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Viruses are thought to facilitate bacterial infections of the respiratory tract, but the mechanisms are poorly understood. The present study analyzed the effect of adenovirus on bacterial adherence to human respiratory tract epithelial cells. The human lung carcinoma cell line A549 was infected with adenovirus of types 1, 2, 3, 4, 5, and 9. At a multiplicity of infection of 75 particles per cell, cytopathic effects occurred in 75 to 100%S of the cells within 48 h. The virus-infected cells were harvested at various times after infection and analyzed for the ability to bind strains of Haemophilus influenzae and Streptococcus pneumoniae. Adenovirus (types 1, 2, 3, and 5) commonly causing respiratory tract infections increased the binding of adherent S. pneumoniae strains to the cells. This effect was not seen for other adenovirus types. Adenovirus infection did not change the adherence of cells of poorly adhering strains of S. pneumoniae or H. influenzae. The increase in adherence of S. pneumoniae could be inhibited by the DNA synthesis inhibitor cytosine arabinofuranoside, which is known to block the late phase of the adenovirus infection. When electron microscopy was used, there was no evidence that virus particles bound directly to bacteria. Adherence was not affected by pretreatment of the cells with virus particles or viral proteins. This suggested that adenovirus infection upregulated receptors for S. pneumonae. The increased attachment may be one mechanism by which viruses precondition the respiratory mucosa for bacterial infection. The upper respiratory tract is an ecological niche for bacteria such as Streptococcus pneumoniae and Haemophilus influenzae. These species are carried by healthy individuals and especially by children (3). The same bacterial strain may, however, also cause infection. It is not clear how the transition from asymptomatic carriage to infection can occur. Adherence facilitates the establishment of bacterial populations at mucosal surfaces. H. influenzae and Pseudomonas aeruginosa adhere to nasopharyngeal epithelial cells as well as respiratory tract mucins (8, 28, 29). Group A streptococci, Neisseria meningitidis, and S. pneumoniae adhere mainly to respiratory tract epithelial cells (8). No clear-cut correlation between in vitro adherence and virulence for the respiratory tract has been established (1). Nasopharyngeal isolates of S. pneumoniae from healthy carriers were found to adhere better to respiratory tract epithelial cells than isolates from the blood or cerebrospinal fluid of patients with pneumonia or meningitis. The in vitro adherence assays are, however, defective with regard to factors that influence adherence in vivo. Viral infections of the upper respiratory tract predispose to bacterial superinfection. The mortality during influenza epidemics has been attributed to bacteria such as Staphylococcus aureus, N. meningitidis, and group A streptococci as well as S. pneumoniae and H. influenzae (12, 35). Both viral and bacterial agents can be isolated from the middle ear fluid...
Viruses are thought to facilitate bacterial infections of the respiratory tract, but the mechanisms are poorly understood. The present study analyzed the effect of adenovirus on bacterial adherence to human respiratory tract epithelial cells. The human lung carcinoma cell line A549 was infected with adenovirus of types 1, 2, 3, 4, 5, and 9. At a multiplicity of infection of 75 particles per cell, cytopathic effects occurred in 75 to 100%S of the cells within 48 h. The virus-infected cells were harvested at various times after infection and analyzed for the ability to bind strains of Haemophilus influenzae and Streptococcus pneumoniae. Adenovirus (types 1, 2, 3, and 5) commonly causing respiratory tract infections increased the binding of adherent S. pneumoniae strains to the cells. This effect was not seen for other adenovirus types. Adenovirus infection did not change the adherence of cells of poorly adhering strains of S. pneumoniae or H. influenzae. The increase in adherence of S. pneumoniae could be inhibited by the DNA synthesis inhibitor cytosine arabinofuranoside, which is known to block the late phase of the adenovirus infection. When electron microscopy was used, there was no evidence that virus particles bound directly to bacteria. Adherence was not affected by pretreatment of the cells with virus particles or viral proteins. This suggested that adenovirus infection upregulated receptors for S. pneumonae. The increased attachment may be one mechanism by which viruses precondition the respiratory mucosa for bacterial infection. The upper respiratory tract is an ecological niche for bacteria such as Streptococcus pneumoniae and Haemophilus influenzae. These species are carried by healthy individuals and especially by children (3). The same bacterial strain may, however, also cause infection. It is not clear how the transition from asymptomatic carriage to infection can occur. Adherence facilitates the establishment of bacterial populations at mucosal surfaces. H. influenzae and Pseudomonas aeruginosa adhere to nasopharyngeal epithelial cells as well as respiratory tract mucins (8, 28, 29). Group A streptococci, Neisseria meningitidis, and S. pneumoniae adhere mainly to respiratory tract epithelial cells (8). No clear-cut correlation between in vitro adherence and virulence for the respiratory tract has been established (1). Nasopharyngeal isolates of S. pneumoniae from healthy carriers were found to adhere better to respiratory tract epithelial cells than isolates from the blood or cerebrospinal fluid of patients with pneumonia or meningitis. The in vitro adherence assays are, however, defective with regard to factors that influence adherence in vivo. Viral infections of the upper respiratory tract predispose to bacterial superinfection. The mortality during influenza epidemics has been attributed to bacteria such as Staphylococcus aureus, N. meningitidis, and group A streptococci as well as S. pneumoniae and H. influenzae (12, 35). Both viral and bacterial agents can be isolated from the middle ear fluid...
A review of the actual problems concerning the meningococcal carriage is presented. The review includes: the epidemiological features of meningococcal carriage, the phenotyping and genotyping characteristics of the carriage strains, the modern models of the carriage, the general and local (mucosal) immune protection induced by the carriage. The significance of genetic and virulence heterogenicity of carriage meningococcal population is underlined.
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