Virus-induced secondary bacterial infection: a concise review

Hendaus, Mohamed A; Jomha, Fatima A; Alhammadi, Ahmed H

Mammalian cells are prone to bacterial attachment during a viral illness. 8, 35 Viruses can debilitate the mucociliary clearance structure, leading to the increased attachment of bacteria to mucins and colonization; moreover, the condensed mucus will impede the penetration of antibacterial material and immune cells. 36 Viruses like the respiratory syncytial virus (RSV) can damage ciliated cells, resulting in ciliostasis and, therefore, deterioration of mucociliary clearance. 37 The same concept applies to an influenza virus infection, leading to decreased tracheal mucociliary velocity and clearance of S. pneumoniae. 35, 38 Moreover, virus-induced cell death debilitates the mechanical elimination of the attached pathogens and displays novice receptors for bacterial adherence. 39 Studies have shown that the RSV virus induces the adherence of S. pneumoniae, Pseudomonas aeruginosa, and Haemophilus influenza to airway epithelial cells. [40] [41] [42] [43] In addition, adenovirus and rhinovirus play the same role in the adherence of S. pneumoniae to the airway epithelial cells; 8, 44 however, the measles virus decreases the risk of adherence of streptococcal bacteria, implying that every virus has a specific mode of changing the host cell membrane. 44 Moreover, bacterial adhesion might also be a result of the upregulation of surface receptors including PAF-r, which is involved in pneumococcal invasion. 45, 46 In patients with cystic fibrosis, bacterial adherence forms a biofilm, creating permanent airway colonization with P. aeruginosa. 47 Viruses such as RSV, rhinovirus, and influenza virus also lead to pneumococcal biofilm formation on the airway lining. 48 Furthermore, RSV increases the risk of adherence of Staphylococcus aureus and Bordetella pertussis to Hep-2 (human epidermoid cancer) epithelial cells. 49, 50 virus effect on the immune system Post-viral sustained desensitization of lung sentinel cells to TLR signals may be one possible contributor to the common secondary bacterial pneumonia associated with viral infection. For instance, TLR4 and TLR5 pathways are altered after influenza virus infection, resulting in decreased neutrophil attraction, thereby leading to increased attachment of S. pneumonia and P. aeruginosa to the airway epithelial cells. 25 The interrelation between host cells and microorganisms during an infection induces immune responses that include the generation of proinflammatory molecules. Despite their crucial role as a bactericidal, proinflammatory cytokines such as TNF-α produced in response to infection could be detrimental to the host cells. 51 During a viral infection, TLR and RIG-I-like receptor activation induces production of type I IFNs, which can augment the inflammatory response to TLR ligands including lipopolysaccharide (LPS). 52, 53 In addition, certain bacteria such as S. aureus integrate into the A549 respiratory epithelial cells (adeno-carcinomic α β