COVID-19 promoting the development of active tuberculosis in a patient with latent tuberculosis infection: A case report

Khayat, Mohammed; Fan, Hanan A.; Vali, Y

doi:10.1016/j.rmcr.2021.101344

Cited by 51 publications

(53 citation statements)

References 9 publications

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“…In addition, cytokines and chemokines are crucial players in COVID-19 and their plasma levels are linked with disease severity [3] . A recent clinical report revealed that CD4 + T-cell deficiency linked with COVID-19 could lead the latent infection to progress in to active tuberculosis [10] . A study from China reported that COVID-19 patients had significant diminution of T-cell lymphocyte counts [11] and CD4 and CD8 counts were drastically decreased [12] .…”

Section: Discussionmentioning

confidence: 99%

Effect of SARS-CoV-2 seropositivity on antigen – specific cytokine and chemokine responses in latent tuberculosis

et al. 2022

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SARS-CoV-2 and latent Mycobacterium tuberculosis infection are both highly co-prevalent in many parts of the globe. Whether exposure to SARS-CoV-2 influences the antigen – specific immune responses in latent tuberculosis has not been investigated. We examined the baseline, mycobacterial antigen and mitogen induced cytokine and chemokine responses in latent tuberculosis (LTBI) individuals with or without SARS-CoV-2 seropositivity, LTBI negative with SARS-CoV-2 seropositivity and healthy controls (LTBI and SARS-CoV-2 negative). Our results demonstrated that LTBI individuals with SARS-CoV-2 seropositivity (LTBI+/IgG+) were associated with increased levels of unstimulated and TB-antigen stimulated IFNγ, IL-2, TNFα, IL-17, IL-1β, IL-6, IL-12, IL-4, CXCL1, CXCL9 and CXCL10 when compared to those without seropositivity (LTBI+/IgG-). In contrast, LTBI+/IgG+ individuals were associated with decreased levels of IL-5 and IL-10. No significant difference in the levels of cytokines/chemokines was observed upon mitogen stimulation between the groups. SARS-CoV-2 seropositivity was associated with enhanced unstimulated and TB-antigen stimulated but not mitogen stimulated production of cytokines and chemokines in LTBI+ compared to LTBI negative individuals. Finally, most of these significant differences were not observed when LTBI negative individuals with SARS-CoV-2 seropositivity and controls were examined. Our data clearly demonstrate that both baseline and TB – antigen induced cytokine responses are augmented in the presence of SARS-CoV-2 seropositivity, suggesting an augmenting effect of prior SARS-CoV-2 infection on the immune responses of LTBI individuals.

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Section: Discussionmentioning

confidence: 99%

Effect of SARS-CoV-2 seropositivity on antigen – specific cytokine and chemokine responses in latent tuberculosis

et al. 2022

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“…To the best of our knowledge, this is an important report of reactivation of prior M. simiae infection following COVID-19. There are several studies on co-infection with tuberculosis (TB) and COVID-19 and also reactivation of latent-TB to acute TB after COVID-19 infection [6] , [7] . However, limited data are available on the COVID-19 infection and nontuberculous mycobacteria infection.…”

Section: Discussionmentioning

confidence: 99%

“…Several reports have indicated that CD4+/CD8+ T-cells play a vital role in defence against mycobacterial infection [6] , [9] . In COVID-19 patients have been shown a significant depletion in the count of T-cell lymphocytes [10] .…”

Section: Discussionmentioning

confidence: 99%

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Reactivation of Mycobacterium simiae after the recovery of COVID-19 infection

Masoumi¹,

Sakhaee²,

Vaziri³

et al. 2021

Journal of Clinical Tuberculosis and Other Mycobacterial Diseas

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“…SARS-CoV-2 and MTb, both infect the same type of cells, which include type II pneumocytes in the lungs and macrophages ( Qian et al, 2013 ; Ganbat et al, 2016 ; Abassi et al, 2020 ). A case study by Khayat et al (2021) reported progression of latent MTb infection (LMTBI) to an active MTb infection following a marked CD4+ T cell depletion associated with COVID-19. Another study involving COVID-19 reported a lower immune response (as measured by IFN-γ response against MTb antigen and SARS-CoV-2 S protein antigen) in MTb-COVID-19 and LMTBI-COVID-19 patients when compared to COVID-19 patients ( Petrone et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Co-infections as Modulators of Disease Outcome: Minor Players or Major Players?

et al. 2021

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Human host and pathogen interaction is dynamic in nature and often modulated by co-pathogens with a functional role in delineating the physiological outcome of infection. Co-infection may present either as a pre-existing pathogen which is accentuated by the introduction of a new pathogen or may appear in the form of new infection acquired secondarily due to a compromised immune system. Using diverse examples of co-infecting pathogens such as Human Immunodeficiency Virus, Mycobacterium tuberculosis and Hepatitis C Virus, we have highlighted the role of co-infections in modulating disease severity and clinical outcome. This interaction happens at multiple hierarchies, which are inclusive of stress and immunological responses and together modulate the disease severity. Already published literature provides much evidence in favor of the occurrence of co-infections during SARS-CoV-2 infection, which eventually impacts the Coronavirus disease-19 outcome. The availability of biological models like 3D organoids, mice, cell lines and mathematical models provide us with an opportunity to understand the role and mechanism of specific co-infections. Exploration of multi-omics-based interactions across co-infecting pathogens may provide deeper insights into their role in disease modulation.

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COVID-19 promoting the development of active tuberculosis in a patient with latent tuberculosis infection: A case report

Cited by 51 publications

References 9 publications

Effect of SARS-CoV-2 seropositivity on antigen – specific cytokine and chemokine responses in latent tuberculosis

Effect of SARS-CoV-2 seropositivity on antigen – specific cytokine and chemokine responses in latent tuberculosis

Reactivation of Mycobacterium simiae after the recovery of COVID-19 infection

Co-infections as Modulators of Disease Outcome: Minor Players or Major Players?

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