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Oral Viruses in Periodontal Disease

Oral Viruses in Periodontal Disease Dr. Afsar Raza Naqvi, PhD

Periodontal disease (PD) is an inflammatory condition of the specialized supporting structures of teeth that if left untreated, can result in tooth loss. The onset of PD is driven by dysbiosis of the normal host microbiome, while disease progression is caused by activation of the host innate and adaptive immune response along with disease enhancement by local and systemic risk factors. Common manifestations of dysbiosis include chronic form or the less common, aggressive form of periodontitis. PD is the 6th most common disease globally and is linked to numerous systemic diseases such as diabetes mellitus, cardiovascular disease and others. Significant pathological findings of PD are linked to aberrant periodontal inflammation impacting both oral and systemic tissues. Research in molecular mechanisms modulating periodontal inflammation is important for our understanding of mucosal immunity, especially oral mucosal immunity for the development and/or improvement of therapeutic approaches. In adult humans, one or more types of viruses are persistently detected signifying HHV adaptation inside human body. Multiple lines of evidence show higher prevalence of these viruses in various oral inflammatory diseases but how HHV exacerbate these infections remains unexplored. A unique feature of HHV, unlike other viruses, is that they also encode viral miRNAs (v-miRs). These viral microRNAs (vmiRs) are multifunctional as they regulate expression of both virus and host derived transcripts and thus control host-virus interaction. In our lab we have been studying the pathological role of five most common oral inflammatory diseases associated HHV viz., HCMV, HSV-1, EBV, KSHV and HHV-6B on periodontal inflammation, a highly common oral inflammatory disease. Given their immunomodulatory role, manipulation of these small RNAs may also be useful in the diagnosis and treatment of oral inflammatory diseases.


Research in Dr. Naqvi’s lab is focused on dissecting epigenetic regulation of (1) peridontal disease and (2) host-pathogen interaction. Using a combinatorial approach of biochemical, genetic and bioinformatics tolos, our lab is interested in understanding immunopathogenesis of periodontal disease and the influence of herpesviruses in disease

proguession/severity. Our long-term goa lis to identify and characterize miRNAs (human or virus-encoded) and long noncoding RNA (LncRNA) whose therapeutic potential translates into clinical application for periodontal disease. This may be in the form of targets to be modified, as biomarkers for disease with prognostic/diagnostic capabilities, or therapeutic agents capable of dynamic modification of gene expression. Knowledge derived from our research will bridge basic and clinical research disciplines. In our lab, we harness the potential of ex vivo biopsies, in vivo murine models of periodontitis and various in vitro models of disease to delineate impairment of pathways with specific focus on innate and adaptive immune responses. In addition, our lab is examining virus-bacterial interaction in periodontal disease. We are currently studying synergy between periodontal herpesviruses and bacteria in context of periodontal disease exacerbation. Finally, we have recently initiated studies to understand immune impairment and microbiome changes influenced by novel coronavirus SARS-CoV-2.

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