Dr.Zaviyalov于2017年5月就职于广州市妇女儿童医疗中心儿科研究所，担任临床免疫学实验室PI。博士毕业于瑞典乌普萨拉大学细胞与分子生物学系，分子生物学专业。曾在乌普萨拉大学（瑞典）进行博士后研究工作，此后先后到新加坡免疫学网络公司担任免疫学研究科学家，夏威夷大学马诺阿分校担任医学免疫学研究助理教授。2011至2016年初，在芬兰图尔库大学研究院任生物技术中心免疫学实验室PI。在俄罗斯读大学时在免疫球蛋白制剂中发现了腺苷脱氨酶（ADA2），此后一直致力于相关研究，曾获得多项国家级研究基金资助，先后在俄罗斯、法国、新加坡、美国等地开展研究工作，与西班牙、瑞典专家开展科研合作。研究期间获得大量科研项目立项，发表SCI论文31篇，包括6篇Cell，2篇Nature，3篇Molecular Cell，1篇JAMA，1篇New England Journal of Medicine等。原核翻译终止和平移的GTPase活性的调控机制相关理论被写入生物化学专业教科书。
Brief description of current research：
It has been shown that adenosine plays an important role in the regulation of immune responses. Adenosine accumulates at sites of inflammation and tumor growth and binds to adenosine receptors that are expressed by immune cells in response to activation signals. However, the role of adenosine deaminases, which decrease the local concentration of adenosine, is still unclear. Moreover, it remains puzzling why humans possess two enzymes, ADA1 and ADA2, with adenosine deaminase activity. ADA1 is largely an intracellular enzyme that breaks down adenosine and reduces the concentration of the adenosine derivatives that are toxic to immune cells. It has been found that mutations in the ADA1 gene lead to a severe combined immunodeficiency that is characterized by decreased antibody production and lower numbers of T and B cells. In contrast to ADA1, ADA2 is a secreted protein expressed mainly by cells of the myeloid lineage, such as macrophages and dendritic cells. Clinical studies have shown that the levels of ADAs in biological fluids are altered in pathophysiological conditions, suggesting that ADA activity could be a convenient marker for the diagnosis of immune diseases such as tuberculosis and oral cancer. We have identified the gene encoding ADA2 and shown that it belongs to a new family of adenosine deaminase growth factors (ADGFs). The crystal structure of ADA2 reveals it to be a dimer with two chemokine-like domains that could potentially bind a putative ADA2 receptor. We found that ADA2 binds to neutrophiles, CD16+ monocytes, NK cells and B cells that do not express CD26, a receptor for ADA1. These observations suggest the existence of a new mechanism by which ADAs bind to and regulate the activity of different lymphocyte subsets. Recently, patients with mutations in the gene encoding ADA2 (DADA2 patients) were identified. These patients display multiple health problems such as early onset systemic inflammation, multiple ischemic strokes, panlymphopenia and hypogammaglobulinemia. The aim of my project is to shed light on the function of ADA2, the enzyme that is currently thought to be a drug candidate to combat solid tumors, and find its clinical applications.