期刊
INFECTION GENETICS AND EVOLUTION
卷 64, 期 -, 页码 105-114出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.meegid.2018.06.025
关键词
Human cytomegalovirus; Innate immunity; DNA sensors; Restriction factors; Interferons; Inflammasome
资金
- Ministry of Education, Universities and Research [2015RMNSTA]
- University of Turin [LANSRILO1701, DELVRILO1701]
The interplay between human cytomegalovirus (HCMV) and the innate immune response is a critical process that has attracted the attention of many research groups. The emerging scenario is that the immune response of an HCMV-infected host is mediated by a plethora of viral DNA sensors acting as pattern recognition receptors (PRRs), which are capable of inhibiting indirectly viral infection through the activation of two distinct downstream signaling cascades. The first one triggers the production of cytokines, chemokines and interferons (IFNs), while the second one leads to inflammasome complex formation, which in turn promotes the maturation and secretion of pro-inflammatory cytokines such as interleukin-1 beta (IL-1 beta). An additional first line of defense against HCMV is represented by a multiplicity of constitutively expressed restriction factors that inhibit viral replication by directly interfering with the activity of essential viral/cellular genes. Here, we take a closer look at some of the most representative intrinsic restriction factors involved in HCMV infection (e.g. IFI16, ND10 complex, viperin and APOBEC3) and review our current understanding of the mechanisms that HCMV has evolved to counteract both IFN and inflammasome responses.
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