The influenza (flu) virus infection induces an upexpression of tlr3, tlr7, tlr8, nfκb1, nfκbiα, nos2, xdh and other genes in mice lung. The nos2 and xdh upexpression causes overproduction of free radicals that lead to lung tissue damage. The upexpression of nfκb1, nfκbiα genes induce incorrect regulation of NF-κB. that regulates expression of the immune, inflammation genes and takes part in flu viral replication. The oligoribonucleotides-D-mannitol complexes (ORNs-D-M) possess antiviral activity against the flu virus in vitro and in vivo. One of mechanisms of the ORNs-D-M anti-influenza activity is direct virucidal action by blocking hemagglutinin–glycan interactions and inhibiting neuraminidase activity of flu virus. However other mechanisms of the ORNs-D-M anti-influenza activity have to be studied.

Current research was aimed at study of the ORNs-D-M effects on expression of the tlr3, tlr7, tlr8, nfkbia, nfnb1 nos2, xdh genes in mice lung under flu virus infection. To achieve this goal we applied a two-step RT-PCR assay. In mice lung after 48 h flu infection it was detected the overexpression of all investigated genes compared to the healthy ones. The ORNs-D-M injection for prevention reduced the mRNA level of tlr3, tlr7, tlr8, nfkbia, nfnb1 nos2, xdh expression by 65, 77, 76, 70, 63, 48, 32 % respectively vs the virus-infected mice. And the ORNs-D-M injection for treatment reduced the mRNA level of tlr3, tlr7, tlr8, nfkbia, nfnb1 nos2, xdh expression by 28, 17, 22, 40, 52, 41, 38 % respectively vs the virus-infected mice.

Our results show that the expression of all investigated genes is modulated by the ORNs-D-M after injection for prevention and treatment of the flu virus infection in vivo. It allows us to assume that by inhibiting the expression of tlr3, tlr7, tlr8, the ORNs-D-M impair the upregulation of nos2, xdh, nfkbia, nfkb1 induced by flu virus.