About: Microglia control the spread of neurotropic virus infection via P2Y12 signalling and recruit monocytes through P2Y12-independent mechanisms

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About: Microglia control the spread of neurotropic virus infection via P2Y12 signalling and recruit monocytes through P2Y12-independent mechanisms Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Microglia control the spread of neurotropic virus infection via P2Y12 signalling and recruit monocytes through P2Y12-independent mechanisms
Creator	Kovacs, Gabor Hortobágyi, Tibor Balázs Gönci, · Bernadett Martinecz, · Boldogkői, Zsolt Connor, · Cserép, Csaba Dénes, · Fekete, Rebeka Ferenczi, Szilamér Kittel, Ágnes Kovács, Krisztina Környei, Zsuzsanna Lénárt, Nikolett Mária Baranyi, · Méhes, Előd Németh, Valéria Orsolits, Barbara Rózsa, Balázs Sperlágh, · Szabó, · Szalay, Gergely Tóth, Krisztina West, Brian
Source	PMC
abstract	Neurotropic herpesviruses can establish lifelong infection in humans and contribute to severe diseases including encephalitis and neurodegeneration. However, the mechanisms through which the brain’s immune system recognizes and controls viral infections propagating across synaptically linked neuronal circuits have remained unclear. Using a well-established model of alphaherpesvirus infection that reaches the brain exclusively via retrograde transsynaptic spread from the periphery, and in vivo two-photon imaging combined with high resolution microscopy, we show that microglia are recruited to and isolate infected neurons within hours. Selective elimination of microglia results in a marked increase in the spread of infection and egress of viral particles into the brain parenchyma, which are associated with diverse neurological symptoms. Microglia recruitment and clearance of infected cells require cell-autonomous P2Y12 signalling in microglia, triggered by nucleotides released from affected neurons. In turn, we identify microglia as key contributors to monocyte recruitment into the inflamed brain, which process is largely independent of P2Y12. P2Y12-positive microglia are also recruited to infected neurons in the human brain during viral encephalitis and both microglial responses and leukocyte numbers correlate with the severity of infection. Thus, our data identify a key role for microglial P2Y12 in defence against neurotropic viruses, whilst P2Y12-independent actions of microglia may contribute to neuroinflammation by facilitating monocyte recruitment to the sites of infection. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s00401-018-1885-0) contains supplementary material, which is available to authorized users.
has issue date	2018-07-19(xsd:dateTime)
bibo:doi	10.1007/s00401-018-1885-0
bibo:pmid	30027450
has license	cc-by
sha1sum (hex)	7421d0a5937f6e1ec30547de88bc4b4148725995
schema:url	https://doi.org/10.1007/s00401-018-1885-0
resource representing a document's title	Microglia control the spread of neurotropic virus infection via P2Y12 signalling and recruit monocytes through P2Y12-independent mechanisms
has PubMed Central identifier	PMC6096730
has PubMed identifier	30027450
schema:publication	Acta Neuropathol
resource representing a document's body	covid:7421d0a5937f6e1ec30547de88bc4b4148725995#body_text
is schema:about of	covid:arg/7421d0a5937f6e1ec30547de88bc4b4148725995 named entity 'IMAGING' named entity 'IDENTIFY' named entity 'VIRUS INFECTION' named entity 'SIGNALLING' named entity 'LEUKOCYTE' named entity 'SELECTIVE' named entity 'USING' named entity 'COMBINED' named entity 'MECHANISMS' named entity 'P2Y12' named entity 'ESTABLISHED' named entity 'CLEARANCE' named entity 'HOURS' named entity 'ENCEPHALITIS' named entity 'SEVERITY' named entity 'ACROSS' named entity 'PROCESS' named entity 'RESULTS' named entity 'MICROGLIA' named entity 'VIRAL INFECTIONS' named entity 'CELLS' named entity 'INDEPENDENT' named entity 'VIRUSES' named entity 'SIGNALLING' named entity 'DIVERSE' named entity 'NUMBERS' named entity 'INCLUDING' named entity 'INFLAMED' named entity 'AUTONOMOUS' named entity '27S' named entity 'CELL' named entity 'RESPONSES' named entity 'MICROGLIA' named entity 'MONOCYTES' named entity 'ALPHAHERPESVIRUS' named entity 'LIFELONG' named entity 'INFECTION' named entity 'ASSOCIATED WITH' named entity 'DISEASES' named entity 'HIGH RESOLUTION MICROSCOPY' named entity 'INFECTED' named entity 'AFFECTED' named entity 'DATA' named entity 'MICROGLIAL' named entity 'ACTIONS' named entity 'NEURONAL' named entity 'TURN' named entity 'LARGELY' named entity 'BRAIN PARENCHYMA' named entity 'SEVERE' named entity 'BRAIN' named entity 'MARKED' named entity 'VIRAL ENCEPHALITIS' named entity 'NEURONS' named entity 'NEURODEGENERATION' named entity 'NEUROLOGICAL SYMPTOMS' named entity 'OUR'

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