Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 11th International Virology Summit Valencia, Spain.

Day 1 :

Keynote Forum

Vsevolod A Zinserling

Saint-Petersburg University, Russia

Keynote: HIV Infection and its complications from pathologist’s point of view

Time : 11:10-11:50

Conference Series Euro Virology 2019 International Conference Keynote Speaker Vsevolod A Zinserling photo

Prof. Zinserling is pathologist working in the field of infectology in Saint-Petersburg, Russia. His research is devoted to  viral, bacterial, fungal and mycoplasma lesions of brain, lung, liver, intestine, placenta on autopsy, clinical and experimental material. Investigations of pathomorphology of Influenza, HIV and its complications, infections due to herpes viruses, viral hepatitis, mixed infections of different localisation are of special interest. Prof. V.A. Zinserling is collaborating at Saint-Petersburg University, Center of infectious pathology at S.P. Botkin hospital for infectious diseases and department of pathomorphology in the Institute of Experimental medicine at National Medical Research Center named after V.A. Almazov. He is active member of European Society of Pathology (working groups infectious diseases, autopsy pathology and history of pathology).  Author of more than 400 publications.


HIV infection remains one of the most dangerous diseases and important causes of death. Numerous investigations are devoted to problems of epidemiology, molecular biology, treatment, psychology etc. The number of studies discussing the results of pathological studies is very limited. Having long term experience in HIV pathology, we can formulate the following items. Most important questions to be studied on the autopsies of the deceased from HIV-infection: exact list of secondary infections and tumors with specification of their localization; evaluation of the efficacy of treatment; revealing of immediate death cause; collection of specimen for further investigations in order to study the mechanisms of the disease and its complications. Methods recommended for postmortem investigation are detailed histological study of all macroscopically changed and not changed organs with use of certain special staining; bacteriological and mycological investigation of all suspected lesions in order to clarify their etiology and certain properties of the pathogens; different virological, molecular-biological methods and immunohistochemistry in order to study the localization of lesions due to HIV and other viruses and some of their properties. Among the most interesting, important and not sufficiently known changes we pay special attention to the brain. We have to distinguish direct and indirect lesions due to HIV virus itself, other pathogens (CMV, Toxoplasma, Cryptococcus, HSV, JCV, EBV first of all) and other influences and follow up them in different decades of epidemics. Some clinico-pathological correlations in perinatal HIV: viral load in pregnant women correlated with the depth of immunosuppression; women without antiretroviral treatment had more expressed grade of immunosuppression; frequency of secondary purulent inflammation correlated with the grade of immunosuppression. Main probable pathogenic mechanisms of Placenta lesion in HIV: direct lesions of placenta macrophages (Hofbauer cells), endotheliocytes and decidual cells with development of typical changes of nuclei, leading role in inflammatory reaction of CD14+ in comparison with CD68+ cells; disturbance of angiogenesis due to hyper expression of anti-angiogenic factor TGFβ; probable disturbances of syncytial-capillary membrane. Main questions for further investigations: clarifying incidence and etiology of placenta inflammation and intrauterine infections in women with HIV; further studies of mechanisms of placenta lesions in HIV infected women; clinico-pathological correlations between morphological changes in placenta and outcome of pregnancy versus antiretroviral treatment; Clinico-pathological correlations between symptoms in children from HIV-infected mothers and post-mortem histology; studying impact of prenatal infections on development of children and morbidity of teenagers and adults. Question for the life-time pathological and cytological diagnostics are study of smears or liquid biopsies of cerebrospinal fluid for evaluating mycobacterium, cryptococci and tumour cells, lymph node biopsies in order to identify the origin of their lesion, needle biopsies of other organs due to clinical necessity.


Keynote Forum

Iva Christova

National Center of Infectious and Parasitic Diseases, Bulgaria

Keynote: Vector borne infections in Bulgaria

Time : 11:50-12:30

Conference Series Euro Virology 2019 International Conference Keynote Speaker Iva Christova photo

Iva Christova is a Professor of Microbiology at the National Center of Infectious and Parasitic Diseases (NCIPD), Sofia, Bulgaria. She is the Deputy Director of NCIPD and Head of National reference vector-borne pathogens laboratory. She published more than 65 papers in reputed journals. Her research interest is focused on ecology, epidemiology, laboratory diagnosis and clinical manifestations of tick-borne and mosquito-borne pathogens. For her outstanding research, she was awarded Morrison Rogosa Award for 2003 from American Society for Microbiology and numerous Bulgarian awards, e.g. award for the most successful young scientist, award for the best research work and award for contribution in medicine. Her area of research interest includes vector-borne.



Located in Southeastern Europe, Bulgaria is an endemic country for Lyme borreliosis and Crimean-Congo haemorrhagic fever (CCHF) and is affected by West Nile virus (WNV). In addition, sporadic cases of Tick-borne encephalitis (TBE) have been also reported. About 500 cases of Lyme borreliosis are detected annually in Bulgaria. Two peaks in the seasonal distribution of cases and more frequent presentation of neuroborreliosis than of Lyme arthritis appear to be characteristics of Lyme borreliosis in the country. With sporadic cases or small outbreaks, CCHF appeared every year. More than 1600 CCHF cases were officially recorded since 1952. Genetic investigations showed that CCHF virus strains causing disease in the country belong to lineage Europe 1. However, two CCHF virus lineages, Europe 1 and Europe 2, are present in ticks in Bulgaria. CCHF seroprevalence among healthy population is 3.7%. In 2018, number of detected WNV human cases in Bulgaria exceeded the total number in the previous seven years, following the same trend in the other affected EU countries. WNV lineage 2 was confirmed as a cause of the human cases. Overall WNV seroprevalence in human population in the country is 1.5%. Tick-borne encephalitis is very unusual. Only a few cases of TBE have been detected. Overall seroprevalence of 0.6% for TBE virus was found in humans.

Keynote Forum

Mohammad Mir

Western University of Health Sciences, USA

Keynote: Hantavirus RdRp requires a host cell factor for Cap Snatching

Time : 17:00-17:40

Conference Series Euro Virology 2019 International Conference Keynote Speaker Mohammad Mir photo

Mohammad Mir did his PhD from Saha Institute of Nuclear Physics, Department of Atomic Energy of India in 2003. He then Moved to University of New Mexico for his Postdoctoral training in Virology, where he worked with hemorrhagic fever viruses. He then joined the University of Kansas, School of Medicine as Assistant Professor in Virology in the year 2009. In 2015, he joined the Western University of Health Sciences, California, as Associate Professor in Virology. His research program at Western University is focused on replication and therapeutic intervention of emerging negative strand RNA viruses.       




The hantavirus RNA-dependent RNA polymerase (RdRp) snatches 5' capped mRNA fragments from the host cell transcripts and uses them as primers to initiate transcription and replication of the viral genome in the cytoplasm of infected cells. Hantavirus nucleocapsid protein (N protein) binds to the 5' caps of host cell mRNA and protects them from the attack of cellular decapping machinery. N protein rescues long capped mRNA fragments in cellular P bodies that are later processed by an unknown mechanism to generate 10- to 14-nucleotide-long capped RNA primers with a 3' G residue. Hantavirus RdRp has an N-terminal endonuclease domain and a C-terminal uncharacterized domain that harbors a binding site for the N protein. The purified endonuclease domain of RdRp nonspecifically degraded RNA in vitro. It is puzzling how such nonspecific endonuclease activity generates primers of appropriate length and specificity during cap snatching. We fused the N-terminal endonuclease domain with the C-terminal uncharacterized domain of the RdRp. The resulting NC mutant, with the assistance of N protein, generated capped primers of appropriate length and specificity from a test mRNA in cells. Bacterially expressed and purified NC mutant and N protein required further incubation with the lysates of human umbilical vein endothelial cells (HUVECs) for the specific endonucleolytic cleavage of a test mRNA to generate capped primers of appropriate length and defined 3' terminus in vitro. Our results suggest that an unknown host cell factor facilitates the interaction between N protein and NC mutant and brings the N protein-bound capped RNA fragments in close proximity to the endonuclease domain of the RdRp for specific cleavage at a precise length from the 5' cap. These studies provide critical insights into the cap-snatching mechanism of cytoplasmic viruses and have revealed potential new targets for their therapeutic intervention.


Keynote Forum

Reza Nassiri

Michigan State University, USA

Keynote: Antimicrobial resistance in HIV patients

Time : 09:30-10:10

Conference Series Euro Virology 2019 International Conference Keynote Speaker Reza Nassiri photo

Reza Nassiri is a former Associate Dean of Global Health at the Michigan State University. He also served as the MSU Director of Institute of International Health. He is currently Professor of Clinical Pharmacology and Toxicology, Professor of Family and Community Medicine and Lecturer in Global Health, Infectious Diseases and Tropical Medicine. He currently works on international public health issues relating to chronic diseases and has expertise in global health. He has made contributions in various fields of medical sciences including clinical investigation and health education. He had served as an Editorial Board Member for the journal of HIV and AIDS Review. He is currently on Editorial Board Member for AIDS Patient Care and STDs, J of AIDS Clin Res., and Int. J. of Global Health. He is the Founder of Michigan State University Osteopathic and Primary Health Clinic in Merida, Yucatan, Mexico. His research interests include Clinical Pharmacology of HIV/AIDS, Viral Pathogenesis, Antibiotic Resistance, Prevention and Control of Infectious Diseases, Tropical Medicine, Global health and Community-based Public Health Interventions.




According to the WHO, there is an estimated 36.7 million people living with the human immunodeficiency virus (HIV). While antiretroviral drug resistance is a common genetic trait of HIV which often results in treatment failure, there is a paucity of information of the development of antibiotic resistance in HIV patients. Along with the CD4 cells, HIV targets other cells of the immune system resulting in immunodeficiency, and thus, such a weakened immune response increases opportunity for bacterial, fungal and other viral infections. Pathogens such as Streptococcus pneumoniae, Salmonella, Hemophilus, Staph aureus, E. coli, Klebsiella and Pseudomonas are the risk pathogens that are encountered in HIV patients. However, the frequency of bacterial infections which are especially common in the lower CD4 counts, necessitate more administration of antibiotics either for prophylaxis or treatment purposes. One of the most clinically challenging threats is the production of extended-spectrum β-lactamases (ESBLs) that impedes the antimicrobial treatment of infections caused by Enterobacteriaceae in HIV patients and is a serious threat to the practice of modern medicine. Antimicrobial resistance in general, is a global health concern within the scientific community. Failure of recognizing antibiotic resistance in HIV/AIDS patients can further complicate the overall therapeutic strategy of the containment of HIV and can also lead to a more compromised quality of life in HIV patients. In summary, antibiotic resistance poses a threat to everyone, but people living with HIV/AIDS are at more significant risk.


Keynote Forum

Tariq M Rana

University of California San Diego, USA

Keynote: Targeting Vif regulatory Axis: developing new AIDS therapies

Time : 10:10-10:50

Conference Series Euro Virology 2019 International Conference Keynote Speaker Tariq M Rana photo

Tariq M Rana is a Scholar, Inventor, Entrepreneur and Multidisciplinary Scientist who is developing new therapies to treat infectious disease, cancer and immune disorders. He is a Professor and Chief of Genetics, V/C for Innovation in Therapeutics in the Department of Pediatrics at the University of California San Diego, School of Medicine, where his laboratory employs mechanisms and technologies of RNA, stem cells and chemical biology to discover new pathways implicated in human disease.



The human host is invaded by a wide range of microbial pathogens and has evolved a number of defensive mechanisms to survive these infections. In addition to adaptive immunity, it is becoming increasingly clear that innate immunity plays an important role in protecting host organisms from infections. One of the innate immune response mechanisms against viral infections involves a protein family, APOBEC3 (apolipoprotein B mRNA editing enzyme catalytic polypeptide 3). The APOBEC3 family of proteins can restrict replication of exogeneous retorviruses as well as Hepatitis B, a DNA virus that replicates through an RNA intermediate, and inhibit replication of retrotransposons. APOBEC3G (A3G) protein exhibits the most potent block to HIV-1 replication. To counteract host defense, HIV-1 expresses Vif protein that targets A3G for proteasomal degradation. Since HIV-1 Vif has no known cellular homologs, this protein represents an extremely attractive, yet unrealized, target for antiviral intervention. I will discuss the strategies to develop therapeutics that antagonize HIV-1 Vif function to inhibit HIV-1 replication. Further mechanistic investigation will be presented showing that Vif inhibitors’ function requires Vif-A3G interactions and restores A3G function. These studies provide proof of principle that the HIV-1 Vif-A3G axis is a valid target for developing small molecule-based new therapies for AIDS or for enhancing innate immunity against viruses.