Resumen
- Epidemiological, clinical and in animal models studies associate primary viral infection with secondary bacterial infections. Biochemical and molecular mechanisms involved on viral bacterial interactions are not well understood, albeit studies on respiratory virus and bacteria co-infections date from the twenty years of last century. Alterations in the infected cell by the virus direct and/or indirect modify the host bactericidal activities. Host cell bactericidal processes start as response to the host recognition of microbial components, known as pathogen associated molecular patterns ((PAMPs) through membrane recognition receptors such as toll like (TLR). PAMPs and TLR interactions activate transduction signals which induce the expression of genes involved in the immune response against bacteria. Control of viral primary infection and the secondary bacterial infection is a multifactor process and requires in tune interaction between host cell, bacteria and virus which easily can be disturbed by co-infection. Here we review cell host changes due to respiratory virus and bacteria that favors co-infection.