Background: Countries in the World Health Organization (WHO) Eastern Mediterranean Region (EMR) are predisposed to highly contagious, severe and fatal, emerging infectious diseases (EIDs), and re-emerging infectious diseases (RIDs). This paper reviews the epidemiological situation of EIDs and RIDs of global concern in the EMR between 2001 and 2018. Methods: To do a narrative review, a complete list of studies in the field was we prepared following a systematic search approach. Studies that were purposively reviewed were identified to summarize the epidemiological situation of each targeted disease. A comprehensive search of all published studies on EIDs and RIDs between 2001 and 2018 was carried out through search engines including Medline, Web of Science, Scopus, Google Scholar, and ScienceDirect. Results: Leishmaniasis, hepatitis A virus (HAV) and hepatitis E virus (HEV) are reported from all countries in the region. Chikungunya, Crimean Congo hemorrhagic fever (CCHF), dengue fever, and H5N1 have been increasing in number, frequency, and expanding in their geographic distribution. Middle East respiratory syndrome (MERS), which was reported in this region in 2012 is still a public health concern. There are challenges to control cholera, diphtheria, leishmaniasis, measles, and poliomyelitis in some of the countries. Moreover, Alkhurma hemorrhagic fever (AHF), and Rift Valley fever (RVF) are limited to some countries in the region. Also, there is little information about the real situation of the plague, Q fever, and tularemia. Conclusion: EIDs and RIDs are prevalent in most countries in the region and could further spread within the region. It is crucial to improve regional capacities and capabilities in preventing and responding to disease outbreaks with adequate resources and expertise.

The mosquito-borne Rift Valley fever (RVF) is a prioritised disease that has been listed by the World Health Organization for urgent research and development of counteraction. Rift Valley fever virus (RVFV) can cause a cytopathogenic effect in the infected cell and induce hyperimmune responses that contribute to pathogenesis. In livestock, the consequences of RVFV infection vary from mild symptoms to abortion. In humans, 1–3% of patients with RVFV infection develop severe disease, manifested as, for example, haemorrhagic fever, encephalitis or blindness. RVFV infection has also been associated with miscarriage in humans. During pregnancy, there should be a balance between pro-inflammatory and anti-inflammatory mediators to create a protective environment for the placenta and foetus. Many viruses are capable of penetrating that protective environment and infecting the foetal–maternal unit, possibly via the trophoblasts in the placenta, with potentially severe consequences. Whether it is the viral infection per se, the immune response, or both that contribute to the pathogenesis of miscarriage remains unknown. To investigate how RVFV could contribute to pathogenesis during pregnancy, we infected two human trophoblast cell lines, A3 and Jar, representing normal and transformed human villous trophoblasts, respectively. They were infected with two RVFV variants (wild-type RVFV and RVFV with a deleted NSs protein), and the infection kinetics and 15 different cytokines were analysed. The trophoblast cell lines were infected by both RVFV variants and infection caused upregulation of messenger RNA (mRNA) expression for interferon (IFN) types I–III and inflammatory cytokines, combined with cell line-specific mRNA expression of transforming growth factor (TGF)-β1 and interleukin (IL)-10. When comparing the two RVFV variants, we found that infection with RVFV lacking NSs function caused a hyper-IFN response and inflammatory response, while the wild-type RVFV suppressed the IFN I and inflammatory response. The induction of certain cytokines by RVFV infection could potentially lead to teratogenic effects that disrupt foetal and placental developmental pathways, leading to birth defects and other pregnancy complications, such as miscarriage.