Abstract
Emerging evidence has unveiled the secondary infection as one of the mortal causes of post-SARS-CoV-2 infection, but the factors related to secondary bacterial or fungi infection remains largely unexplored. We here systematically investigated the factors that might contribute to secondary infection. By clinical examination index analysis of patients, combined with the integrative analysis with RNA-seq analysis in the peripheral blood mononuclear cell isolated shortly from initial infection, this study showed that the antibiotic catabolic process and myeloid cell homeostasis were activated while the T-cell response were relatively repressed in those with the risk of secondary infection. Further monitoring analysis of immune cell and liver injury analysis showed that the risk of secondary infection was accompanied by severe lymphocytopenia at the intermediate and late stages and liver injury at the early stages of SARS-CoV-2. Moreover, the metagenomics analysis of bronchoalveolar lavage fluid and the microbial culture analysis, to some extent, showed that the severe pneumonia-related bacteria have already existed in the initial infection.
Highlights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a kind of beta coronavirus that infects the host cell via its interaction with the angiotensin-converting enzyme–related carboxypeptidase (ACE2), has become the greatest scourge for humanity since the 1918 influenza [1, 2]
There are many opportunistic pathogens existing in human body, such as Mycoplasma pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, Haemophilus influenzae, Staphylococcus aureus, Streptococcus pneumoniae and other resistant Enterobacteriaceae [16,17,18], with the changes of the immune system and micro-environment when fighting against the viral infection, these opportunists look to expand rapidly and cause severe secondary infection post-SARS-CoV-2-infection [19, 20]
In the face of the COVID-19, currently rampaging around the world and continues to spread, the secondary infection has been reported to be an adverse prognostic marker for the severe illness and mortality of SARS-CoV-2 [8, 31]. It was documented than the mortality rate of secondary bacterial infections among COVID-19 patients admitted to the intensive care unit (ICU) was as high as 95% [32]
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a kind of beta coronavirus that infects the host cell via its interaction with the angiotensin-converting enzyme–related carboxypeptidase (ACE2), has become the greatest scourge for humanity since the 1918 influenza [1, 2]. There are many opportunistic pathogens existing in human body, such as Mycoplasma pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, Haemophilus influenzae, Staphylococcus aureus, Streptococcus pneumoniae and other resistant Enterobacteriaceae [16,17,18], with the changes of the immune system and micro-environment when fighting against the viral infection, these opportunists look to expand rapidly and cause severe secondary infection post-SARS-CoV-2-infection [19, 20]
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