Viruses are thought to facilitate bacterial infections of the respirat
ory tract, but the mechanisms are poorly understood. The present study
analyzed the effect of adenovirus on bacterial adherence to human res
piratory tract epithelial cells. The human lung carcinoma cell line A5
49 was infected with adenovirus of types 1, 2, 3, 4, 5, and 9. At a mu
ltiplicity of infection of 75 particles per cell, cytopathic effects o
ccurred in 75 to 100% of the cells within 48 h. The virus-infected cel
ls were harvested at various times after infection and analyzed for th
e ability to bind strains of Haemophilus influenzae and Streptococcus
pneumoniae. Adenovirus (types 1, 2, 3, and 5) commonly causing respira
tory tract infections increased the binding of adherent S. pneumoniae
strains to the cells. This effect was not seen for other adenovirus ty
pes. Adenovirus infection did not change the adherence of cells of poo
rly adhering strains of S. pneumoniae or H. influenzae. The increase i
n adherence of S. pneumoniae could be inhibited by the DNA synthesis i
nhibitor 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 pa
rticles or viral proteins. This suggested that adenovirus infection up
regulated receptors for S. pneumoniae. The increased attachment may be
one mechanism by which viruses precondition the respiratory mucosa fo
r bacterial infection.