Cytomegalovirus immune evasion of myeloid lineage cells
Medical Microbiology and Immunology, ISSN: 1432-1831, Vol: 204, Issue: 3, Page: 367-382
2015
- 33Citations
- 51Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations33
- Citation Indexes33
- 33
- CrossRef21
- Captures51
- Readers51
- 51
Review Description
Cytomegalovirus (CMV) evades the immune system in many different ways, allowing the virus to grow and its progeny to spread in the face of an adverse environment. Mounting evidence about the antiviral role of myeloid immune cells has prompted the research of CMV immune evasion mechanisms targeting these cells. Several cells of the myeloid lineage, such as monocytes, dendritic cells and macrophages, play a role in viral control, but are also permissive for CMV and are naturally infected by it. Therefore, CMV evasion of myeloid cells involves mechanisms that qualitatively differ from the evasion of non-CMV-permissive immune cells of the lymphoid lineage. The evasion of myeloid cells includes effects in cis, where the virus modulates the immune signaling pathways within the infected myeloid cell, and those in trans, where the virus affects somatic cells targeted by cytokines released from myeloid cells. This review presents an overview of CMV strategies to modulate and evade the antiviral activity of myeloid cells in cis and in trans.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84929965926&origin=inward; http://dx.doi.org/10.1007/s00430-015-0403-4; http://www.ncbi.nlm.nih.gov/pubmed/25776081; http://link.springer.com/10.1007/s00430-015-0403-4; https://dx.doi.org/10.1007/s00430-015-0403-4; https://link.springer.com/article/10.1007/s00430-015-0403-4
Springer Science and Business Media LLC
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