Augmented adherence and internalization of group A Streptococcus pyogenes to influenza A virus infected MDCK cells.

Respiratory tract infections are one of the leading causes of morbidity and mortality. There is considerable epidemiologic evidence that infection with respiratory viruses increases the incidence and severity of secondary bacterial complications. However, very limited number of studies were concerned with the mechanism behind such synergy. In this context, our study aimed to explore the interaction between Group A Streptococcus pyogenes (GAS) and Influenza A virus (IAV). Our results revealed that the GAS adherence and internalization into Madin-Darby canine kidney (MDCK) cells markedly increased after IAV infection. When M6 protein defective mutant of GAS was used, the virus enhanced adherence and internalization was nearly abolished indicating the involvement of M protein binding sites on the MDCK cell surface. Interestingly, the modulation of some O-linked glycolproteins as well as sialic acid, mucin and fibrinogen-like residues on the surface of MDCK cells contributed to augmented bacterial adherence and/or internalization. In the same way, qRT-PCR experiments showed an overexpression of the membrane associated mucin (MUC1) on the surface of the MDCK cells after IAV infection. Altogether, the present study revealed that IAV infection augments the adherence and internalization of GAS to MDCK cells via modulation of membrane associated O-linked glycoproteins, fibrinogen, sialic acid residues and the mucin, MUC1 on the surface of MDCK cell.