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Eucalyptus is a large genus of the Myrtaceae family with high value in various fields of industry. Recently, attention has been focused on the functional properties of Eucalyptus extracts. These extracts have been traditionally used to combat various infectious diseases, and volatile oils are usually considered to play a major role. But the positive effects of non-volatile acylphloroglucinols, a class of specialized metabolites with relatively high content in Eucalyptus, should not be neglected. Herein, non-volatile acylphloroglucinols from leaves of Eucalyptus robusta were evaluated for their abilities to inhibit Zika virus (ZIKV) which is associated with severe neurological damage and complications. The results showed eucalyprobusone G, a new symmetrical acylphloroglucinol dimer, possessed the significant ability to inhibit ZIKV without inducing cytotoxicity. The EC50 values of eucalyprobusone G against the African lineage (MR766) and Asian lineage (SZ-WIV01) of ZIKV were 0.43 ± 0.08 and 10.10 ± 3.84 μM which were 110 times and 5.8 times better than those of the reference compound ribavirin, respectively. Further action mode research showed that eucalyprobusone G impairs the viral binding and RdRp activity of NS5. The results broaden the functional properties of Eucalyptus robusta and indicate acylphloroglucinol dimers could be developed as anti-ZIKV agents.

HIV-1 depends on host-cell-encoded factors to complete its life cycle. A comprehensive understanding of how HIV-1 manipulates host machineries during viral infection can facilitate the identification of host targets for antiviral drugs or gene therapy. The cellular protein Naf1 (HIV-1 Nef-associated factor 1) is a CRM1-dependent nucleo-cytoplasmic shuttling protein, and has been identified to regulate multiple receptor-mediated signal pathways in inflammation. The cytoplasm-located Naf1 can inhibit NF-κB activation through binding to A20, and the loss of Naf1 controlled NF-κB activation is associated with multiple autoimmune diseases. However, the effect of Naf1 on HIV-1 mRNA expression has not been characterized. In this study we found that the nucleus-located Naf1 could promote nuclear export of unspliced HIV-1 gag mRNA. We demonstrated that the association between Naf1 and CRM1 was required for this function as the inhibition or knockdown of CRM1 expression significantly impaired Naf1-promoted HIV-1 production. The mutation of Naf1 nuclear export signals (NESs) that account for CRM1 recruitment for nuclear export decreased Naf1 function. Additionally, the mutation of the nuclear localization signal (NLS) of Naf1 diminished its ability to promote HIV-1 production, demonstrating that the shuttling property of Naf1 is required for this function. Our results reveal a novel role of Naf1 in enhancing HIV-1 production, and provide a potential therapeutic target for controlling HIV-1 infection.

Recently, more and more studies suggested a new, possible role of markers of infection and inflammation beyond traditional cardiovascular risk factors, in the development and progression of atherosclerosis. Our aim was to study the mechanism of MCMV infection contributing to atherogenesis. ApoE knockout C57BL/6 mice were fed with hypercholesterol diet and inoculated ip with 3×10 pfu/100 μl MCMV. The plasma concentrations of cholesterol and the expression of MCP-1, GRO-α, FKN, RANTES, IL-4 and IFN-γ were detected in the atherosclerosis lesion. Results showed that the concentration of plasma cholesterol increased over 500 mg/dl and distinct atherosclerotic plaque could be observed in aorta after 12 weeks with hypercholesterol diet. In MCMV infection, impressive atherosclerotic plaques were observed in the aorta and the infiltration of inflammatory cells in endothelium were significantly enhanced. RT-PCR results showed that MCMV infection could induce the expression of MCP-1, GRO-α, FKN and RANTES on the atherosclerotic lesion and correlated with the atherosclerotic plaque. The local expression of cytokine IFN-γ was enhanced in MCMV infection. Our findings showed that MCMV infection contributed to atherogenesis probably by inducing expression of chemokines and immune response deviation to Th1 response. Surely, there will be other pathways involved the atherogenesis.