Influenza A virus lacking the effector and C terminal domains of NS1 protein induces cytokines associated with high pathogenicity in mice.

Non-structural NS1 protein of influenza A virus counters host antiviral defences by antagonizing the interferon response. The C-terminal effector domain suppresses the host response and is associated with the pathogenicity of the virus.  To better understand the regulatory role of the C-terminal domain, we used reverse genetics system to generate NS1-truncated virus (NS80) and compared the cytokine profiles in the lungs of mice infected with the NS80 mutant and with the control virus A/WSN/33 (WSN).

Comparison of cytokine profiles induced by nonlethal and lethal doses of influenza A virus in mice.

Influenza viruses are among the most common human pathogens and are responsible for causing extensive seasonal morbidity and mortality. To investigate the immunological factors associated with severe influenza infection, the immune responses in mice infected with nonlethal (LD0) doses of A/PR/8/34 (H1N1) influenza virus were compared with those of mice infected with a lethal dose (LD100) of the virus. The virus titer and activation of retinoic acid-inducible gene (RIG)-I-like receptor signaling pathways were similar in the mice infected with LD0 and LD100 at 2 days post-infection; however, mice infected with LD100 exhibited a greater abundance of cytokines and a more diverse cytokine profile.

Comparison of transcriptional profiles of interferons, CXCL10 and RIG-1 in influenza infected A549 cells stimulated with exogenous interferons.

Type I and type III interferons (IFNs) are induced by viral infection. It was concluded that these IFN species are identical in regulation and biological functions. However, these two systems differ in the tissue expression of their receptors and their transcriptional regulation is fundamentally different as well as cellular signaling pathways that drive expression of each IFN.

Cytokines Induced During Influenza Virus Infection.

Influenza A virus is one of the major human pathogens. The influenza infection can pass out without any subclinical symptoms or infestation can appear in upper respiratory tract as well as in lower respiratory tract where it can result in lethal outcome. Both innate and adaptive immune responses are activated shortly after infection providing protection against infection.

Transforming Activity of Murine Herpesvirus 68 Putative Growth Factor Is Related to the Ability to Change Cytoskeletal Structure.

Murine herpesvirus 68 (MHV-68) can transform cells in vitro and in vivo. We investigated putative murine herpesvirus growth factors (MHGFs) obtained by the separation of cell-free media from MHV-68-transformed cells on an FPLC Sephadex G15 column. The transforming activity of the MHGFA fraction was related to depolymerization of actin, disruption of the microtubule network, and punctate-reticular changes of the Golgi.