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Assoc. Prof. Roberta Rizzo

University of Ferrara, Italy




“Human herpesviruses – biology, epidemiology and disease association”

Department of Medical Sciences, Section of Microbiology and Medical Genetics, University of Ferrara, Ferrara (Italy)
Of the more than 100 known herpesviruses, 8 routinely infect only humans: α herpesviruses (herpes simplex virus types 1 and 2, varicella-zoster virus), β herpesviruses (cytomegalovirus, human herpesvirus 6 (variants A and B), human herpesvirus 7), and γ herpesviruses (Epstein-Barr virus, Kaposi's sarcoma virus or human herpesvirus 8). Herpesviruses have a unique four-layered structure: a core containing the large, double-stranded DNA genome is enclosed by an icosapentahedral capsid which is composed of capsomers. The capsid is surrounded by an amorphous protein coat called the tegument. It is encased in a glycoprotein-bearing lipid bilayer envelope. Herpesviruses are among the most successful human pathogens. In healthy individuals, primary infection is most often inapparent. After primary infection, the virus becomes latent in ganglia or blood mononuclear cells. Each herpesvirus has evolved its own unique ecological niche within the host that allows the maintenance of latency over the life of the individual (e.g. the adaptation to specific cell types in establishing latent infection and the mechanisms, including expression of different sets of genes, by which the virus remains latent). Neurotropic α herpesviruses become latent in dorsal root ganglia and reactivate to produce epidermal ulceration, either localized (herpes simplex types 1 and 2) or spread over several dermatomes (varicella-zoster virus). Human cytomegalovirus, the prototype β herpesvirus, establishes latency in bone marrow-derived myeloid progenitor cells. Reactivation of latent virus is especially serious in transplant recipients and AIDS patients. Lymphotropic γ herpesviruses (Epstein-Barr virus) reside latently in resting B cells and reactivate to produce various neurologic complications. This review will describe the biology, epidemiology and disease association of the human herpesviruses.




I’m Associate Professor in Microbiology at the at University of Ferrara (Italy) and I’m supervising a number of projects in the field of immunological and virological implications in pregnancy, female infertility, tumours and autoimmune diseases. During my career I made important research in unraveling of networks of immunological tolerance during pregnancy, first by evidencing the importance of HLA-G molecules in embryo implantation and pregnancy outcome working in the group of Prof. Olavio Baricordi. More recently, I become an independent researcher in the field of host immune response towards microbiological infections elucidating the role of NK cell KIR receptors in the control of herpesvirus infections. During the last ten years, I performed works in the characterization of the mechanisms underlying the function of innate immunity, and I contributed in elucidating the role of NK cells promoting herpesvirus infection control. I demonstrated that NK cell activation can be controlled in a different way on the basis of the expression of specific KIR receptors, and the modification of the KIR subset could modify the ability to counteract infection chronicity. I’m currently involved in the identification of the specific marker for female infertility including HLA-G molecules and the implication of herpesvirus infections.
I have established internal and external National and International Collaborations with leading group in the field of pregnancy and autoimmune diseases. These collaborations have been instrumental for developing the study of the role of host response to microbiological infections.