TBC and COVID: an interplay between two infections

ABSTRACT

Introduction

In a historical era dominated by the SARS-CoV-2 pandemic, a fact of growing interest emerges regarding co-infection with Mycobacterium tuberculosis (M. tuberculosis). This represents today an important clinical and diagnostic challenge, as the two pathogens are capable, through specific immunopathological mechanisms, of interacting with each other, determining a severe respiratory condition with a severe prognosis.

Areas covered

With this review, we wanted to collect and analyze the latest scientific evidence concerning the main immunopathogenetic mechanisms shared by these two respiratory pathogens, with particular interest in the possible iatrogenic factors favoring coinfection and the need to define multidisciplinary and standardized screening tools aimed to identify coinfection early, ensuring the best clinical and therapeutic management.

Expert opinion

The existence of a direct immunopathogenetic link between COVID-19 and TB indirectly contributes to mutual morbidity and mortality. The identification and application of early and standardized screening tools aimed at the identification of this condition is essential, in addition to vaccine prevention.

KEYWORDS:

• Coinfection
• immunopathogenesis
• Mycobacterium tuberculosis
• SARS-CoV-2
• LTBI

Article highlights

• Overproduction of IFN and its types I and III responses are significantly upregulated in severe disease in both COVID-19 and TB and can lead to disease progression and serious/fatal outcomes;

• The use of immunosuppressive (including high-dose corticosteroids) and biological therapies (especially TNF-α inhibitors) for severe SARS-CoV-2 infections increase the risk of LTBI reactivation;

• BCG-based vaccines would be able to protect against the main circulating variants of SARS-CoV-2 by stimulating the production of virus-specific IgG antibodies;

• To reduce the risk of LTBI reactivation in COVID-19 patients, TB screening by immunoassays (e.g. IGRA or QFT) is recommended before the start of anti-TNF-α drugs or immunosuppressants.

Declaration of interests

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Author contribution statement

Each authors contributed in drafting of the article. In particular, G Murdaca and S Gangemi contributed in the design and final revision. F Paladin, G Mangini, and D Tiso wrote the article.

Additional information

Funding

This paper was not funded.