The microbial coinfection in COVID-19

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel β-coronavirus, is the main pathogenic agent of the rapidly spreading pneumonia called coronavirus disease 2019 (COVID-19). SARS-CoV-2 infects much more people, especially the elder population, around the world than other coronavirus, such as SARS-CoV and MERS-CoV, which is challenging current global public health system. Beyond the pathogenesis of SARS-CoV-2, microbial coinfection plays an important role in the occurrence and development of SARS-CoV-2 infection by raising the difficulties of diagnosis, treatment, prognosis of COVID-19, and even increasing the disease symptom and mortality. We summarize the coinfection of virus, bacteria and fungi with SARS-CoV-2, their effects on COVID-19, the reasons of coinfection, and the diagnosis to emphasize the importance of microbial coinfection in COVID-19. Key points • Microbial coinfection is a nonnegligible factor in COVID-19. • Microbial coinfection exacerbates the processes of the occurrence, development and prognosis of COVID-19, and the difficulties of clinical diagnosis and treatment. • Different virus, bacteria, and fungi contributed to the coinfection with SARS-CoV-2.

Neuroimaging manifestations in children with SARS-CoV-2 infection: a multinational, multicentre collaborative study

“…These four cases emphasise the potential for SARS-CoV-2 to impede the host's normal immune responses such that co-infections can work synergistically, contributing to a more severe clinical evolution of infection. 24 , 25 …”

Dysregulated Interferon Response Underlying Severe COVID-19

“…Further data from in vivo mouse models indicate that the inductive expression of IFN-α/β and IFN-λ2/3 by the lung immune cells (primarily dendritic cells) causes damage to the lung epithelium, which hampers lung repair and increases susceptibility to lethal bacterial coinfections [ 44 , 45 , 46 ]. Indeed, a meta-analysis evaluated 4.3–9.5% of COVID-19 patients with a bacterial infection, which was more common in severe patients (8.1%) [ 47 ] and so were the incidences of co-infection from other microbes, including fungi and other viruses, in critically ill COVID-19 patients who suffer dysfunctional IFN and other immune reactions [ 48 ]. As mammalian IFN-α and IFN-λ2/3 subtypes evolve more inductive and antiviral activity than the epithelial-specific IFN subtypes (such as IFN-β and IFN-λ1) [ 49 , 50 ], the robust reaction of inflammatory IFN responses via recruited immune cells in the lung certainly deteriorate the pulmonary homeostasis maintained by the epithelial IFN subtypes, which is more constitutively expressed by pneumocytes prior to immunopathic IFN responses in severe COVID-19.…”

Plasma Metabolomic Profiles and Clinical Features in Recovered COVID-19 Patients Without Previous Underlying Diseases 3 Months After Discharge

“…Except the infection of SARS-CoV-2, microbial coinfection was very common, including various viruses, bacteria, and fungi, which not only rendered the diagnosis and treatment of COVID-19 di cult, but also put patients on the risk of unfavorable clinical outcomes. 29,30 Homotyrosine has been reported to be associated with the fungal infection and sulfated homotyrosine echinocandin variants are essential to pathogenicity of some fungi. 31 Indolelactate is one of the bacterial tryptophan metabolites 32 which have been reported to be related to colon cancer, serving as promoters of the disease.…”