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A ZIKA VIRUS PRIMARY ISOLATE INDUCES NEUROINFLAMMATION, COMPROMISES THE BLOOD-BRAIN BARRIER AND UPREGULATES CXCL12 IN ADULT MACAQUES
Neuroinflamação
CXCL12
Comprometimento da barreira hematoencefálica
Macacos adultos
Neuroinflammation
Compromises the blood-brain barrieR
CXCL12
Vírus Zika
Adult macaques
Autor
Afiliación
Division of Microbiology. Tulane National Primate Research Center. Covington, LA, USA.
Division of Microbiology. Tulane National Primate Research Center. Covington, LA, USA.
Department of Microbiology and Molecular Cell Biology. Eastern Virginia Medical School. Norfolk, VA, USA.
Department of Microbiology and Molecular Cell Biology. Eastern Virginia Medical School. Norfolk, VA, USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Molecular de Flavivírus. Rio de Janeiro, RJ, Brasil.
Division of Microbiology. Tulane National Primate Research Center. Covington, LA, USA.
Division of Microbiology. Tulane National Primate Research Center. Covington, LA, USA.
Department of Microbiology and Molecular Cell Biology. Eastern Virginia Medical School. Norfolk, VA, USA.
Division of Microbiology. Tulane National Primate Research Center. Covington, LA, USA.
Department of Microbiology and Molecular Cell Biology. Eastern Virginia Medical School. Norfolk, VA, USA.
Department of Microbiology and Molecular Cell Biology. Eastern Virginia Medical School. Norfolk, VA, USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Molecular de Flavivírus. Rio de Janeiro, RJ, Brasil.
Division of Microbiology. Tulane National Primate Research Center. Covington, LA, USA.
Division of Microbiology. Tulane National Primate Research Center. Covington, LA, USA.
Department of Microbiology and Molecular Cell Biology. Eastern Virginia Medical School. Norfolk, VA, USA.
Resumen en ingles
Zika virus (ZIKV) is a flavivirus that can cause neuropathogenesis in adults and fetal neurologic malformation following the infection of pregnant women. We used a nonhuman primate model, the Indian-origin Rhesus macaque (IRM), to gain insight into virus-associated hallmarks of ZIKV-induced adult neuropathology. We find that the virus causes prevalent acute and chronic neuroinflammation and chronic disruption of the blood-brain barrier (BBB) in adult animals. ZIKV infection resulted in specific short- and long-term augmented expression of the chemokine CXCL12 in the central nervous system (CNS)of adult IRMs. Moreover, CXCL12 expression persists long after the initial viral infection is apparently cleared. CXCL12 plays a key role both in regulating lymphocyte trafficking through the BBB to the CNS and in mediating repair of damaged neural tissue including remyelination. Understanding how CXCL12 expression is controlled will likely be of central importance in the definition of ZIKV-associated neuropathology in adults.
Palabras clave en portugues
Isolado primárioNeuroinflamação
CXCL12
Comprometimento da barreira hematoencefálica
Macacos adultos
Palabras clave en ingles
Primary isolateNeuroinflammation
Compromises the blood-brain barrieR
CXCL12
Vírus Zika
Adult macaques
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