Department of Microbiology, University of Dhaka, Dhaka, 1000, Bangladesh; Department of Gynecology, Obstetrics and Reproductive Health, Bangabandhu Sheikh Mujibur Rahman Agricultural University (BSMRAU), Gazipur, 1706, Bangladesh.
Department of Microbiology, University of Dhaka, Dhaka, 1000, Bangladesh; Department of Microbiology, Jahangirnagar University, Savar, Dhaka, 1342, Bangladesh.
Microb Pathog. 2021 Jul;156:104941. doi: 10.1016/j.micpath.2021.104941. Epub 2021 May 4.
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.
新型冠状病毒病 2019（COVID-19）由严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）引起，正在进行的破坏性大流行使全世界受到创伤。大量微生物领域包括病毒（除 SARS-CoV-2 外）、细菌、古菌和真菌共同进化，并与 SARS-CoV-2 一起在复杂的分子发病机制中相互作用。然而，其他微生物共病原体的参与以及导致 COVID-19 重症患者病情加重的潜在分子机制尚未得到广泛审查。尽管实验室确诊的 COVID-19 病例中合并感染的发生率高达 94.2%，但 SARS-CoV-2 感染宿主中合并感染的命运往往取决于宿主保护性免疫和免疫病理学之间的平衡。SARS-CoV-2 的主要共病原体是细菌，如肺炎链球菌、金黄色葡萄球菌、肺炎克雷伯菌、流感嗜血杆菌、肺炎支原体、鲍曼不动杆菌、嗜肺军团菌和肺炎衣原体，其次是病毒，包括流感、冠状病毒、鼻病毒/肠道病毒、副流感、副流感病毒、乙型流感病毒和人类免疫缺陷病毒。共病原体（特别是肺部微生物组）、SARS-CoV-2 和宿主之间的串扰是一个重要因素，最终增加了 COVID-19 的诊断、治疗和预后的难度。同时，合并感染的微生物群可能通过改变固有和适应性免疫反应来逃避宿主防御机制，从而进一步加重 SARS-CoV-2 的发病机制，从而利用新的策略。更好地了解 COVID-19 中的合并感染对于有效管理患者、治疗和控制 SARS-CoV-2 至关重要。因此，本综述需要对 COVID-19 中常见报道的微生物共病原体及其传播模式以及合并感染的可能机制和结果进行全面调查。因此，确定 SARS-CoV-2 发病过程中的可能共病原体及其潜在分子机制，可能为当前大流行中疑似 SARS-CoV-2 呼吸道感染的诊断、适当的治疗和预防干预措施提供思路。
