Asset Details
Do you wish to reserve the book?
Recognition of herpesviruses by the innate immune system
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Recognition of herpesviruses by the innate immune system
Do you wish to request the book?
Recognition of herpesviruses by the innate immune system
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Recognition of herpesviruses by the innate immune system
2011
Overview
Key Points
Herpesviruses are a large family of DNA viruses, eight of which can cause diseases in humans, particularly in children and immunocompromised individuals. All herpesviruses have the capacity to cause lytic infection in permissive cells and to establish latent or recurrent infections in other cell types.
The innate immune system detects infections using germline-encoded pattern recognition receptors (PRRs). Toll-like receptors (TLRs) are membrane-bound PRRs that detect microorganisms in extracellular and endosomal locations. TLR2, TLR3 and TLR9 are well-described sensors of herpesvirus infections.
In the cytoplasm, active innate immune surveillance takes place and is mediated by nucleic acid sensors. Herpesvirus infections are sensed by both RNA and DNA sensing systems, and recent reports suggest a particularly important role for the cytosolic DNA-sensing AIM2-like receptor (ALR) family in intracellular detection of herpesviruses.
Given the relatively slow replication cycle of herpesviruses and the establishment of life-long infections, these viruses are highly dependent on efficient immune evasion strategies. It is now known that herpesviruses evade all classes of PRRs (including ALRs), as well as the downstream signalling machinery.
Innate immune defence against herpesviruses is highly dependent on the type I interferon system and natural killer cells. Model studies in mice and genetic data from humans have revealed essential roles for both TLRs and intracellular DNA sensors in mounting protective immune responses against herpesviruses.
Here the authors describe how multiple pattern recognition receptors, at the host cell surface, in endosomes and in the cytoplasm, are involved in detecting herpesviruses. How do they each contribute to immune defence against the virus, and how does the virus evade this detection and persist in the host?
Advances in innate immunity over the past decade have revealed distinct classes of pattern recognition receptors (PRRs) that detect pathogens at the cell surface and in intracellular compartments. This has shed light on how herpesviruses, which are large disease-causing DNA viruses that replicate in the nucleus, are initially recognized during cellular infection. Surprisingly, this involves multiple PRRs both on the cell surface and within endosomes and the cytosol. In this article we describe recent advances in our understanding of innate detection of herpesviruses, how this innate detection translates into anti-herpesvirus host defence, and how the viruses seek to evade this innate detection to establish persistent infections.
Publisher
Nature Publishing Group UK,Nature Publishing Group
