Journal
VIRAL IMMUNOLOGY
Volume 32, Issue 10, Pages 424-429Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/vim.2019.0097
Keywords
herpes simplex virus type 1; latent infection; innate immunity; adaptive immunity
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Funding
- Higher Education Commission (HEC)-Pakistan
- University of the Punjab, Lahore, Pakistan
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Herpes simplex virus type 1 (HSV-1) infection activates a rapid stimulation of host innate immune responses and a delicate interplay between virus and host immune elements regulates the whole events. Although host immune elements play well in limiting the HSV-1 infection by interfering viral replication, they are still unable to remove the virus completely, because HSV-1 proteins are efficient enough to bypass the host antiviral immune responses and virus succeed to reactivate again from latency at opportune time. Type 1 interferon signaling pathway is the central point of innate immunity along with some of the activated neutrophils, monocytes, macrophages, and dendritic cells, and some natural killer cells play role, while the CD8(+) T cells are crucial in adaptive immunity. In this review, the current knowledge of host and HSV-1 interaction has been described that how the host antiviral immune responses occur and what are the mechanisms of viral evasion adapted by virus to counteract with both arms of immunity.
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