Day 2 :
Keynote Forum
Roger M Loria
Virginia Commonwealth University , USA
Keynote: Enhancing host resistance to infections
Time : 09:00-09:40
Biography:
Roger M Loria is an Emeritus Professor in Microbiology, Immunology with joint appointments in Pathology and Emergency Medicine. He has obtained his Doctorate from Boston University, Postdoctoral studies by the Massachusetts Heart Association, Greater Boston Chapter and a sabbatical at Harvard Medical School, Boston, MA. He is a Research Fellow in Children’s Hospital in Infectious Disease Unit. He has more than 80 publications in peer reviewed journal and more that 25 patents. He is a Member of several Editorial Boards.
Abstract:
β Androstanediol epimers (Δ5 androstane, 3β, 17α diol; and Δ5 androstane, 3β, 17β diol) consist of a metabolic endocrine node which functions to regulate host resistance to infections and malignancies. The β Androstane steroids (17β AED/AET) up-regulate immunity and increase host resistance against lethal infection by viruses, and bacteria. The β Androstenes increase the levels of the TH1 cytokines, IL-2, IL-3, and IFNγ and counteract hydrocortisone mediated immune suppression. Treatment with a single dose of either 17β AED or 17β AET protected the host from whole body lethal radiation and led to the recovery of the remaining hematopoietic precursor cells. Increased host resistance protected the host from lethal infection by DNA or RNA viruses such as herpes virus, coxsackievirus B4, influenza, and arthropod borne viruses. Similar protection against lethal Gram positive and Gram-negative bacteria infections has been observed. The specificity of 17β AED/17β AET is illustrated by the finding that the 17α epimer (17α AED inhibits proliferation and mediates apoptosis in tumor cells of murine and human origin and induces autophagy in human glioblastoma. In summary, these agents provide a unique new avenue for the control, mitigation, and prevention of diseases by viral, bacterial infections. The androstenes are a new subclass of steroid hormones with specific and unique physiological properties.
Keynote Forum
Sharad Kumar Yadav
DUVASU, India
Keynote: Recent advances in molecular characterization of Bovine herpesvirus-4
Time : 09:40-10:20
Biography:
Sharad Kumar Yadav has 28 years of teaching and research experience and has served to various senior positions of the University including Registrar of the DUVASU University. He is currently Professor, Head of Department of Veterinary Microbiology, and Director at Cow Research Institute at DUVASU, Mathura, India. He has published number of papers in reputed International and National journals and has a vast experience in the arena of BHV-I virus.
Abstract:
Bovine herpesvirus 4 (BoHV-4) is an important viral pathogen negatively affecting the livestock production because of abortion and associated ill effects. BoHV-4 is a member of the genus Rhadinovirus in the sub family Gammaherpesvirinae, belonging to the family Herpesviridae. BoHV 4 can affect cattle, buffalo, sheep, goats, bison and large cats. The property of establishing a latent state in ganglionic neurons after infection allocates the BoHV-4 virus to persist in the body and spread the disease from a latently infected carrier to a non-infected herd. Bovine herpesviruses 4 can generally be transmitted by horizontal and vertical routes. The horizontal transmission occurs by close contact with moist contaminated surfaces, but droplet infections are also common. Vertical transmission via fetal infection occurs during parturition, hence mostly associated with reproductive disorders. Because bovine herpesviruses are highly labile once shed from the body and are readily inactivated by sunlight or drying, milk represents a good candidate as a vehicle for BoHV-4 shedding and transmission. BoHV-4 infection can be diagnosed efficiently by molecular techniques such as PCR, restriction enzyme analysis, detection by probe and Southern hybridization. BoHV-4 has also been isolated by using cell culture propagation, histopathology, serology, PCR, and electron microscopy from animals with symptoms of respiratory and ocular infections, vulvovaginitis, mastitis, abortions, endometritis and even from apparently healthy animals throughout the world. Molecular studies on molecular and phylogenic analysis are scarce but recent studies showed popularity and reliability on advance molecular techniques. Further, molecular studies on BoHV-4 are warranted and needed to know about virus entry into target cells, viral gene expression inside, DNA replication, and phylogenetic relationship with other related Bovine herpes virus for providing proper protection to susceptible animals against hidden threat of BoHV-4. Considering the unusual rate of spread of the infection related with economic aspects, the current study is addressed to discuss comprehensive diagnostic strategy specifically focusing on new upcoming advances in molecular diagnosis of BoHV-4 in different parts of the world
- Sessions: Global Epidemiology of HIV/AIDS, STDs, & STIs | Viral Hepatitis | Veterinary Virology | General Virology and Basic Science | Viral Pathogenesis,Virulence & Latency | Bacterial Virology | Viruses and Diseases
Chair
Shubhada Bopegamage
Slovak Medical University, Slovakia
Co-Chair
Abdelouaheb Benani
Pasteur Institute of Morocco, Morocco
Session Introduction
Shubhada Bopegamage
Slovak Medical University, Slovak Republic
Title: In vivo mouse model for coxsackievirus infections: our story
Time : 10:35-10:55
Biography:
Shubhada Bopegamage is a Virologist. Currently, she is the Head of the Enterovirus Laboratory and the National Reference Center for Identification of Enteroviruses at the Medical Faculty of the Slovak Medical University in Bratislava, Slovakia. Her work is focused on the pathogenesis and diagnosis of Enteroviruses. She received her BSc Microbiology degree from Pune, India and MSc Microbiology degree from Mumbai, India. She got her PhD in Biological Sciences from the Academy of Medical Sciences, Moscow, Russia. She is known in the Enterovirus research, since 2005, for her work on the in vivo experimental coxsackievirus oral infection of mice, and experimental coxsackievirus infection during gravidity. She is involved in research and teaching and has guided several MSc and PhD students. She has Coordinated and has lead several national and international projects as a Principal or Co-investigator
Abstract:
Statement of the Problem: The introduction of cell culture techniques has simplified the work of Virologists. Scientific history shows us, however, that we cannot study a disease completely without using animal models. Though, humans are the natural hosts for coxsackieviruses B (CVB), mice have been shown to be susceptible. In mice, these viruses induce diseases like those which they cause in humans. The experimental animal models allow investigation at a pathophysiological level where the biological picture and functioning is depicted. Though the closest experimental models for the Enteroviruses and human diseases are maybe chimpanzees, the murine models (mice), are one of the best models for studying coxsackieviruses.
Methodology & Theoretical Orientation: We studied genetically different mice strains. Permission for the animal work was obtained from the Ethics Committee of the Slovak Health University and the State Veterinary and Food Control Authority of the Slovak Republic. Mice were infected with different CVB strains and control mice with PBS by oral gavage. Organs were collected from infected mice/groups and control (mock infected) mice/groups at different days post infection. Organs were fixed for histology and immunohistochemistry in formalin and snap frozen and stored at -80ºC for detection of the viral RNA by polymerase chain reaction (PCR).
Findings & Conclusions: Our work showed differences between the oral route and intraperitoneal routes of infection. The differences were mainly in the histopathology of the pancreas, they also depended on the genetic background of the mice. We also showed pancreatitis in challenged pups of mice orally infected dams during gravidity at different times. Our work characterizes and shows the application of our model of the natural ‘oral’ route of infection to understand the pathogenesis of CV infections.