Chengyu Liang is an Assistant Professor (tenure-track) at the Keck School of Medicine of the University of Southern California. Research in Liang’s lab is centered on investigating the basic principle of cellular processes including apoptosis and autophagy, and genomic stability, as well as intracellular trafficking pathways in viral entry, replication, pathogenesis and cancer biology. She was the first to identify UVRAG as an autophagic tumor suppressor in cancer anddictate its important roles in synchronizing diverse cellular processes in human diseases including viral infection (Nature Cell Biology 2006, 2007, 2008, 2009, 2013; Dev Cell 2012). She had achieved extensive training and accomplishments in the molecular study of KSHV and γHV68 at Harvard Medical School, and pioneered the study of structural bases and functions of vBcl-2-mediated anti-autophagy and anti-apoptosis in AIDS-associated g-herpesviruses infection (PLoS pathogen 2008, 2009). Due to the remarkable nature of these findings, Dr. Liang has been granted the Leukemia & Lymphoma Society Fellow, the Wright Foundation Young Investigator Award, the Baxter Foundation Junior Faculty Award, and American Cancer Society Research Scholar. She successfully administered the projects, collaborated with other researchers, and produced several peer-reviewed high-profile publications from each project. She also serves as the director of confocal imaging core of the department.

Negative-strand RNA viruses are highly pathogenic and cause many severe diseases in humans and animals. These viruses generally use existing cellular pathways to enter cells, which involves intensive interaction with the endomembrane network, offering the endocytic pathway as an attractive scheme for therapeutic intervention. The molecular mechanisms governing virus entry remain incompletely understood. We found that UVRAG, well-known for regulating autophagy and intracellular trafficking, is a critical factor for virus entry through combinatorial interactions with a tether and endosomal SNAREs. UVRAG mediates viral endocytic transport and membrane penetration through interactions with the class C Vps complex and endosomal Q-SNAREs, leading to the assembly of a fusogenic trans-SNARE complex involving VAMP8, but not VAMP7. Indeed, UVRAG stimulates VAMP8 translocation to virus-bearing endosomes. Inhibition of VAMP8, but not VAMP7, reduces viral entry. Understanding the mechanism that allows the virus to interact with late endocytic organelles could identify the specific set of proteins that have a role in virus entry, which help us to design specific therapeutic agents against virus entries

Zorraga Mokhtar has completed medicine studies at the age of 28 years from El Manar University, Faculty of Medicine of Tunis. He has Doctoral thesis in Medicinernon 5-07-2001, Master of Advanced Studies in Emergency in the Faculty of Medicine of Tunis on 2012,Master of Advanced Studies in Travel medecine in the Facultyrnof Medicine of Tunis on 2014,ALS (Advanced life support) certificate of European Resuscitation Council at March 2013.He is the coordinator of influenza programrnin Tunisia that supported by US / CDC, part of InPRIS project (Building and Strenghtening Core Capacities for Influenza Preparedness and Response in Supportrnof International Health Regulation (2005) implementation in selected countries.He has published some papers in reputed journals, the last one in EID journal (rnemerging infectious desaease) / CDC : “Family Cluster of Middle East Respiratory Syndrome Coronavirus Infections, Tunisia, 2013” on September 2014.

Influenza surveillance in Tunisia has been in place since 1999 with the creation of network sentinel sites,but it has developedrnsignificantly on March 2014, with the implementation of electronic surveillance system.In Tunisia, clinical, epidemiological andrnvirological surveillance of influenza began in week 40/2014 (1 October 2014) and ended in week 18/2015 (30 April 2015). Duringrnthe period of study:123 719 cases ILI(Influenza-like illness) were collected from a total of 1 619 146 patients seen at sentinel sites,rnrepresenting 7.7% of total patients.rnThe influenza epidemic was spreading in the winter season 2014/2015 during eight weeks from 18 January 2015(2015 /rnS3) to 17 March 2015 (2015/ S11), it was as ordinary as the last five seasonal epidemics.The epidemic peak was observed duringrnthe week of 16 to 21 February 2015 (2015/ S08), with an incidence rate of 10.7%.On the other hand,Influenza epidemic of2014-rn2015 season was mild in intensity and started earlier than that of the previous year. These findings were also observed in Europernand in USA. Among the consultants for influenza-like illness (ILI), 263 severe cases (0.2%) were hospitalized; significantlyrnhigher proportion than the previous season.The lethality of severe cases was higher than that observed in the previous seasonrn(3%), these severe cases were mainly infected with A (H1N1) pmd09 virus.All of the 24 governorates of Tunisia have been affectedrnby the influenza and the incidence is higher in regions that are the most populated. Children 5to 16 years aremost affected.rnEpidemiological surveillance of influenza on the Tunisian territory has shown that the epidemic peak was recorded during therncoldest weeks (S08), in fact there is an inversetr end of monthly average temperature and influenza incidence, this remarkablerncorrelation shows that the rate of influenza incidence increased as the temperatures gradually decline. The hypothes is that thernvirus is favored by low temperatures and inhibited by higher temperatures is confirmed in our study.Influenza virus type B, Arn(H1N1) and A(H3N2) circulated with an initial dominance of type B virus that was reversed in favor of the type A (H1N1)rnpmd09 in the beginning of February.The seasonal distribution of three types of influenza viruses was: Virus B (58.4%), Arn(H1N1) pmd09(28.4%),Virus A (H3N2) (13.2%), The positivity rate for influenza was 28.4%.