Comparisons between groups were calculated by Mann-Whitney rank sum. Further statistical analyses were done by Kruskal-Wallis test followed by Dunn's multiple comparison tests. P values of ,0.05 were considered to be statistically significant. Figure S1 Complete profile of the levels (pg/ml) of cytokines, chemokines and growth factors determined by multiplex-bead arrays from blood samples collected from CHIKV-infected patients and healthy control subjects.  Avian Influenza: Should China Be Alarmed? Avian influenza has emerged as one of the primary public health concern of the 21st century. Influenza strain H5N1 is capable of incidentally infecting humans and other mammals. Since their reemergence in 2003, highly pathogenic avian influenza A (H5N1) viruses have been transmitted from poultry to humans (by direct or indirect contact with infected birds) in several provinces of Mainland China, which has resulted in 22 cases of human infection and has created repercussions for the Chinese economy. People have been concerned whether a new pandemic will occur in the future. The eradication of pathogenic avian influenza viruses appears to be the most effective way to prevent an influenza pandemic. This paper will examine the features of H5N1, including incidence, infection, immunity, clinical management, prevention and control, and therapy in Mainland China.  Rift Valley Fever Virus NSs Protein Promotes Post-Transcriptional Downregulation of Protein Kinase PKR and Inhibits eIF2α Phosphorylation Rift Valley fever virus (RVFV) (genus Phlebovirus, family Bunyaviridae) is a negative-stranded RNA virus with a tripartite genome. RVFV is transmitted by mosquitoes and causes fever and severe hemorrhagic illness among humans, and fever and high rates of abortions in livestock. A nonstructural RVFV NSs protein inhibits the transcription of host mRNAs, including interferon-β mRNA, and is a major virulence factor. The present study explored a novel function of the RVFV NSs protein by testing the replication of RVFV lacking the NSs gene in the presence of actinomycin D (ActD) or α-amanitin, both of which served as a surrogate of the host mRNA synthesis suppression function of the NSs. In the presence of the host-transcriptional inhibitors, the replication of RVFV lacking the NSs protein, but not that carrying NSs, induced double-stranded RNA-dependent protein kinase (PKR)–mediated eukaryotic initiation factor (eIF)2α phosphorylation, leading to the suppression of host and viral protein translation. RVFV NSs promoted post-transcriptional downregulation of PKR early in the course of the infection and suppressed the phosphorylated eIF2α accumulation. These data suggested that a combination of RVFV replication and NSs-induced host transcriptional suppression induces PKR-mediated eIF2α phosphorylation, while the NSs facilitates efficient viral translation by downregulating PKR and inhibiting PKR-mediated eIF2α phosphorylation. Thus, the two distinct functions of the NSs, i.e., the suppression of host transcription, including that of type I interferon mRNAs, and the downregulation of PKR, work together to prevent host innate antiviral functions, allowing efficient replication and survival of RVFV in infected mammalian hosts. Rift Valley fever virus (RVFV) is a mosquito-borne zoonotic pathogen, which is distributed in sub-Saharan Africa [1] and has also caused large outbreaks in Madagascar [2] , Egypt [3, 4, 5] , Saudi Arabia [6] , and Yemen [6] . In endemic areas, RVFV naturally circulates among mosquitoes and ruminants, such as sheep, goat and cattle [7] . RVFV infection in adult ruminants causes febrile illness and a high rate of abortions, while some newborn animals less than 1-2 weeks of age develop an acute infection which results in higher mortality rates than those in adults [8] . Humans infected with RVFV usually develop an acute febrile myalgic syndrome; however, a small percentage of patients have a lethal illness that results in hepatic damage, hemorrhagic fever-like illness, encephalitis and/or retinal vasculitis [8] .