Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 8th Clinical Microbiology Conference Paris, France.

Day 1 :

Keynote Forum

Gerald Kleymann

University of Tubingen, Germany

Keynote: Novel agents and strategies to treat herpes simplex virus infections
Conference Series Clinical Microbiology 2017 International Conference Keynote Speaker Gerald Kleymann photo

Gerald Kleymann has received his PhD from the Max Planck Institute of Biophysics and the University of Frankfurt in 1994. He worked with Bayer Pharmaceuticals as a Lab Head and Coordinator of strategic projects where he discovered the helicase primase inhibitors to treat herpes disease. He was appointed as Apl. Professor at the University of Tübingen in 2009. He has founded diverse companies e.g. the private clinic Primedica, Innovative Molecules and Your Lab. He has published numerous papers, patents, review articles and book chapters.


After first evidence that nucleosides such as idoxuridine may also be useful to treat herpes disease in the 1950, research in the field was intensified. The milestone publication of acyclovir in 1978 subsequently leads to a new era of DNA polymerase inhibitors to treat herpes infections. For the underlying strategy of anti-metabolite research, the noble price was awarded to Gertrude Elion in 1988. Since the eighties the prodrug acyclovir became the gold standard to treat herpes infections, predominantly HSV and VZV. In the nineties the pre-prodrugs of acyclovir and penciclovir, a close congener of ACV, named valacyclovir and famciclovir with a more convenient dosing schedule were launched. These anti-herpes nucleosidic drugs are virostatic but they do not cure the key clinical issue of herpes infections which is recurrent disease. In 2002, helicase primase inhibitors of HSV and VZV that are two orders of magnitude more potent than acyclovir in vitro and at least 10 times more efficacious in vivo were published and subsequently developed. Published animal models and current clinical trials indicate that the frequency of recurrent herpes disease can be reduced.

Keynote Forum

Walter Fierz

labormedizinisches zentrum Dr Risch, Liechtenstein

Keynote: Multiple sclerosis and age-related macular degeneration: examples of pathogenic viral interaction with the immune system?

Time : 11:15-12:15

Conference Series Clinical Microbiology 2017 International Conference Keynote Speaker Walter Fierz photo

Walter Fierz is a Clinical Immunologist with basic training in experimental cellular immunology at the Transplantation Immunology Unit of the Clinical Research Center in Harrow, London (UK) and at the Max-Planck-Society group for Multiple Sclerosis research in Würzburg (Germany). Later work involved running of a Diagnostic Cellular Immunology Laboratory at the University of Zürich (Switzerland) and further as Medical Director at private laboratories. He also achieved a Master of Health Information Management (MHIM) at the Erasmus University in Rotterdam (The Netherlands). For some years, he was Member of the Scientific Advisory Group of the Swiss Society of Multiple Sclerosis.


A hypothesis is formulated on viral interaction between HHV-6A and EBV as a pathogenic mechanism in Multiple Sclerosis (MS). Evidence of molecular and genetic mechanisms suggests a link between HHV-6A infection and EBV activation in the brain of MS patients leading to intrathecal B-cell transformation. Consequent T-cell immune response against the EBVinfected cells is postulated as a pathogenic basis for inflammatory lesion formation in the brain of susceptible individuals. A more subtle pathogenic mechanism can be seen in the down-regulation of CD46 on astrocytes by the infecting HHV-6A. Since CD46 is central in regulating the complement system, a lack of CD46 leads to hyper-activation of the complement system. In fact, activation of the complement system in brain lesions is one of the pathogenic mechanism in MS. A similar mechanism is suspected to be central in the development of age-related macular degeneration (AMD). One of the earliest changes in the retina of AMD patients is the loss of CD46 expression in the retinal pigment epithelium (RPE) during geographic atrophy. Furthermore, CD46 deficient mice spontaneously develop dry-type AMD-like changes in their retina. It is also well known that certain genetic polymorphisms in the complement-inhibiting pathways correlate with higher risks of AMD development. The hypothesis here is that HHV-6A infection of the retina leads to down-regulation of CD46 and consequently to hyper-activation of the complement system in the eyes of susceptible individuals as a pathogenic mechanism. Interaction of HHV-6A with
CD46 also plays a role in triggering autophagy providing a further link to AMD.