a Therapy for the Treatment of COVID-19. Med (N Y) 2020;1:90-102.  Back to cited text no. 36
Botha T, Ryffel B. Reactivation of latent tuberculosis by an inhibitor of inducible nitric oxide synthase in an aerosol murine model. Immunology 2002;107:350-7.  Back to cited text no. 37
Khayat M, Fan H, Vali Y. COVID-19 promoting the development of active tuberculosis in a patient with latent tuberculosis infection: A case report. Respir Med Case Rep 2021;32:101344.  Back to cited text no. 38
Chen G, Wu D, Guo W, Cao Y, Huang D, Wang H, et al. Clinical and immunological features of severe and moderate coronavirus disease 2019. J Clin Invest 2020;130:2620-9.  Back to cited text no. 39
Sheerin D, Abhimanyu, Wang X, Johnson WE, Coussens A. Systematic evaluation of transcriptomic disease risk and diagnostic biomarker overlap between COVID-19 and tuberculosis: a patient-level meta-analysis. medRxiv Prepr Serv Heal Sci Cold Spring Harbor Laboratory; 2020;2020.11.25.20236646.  Back to cited text no. 40
Zhang D, Guo R, Lei L, Liu H, Wang Y, Wang Y, et al. COVID-19 infection induces readily detectable morphologic and inflammation-related phenotypic changes in peripheral blood monocytes. J Leukoc Biol Wiley-Blackwell; 2020.  Back to cited text no. 41
Merad M, Martin JC. Author correction: Pathological inflammation in patients with COVID-19: A key role for monocytes and macrophages. Nat Rev Immunol 2020;20:448.  Back to cited text no. 42
Lastrucci C, Bénard A, Balboa L, Pingris K, Souriant S, Poincloux R, et al. Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis. Cell Res 2015;25:1333-51.  Back to cited text no. 43
Zheng M, Gao Y, Wang G, Song G, Liu S, Sun D, et al. Functional exhaustion of antiviral lymphocytes in COVID-19 patients. Cell Mol Immunol 2020;17:533-5.  Back to cited text no. 44
Khan N, Vidyarthi A, Amir M, Mushtaq K, Agrewala JN. T-cell exhaustion in tuberculosis: Pitfalls and prospects. Crit Rev Microbiol 2017;43:133-41.  Back to cited text no. 45
Volkert M, Pierce C, Horsfall FL, Dubos RJ. The enhancing effect of concurrent infection with pneumotropic viruses on pulmonary tuberculosis in mice. J Exp Med 1947;86:203-14.  Back to cited text no. 46
Redford PS, Mayer-Barber KD, McNab FW, Stavropoulos E, Wack A, Sher A, et al. Influenza A virus impairs control of Mycobacterium tuberculosis coinfection through a type I interferon receptor-dependent pathway. J Infect Dis 2014;209:270-4.  Back to cited text no. 47
Pathak L, Gayan S, Pal B, Talukdar J, Bhuyan S, Sandhya S, et al. Corona virus activates a stem cell mediated defense mechanism that accelerates activation of dormant tuberculosis: implications for the COVID-19 pandemic. bioRxiv 2020;2020.05.06.077883.   Back to cited text no. 48
Tan L, Wang Q, Zhang D, Ding J, Huang Q, Tang YQ, et al. Lymphopenia predicts disease severity of COVID-19: A descriptive and predictive study. Signal Transduct Target Ther 2020;5:33.  Back to cited text no. 49
De Biasi S, Meschiari M, Gibellini L, Bellinazzi C, Borella R, Fidanza L, et al. Marked T cell activation, senescence, exhaustion and skewing towards TH17 in patients with COVID-19 pneumonia. Nat Commun 2020;11:3434.  Back to cited text no. 50
Yuki K, Fujiogi M, Koutsogiannaki S. COVID-19 pathophysiology: A review. Clin Immunol 2020;215:108427.  Back to cited text no. 51
Ge H, Wang X, Yuan X, Xiao G, Wang C, Deng T, et al. The epidemiology and clinical information about COVID-19. Eur J Clin Microbiol Infect Dis 2020;39:1011-9.  Back to cited text no. 52
Srivastava K, Kant S, Verma A. Role of environmental factors in transmission of tuberculosis. Dyn Hum Heal 2015;2:12.  Back to cited text no. 53
Sanyaolu A, Okorie C, Marinkovic A, Patidar R, Younis K, Desai P, et al. Comorbidity and its impact on patients with COVID-19. SN Compr Clin Med 2020;2:1069-76.  Back to cited text no. 54
Sy KT, Haw NJ, Uy J. Previous and active tuberculosis increases risk of death and prolongs recovery in patients with COVID-19. Infect Dis (Lond) 2020;52:902-7.  Back to cited text no. 55
Visca D, Ong CW, Tiberi S, Centis R, D'Ambrosio L, Chen B, et al. Tuberculosis and COVID-19 interaction: A review of biological, clinical and public health effects. Pulmonology 2021;27:151-65.  Back to cited text no. 56
Minozzi S, Bonovas S, Lytras T, Pecoraro V, González-Lorenzo M, Bastiampillai AJ, et al. Risk of infections using anti-TNF agents in rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis: A systematic review and meta-analysis. Expert Opin Drug Saf 2016;15:11-34.  Back to cited text no. 57
Yang H, Lu S. COVID-19 and Tuberculosis. J Transl Int Med 2020;8:59-65.  Back to cited text no. 58
Riou C, du Bruyn E, Stek C, Daroowala R, Goliath RT, Abrahams F, et al. Relationship of SARS-CoV-2-specific CD4 response to COVID-19 severity and impact of HIV-1 and tuberculosis coinfection. J Clin Invest 2021;131:149125.  Back to cited text no. 59
Reisinger AC, Hermann J, Vagena FR, Hackl G, Eller P. Tuberculosis sepsis after tocilizumab treatment. Clin Microbiol Infect 2020;26:1493-4.  Back to cited text no. 60
Patil S, Jadhav A. Short course of high-dose steroids for anaphylaxis caused flare up of tuberculosis: A case report. J Transl Int Med 2019;7:39-42.  Back to cited text no. 61
Singh V, Batta A. Suspected reactivation of extrapulmonary tuberculosis focus after non-medical abuse of anabolic androgenic steroids: a case report. J Basic Clin Physiol Pharmacol De Gruyter; 2020;31.  Back to cited text no. 62
Garg N, Lee YI. Reactivation tb with severe COVID-19. Chest Am Coll Chest Physicians 2020;158:A777.  Back to cited text no. 63
Al Lawati R, Al Busaidi N, Al Umairi R, Al Busaidy M, Al Naabi HH, Khamis F. COVID-19 and pulmonary Mycobacterium tuberculosis coinfection. Oman Med J 2021;36:e298.  Back to cited text no. 64
Yasri S, Wiwanitkit V. Tuberculosis and novel Wuhan coronavirus infection: Pathological interrelationship. Indian J Tuberc 2020;67:264.  Back to cited text no. 65
Cox MJ, Loman N, Bogaert D, O'Grady J. Co-infections: Potentially lethal and unexplored in COVID-19. Lancet Microbe 2020;1:e11.  Back to cited text no. 66
Gupta U, Prakash A, Sachdeva S, Pangtey GS, Khosla A, Aggarwal R, et al. COVID-19 and tuberculosis: A meeting of two pandemics! J Assoc Physicians India 2020;68:69-72.  Back to cited text no. 67
Pinky L, González-Parra G, Dobrovolny HM. Superinfection and cell regeneration can lead to chronic viral coinfections. J Theor Biol 2019;466:24-38.  Back to cited text no. 68
Tapela K, Ochieng' Olwal C, Quaye O. Parallels in the pathogenesis of SARS-CoV-2 and M. tuberculosis: A synergistic or antagonistic alliance? Future Microbiol 2020;15:1691-5.  Back to cited text no. 69
Mousquer GT, Peres A, Fiegenbaum M. Pathology of TB/COVID-19 co-infection: The phantom menace. Tuberculosis (Edinb) 2021;126:102020.  Back to cited text no. 70


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