Microbial co-infections in COVID-19: Associated microbiota and underlying mechanisms of pathogenesis

Abstract

The novel coronavirus infectious disease-2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has traumatized the whole world with the ongoing devastating pandemic. A plethora of microbial domains including viruses (other than SARS-CoV-2), bacteria, archaea and fungi have evolved together and interact in complex molecular pathogenesis along with SARS-CoV-2. However, the involvement of other microbial co-pathogens and underlying molecular mechanisms leading to extortionate ailment in critically ill COVID-19 patients has yet not been extensively reviewed. Although, the incidence of co-infections could be up to 94.2% in laboratory-confirmed COVID-19 cases, the fate of co-infections among SARS-CoV-2 infected hosts often depends on the balance between the host's protective immunity and immunopathology. Predominantly identified co-pathogens of SARS-CoV-2 are bacteria such as Streptococcus pneumoniae, Staphylococcus aureus, Klebsiella pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Acinetobacter baumannii , Legionella pneumophila and Clamydia pneumoniae followed by viruses including influenza, coronavirus, rhinovirus/enterovirus, parainfluenza, metapneumovirus, influenza B virus, and human immunodeficiency virus. The cross-talk between co-pathogens (especially lung microbiomes), SARS-CoV-2 and host is an important factor that ultimately increases the difficulty of diagnosis, treatment, and prognosis of COVID-19. Simultaneously, co-infecting microbiotas may use new strategies to escape host defense mechanisms by altering both innate and adaptive immune responses to further aggravate SARS-CoV-2 pathogenesis. Better understanding of co-infections in COVID-19 is critical for the effective patient management, treatment and containment of SARS-CoV-2. This review therefore necessitates the comprehensive investigation of commonly reported microbial co-pathogens amid COVID-19, their transmission pattern along with the possible mechanism of co-infections and outcomes. Thus, identifying the possible co-pathogens and their underlying molecular mechanisms during SARS-CoV-2 pathogenesis may shed light in developing diagnostics, appropriate curative and preventive interventions for suspected SARS-CoV-2 respiratory infections in the current pandemic.

Dysbiosis of Oral and Gut Microbiomes in SARS-CoV-2 Infected Patients in Bangladesh: Elucidating the Role of Opportunistic Gut Microbes

“…The inhaled SARS-CoV-2 virus particle binds to the human angiotensin-converting enzyme 2 (hACE2) receptor on epithelial cells lining the respiratory and digestive tracts of the patients, starts replicating, migrates down the respiratory tract along the conducting airways, and a more robust innate immune response is triggered (3,4). It is assumed that during this propagation, migration, and immune response, the microbiomes throughout the respiratory airways and digestive systems might be altered or changed, and some of them may contribute to further complicating the disease progression (5,6). The most common clinical features of COVID-19 include fever, dry cough, fatigue, sore throat, diarrhea, difficulty in breathing or shortness of breath, chest pain or pressure, and loss of speech or movement (5)(6)(7).…”

“…It is assumed that during this propagation, migration, and immune response, the microbiomes throughout the respiratory airways and digestive systems might be altered or changed, and some of them may contribute to further complicating the disease progression (5,6). The most common clinical features of COVID-19 include fever, dry cough, fatigue, sore throat, diarrhea, difficulty in breathing or shortness of breath, chest pain or pressure, and loss of speech or movement (5)(6)(7). The coinfection of the SARS-CoV-2 with other microorganisms is a very important factor in COVID-19 pathogenesis that may complicate the accurate diagnosis, treatment, prognosis of COVID-19, and even increase the mortality rates.…”

Genomic characterization of the dominating Beta, V2 variant carrying vaccinated (Oxford−AstraZeneca) and nonvaccinated COVID‐19 patient samples in Bangladesh: A metagenomics and whole‐genome approach

“…This might happen due to immune-suppression upon SARS-CoV-2 infection that leads to other viral coinfections or vice versa. 73,74 However, further careful observation on microbial coinfection is warranted for understanding this phenomenon.…”

Does the Fetus Limit Antibiotic Treatment in Pregnant Patients with COVID-19?

“…On the other hand, superinfection is when a pathogen infects the host shortly before a second infection with another pathogen. In both cases, the state of the host depends mainly on the balance between the immunopathology exerted by the pathogens and the immunity of the host [ 33 ].…”

“…Clinical trials and metagenomic investigations indicated the co-presence of other viruses, bacteria, archaea, and fungi with SARS-CoV-2 in COVID-19 patients. Approximately 50% of the patients who died from SARS-CoV-2 had secondary bacterial infections that promoted COVID-19 pathophysiological progression [ 33 ].…”