Aquatic birds are the main reservoir of influenza A viruses (IAVs). These viruses can infect humans repeatedly and cause acute respiratory disease with potential of spread in the form of epidemics. In addition, avian influenza viruses that overcome the interspecies barrier and adapt to humans can cause a worldwide pandemic with severe consequences to human health. Therefore, scientists are focused on the development of a "universal" vaccine with a broad protective efficacy, i.e. against different subtypes of influenza A viruses and not only against the currently co-circulating human epidemic strains. Nowadays, several new vaccine design strategies have been described. Most of them utilize the conserved stem part of influenza surface glycoprotein hemagglutinin (HA) or the ectodomain of M2 (M2e) protein with proton-channel activity. A comparison of the effectivity of novel vaccines and their protective mechanisms against influenza infection is discussed in this review and should be considered for the construction of the most effective broadly protective vaccine with minimal side effects. This is the essential goal in influenza virus research today, especially when the infection with new human coronavirus SARS-CoV-2 can interfere with the course of influenza virus infection.

The oncogenic gammaherpesviruses, Epstein-Barr virus (EBV) and Kaposi's sarcoma herpesvirus (KSHV), are etiologically associated with a variety of human cancers, including Burkitt's lymphoma (BL), Hodgkin lymphoma (HL), Kaposi's sarcoma (KS), and primary effusion lymphoma (PEL). Recently, we demonstrated KSHV infection of B- and endothelial cells to significantly upregulate the expression of interferon induced transmembrane protein 1 (IFITM1) which in turn enhances virus entry. This is an extension of the above study. In here, we determined EBV infection of cells to trigger IFITM1 expression, in vitro. Silencing IFITM1 expression using siRNA specifically lowered gammaherpesvirus infection of cells at a post binding stage of entry. A natural model system to explore the effect of IFITM1 on gammaherpesvirus infection in vivo is infection of BALB/c mice with murine gammaherpesvirus 68 (MHV-68). Priming mice with siRNA specific to IFITM1 significantly lowered MHV-68 titers in the lung specimens compared to priming with (NS)siRNA or PBS. MHV-68 titers were monitored by plaque assay and qPCR. Taken together, for the first time, this study provides insight into the critical role of IFITM1 to promoting in vivo gammaherpesvirus infections.

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