Xanthenedione (and intermediates involved in their synthesis) inhibit Zika virus migration to the central nervous system in murine neonatal models

2020 ◽  
Vol 22 (9) ◽  
pp. 489-499
Author(s):  
Ítalo Esposti Poly da Silva ◽  
Milene Lopes da Silva ◽  
Roberto Sousa Dias ◽  
Edjon Gonçalves Santos ◽  
Maria Cecília Brangioni de Paula ◽  
...  
Cell ◽  
2017 ◽  
Vol 169 (4) ◽  
pp. 610-620.e14 ◽  
Author(s):  
Malika Aid ◽  
Peter Abbink ◽  
Rafael A. Larocca ◽  
Michael Boyd ◽  
Ramya Nityanandam ◽  
...  

2018 ◽  
Vol 45 (2) ◽  
pp. 152-153 ◽  
Author(s):  
Bruno Niemeyer de Freitas Ribeiro ◽  
Bernardo Carvalho Muniz ◽  
Emerson Leandro Gasparetto ◽  
Edson Marchiori

2018 ◽  
Vol 2 (4) ◽  
pp. 106-111
Author(s):  
Sâmia Israele Braz do Nascimento ◽  
Sheezara Teles Lira dos Santos ◽  
Bárbara Torquato Alves ◽  
Kevellyn Cruz Aguilera ◽  
Airton César Pinheiro de Menezes ◽  
...  

Since the twentieth century, humanity has been experiencing a public health reality marked by numerous mosquito-borne diseases (belonging to the arthropod class), known as arboviruses. The Zika virus has become in recent years a risk to Brazilian and international public health due to its devastating effect due to its pathogenesis but also to fetal neurological development, causing serious health problems such as microcephaly and Guillain-Barré Syndrome, but also myelitis and meningoencephalitis. However, scientists studying the Zika virus have been trying to use the agent's ability to cause infections in healthy cells to attack and destroy cancer cells, such as the case of grade IV astrocytoma known as Gliobastoma Multiforme (GBM), which is a tumor of the very aggressive central nervous system and worse prognosis among primary cancers. As a result of effective therapy for GBM and the tropism of this etiological agent for brain cells, the hypothesis is that this virus would cause cell death in glioblastomas through metabolic alterations induced by the induced viral infection, but further studies must be carried out to demonstrate this therapeutic advantage in using the virus for the treatment of this malignant disease. Keywords: Zika virus; Gliobastoma Multiforme; Tumor of the Central Nervous System.


2017 ◽  
Vol 75 (6) ◽  
pp. 381-386 ◽  
Author(s):  
Vanessa van der Linden ◽  
Hélio van der Linden Junior ◽  
Mariana de Carvalho Leal ◽  
Epitacio Leite Rolim Filho ◽  
Ana van der Linden ◽  
...  

ABSTRACT Congenital Zika syndrome is an emergent cause of a congenital infectious disorder, resulting in severe damage to the central nervous system and microcephaly. Despite advances in understanding the pathophysiology of the disease, we still do not know all the mechanisms enrolled in the vertical transmission of the virus. As has already been reported in other types of congenital infectious disorders in dizygotic twin pregnancies, it is possible that the virus affects only one of the fetuses. In this article, we report on two cases of twin pregnancies exposed to the Zika virus, but with only one of the fetuses affected with microcephaly and brain damage. This indicates the urgent need for more studies regarding the pathophysiology of viral infection and the mechanisms involved in the natural protection against the virus.


2020 ◽  
Vol 16 (5) ◽  
pp. e1008204 ◽  
Author(s):  
Jihye Kim ◽  
Brian Alejandro ◽  
Michal Hetman ◽  
Eyas M. Hattab ◽  
Joshua Joiner ◽  
...  

2021 ◽  
Vol 118 (49) ◽  
pp. e2111266118
Author(s):  
Natasha W. Hanners ◽  
Katrina B. Mar ◽  
Ian N. Boys ◽  
Jennifer L. Eitson ◽  
Pamela C. De La Cruz-Rivera ◽  
...  

Flaviviruses such as Zika virus and West Nile virus have the potential to cause severe neuropathology if they invade the central nervous system. The type I interferon response is well characterized as contributing to control of flavivirus-induced neuropathogenesis. However, the interferon-stimulated gene (ISG) effectors that confer these neuroprotective effects are less well studied. Here, we used an ISG expression screen to identify Shiftless (SHFL, C19orf66) as a potent inhibitor of diverse positive-stranded RNA viruses, including multiple members of the Flaviviridae (Zika, West Nile, dengue, yellow fever, and hepatitis C viruses). In cultured cells, SHFL functions as a viral RNA-binding protein that inhibits viral replication at a step after primary translation of the incoming genome. The murine ortholog, Shfl, is expressed constitutively in multiple tissues, including the central nervous system. In a mouse model of Zika virus infection, Shfl−/− knockout mice exhibit reduced survival, exacerbated neuropathological outcomes, and increased viral replication in the brain and spinal cord. These studies demonstrate that Shfl is an important antiviral effector that contributes to host protection from Zika virus infection and virus-induced neuropathological disease.


Cytokine ◽  
2018 ◽  
Vol 111 ◽  
pp. 255-264 ◽  
Author(s):  
Jorge Rodrigues de Sousa ◽  
Raimunda do Socorro da Silva Azevedo ◽  
Arnaldo Jorge Martins Filho ◽  
Marialva Tereza Ferreira de Araujo ◽  
Ermelinda do Rosário Moutinho Cruz ◽  
...  

Author(s):  
Geraldo Duarte ◽  
Antonio Moron ◽  
Artur Timerman ◽  
César Fernandes ◽  
Corintio Mariani Neto ◽  
...  

AbstractFrom the discovery of the Zika virus (ZIKV) in 1947 in Uganda (Africa), until its arrival in South America, it was not known that it would affect human reproductive life so severely. Today, damage to the central nervous system is known to be multiple, and microcephaly is considered the tip of the iceberg. Microcephaly actually represents the epilogue of this infection's devastating process on the central nervous system of embryos and fetuses. As a result of central nervous system aggression by the ZIKV, this infection brings the possibility of arthrogryposis, dysphagia, deafness and visual impairment. All of these changes of varying severity directly or indirectly compromise the future life of these children, and are already considered a congenital syndrome linked to the ZIKV. Diagnosis is one of the main difficulties in the approach of this infection. Considering the clinical part, it has manifestations common to infections by the dengue virus and the chikungunya fever, varying only in subjective intensities. The most frequent clinical variables are rash, febrile state, non-purulent conjunctivitis and arthralgia, among others. In terms of laboratory resources, there are also limitations to the subsidiary diagnosis. Molecular biology tests are based on polymerase chain reaction (PCR) with reverse transcriptase (RT) action, since the ZIKV is a ribonucleic acid (RNA) virus. The RT-PCR shows serum or plasma positivity for a short period of time, no more than five days after the onset of the signs and symptoms. The ZIKV urine test is positive for a longer period, up to 14 days. There are still no reliable techniques for the serological diagnosis of this infection. If there are no complications (meningoencephalitis or Guillain-Barré syndrome), further examination is unnecessary to assess systemic impairment. However, evidence is needed to rule out other infections that also cause rashes, such as dengue, chikungunya, syphilis, toxoplasmosis, cytomegalovirus, rubella, and herpes. There is no specific antiviral therapy against ZIKV, and the therapeutic approach to infected pregnant women is limited to the use of antipyretics and analgesics. Anti-inflammatory drugs should be avoided until the diagnosis of dengue is discarded. There is no need to modify the schedule of prenatal visits for pregnant women infected by ZIKV, but it is necessary to guarantee three ultrasound examinations during pregnancy for low-risk pregnancies, and monthly for pregnant women with confirmed ZIKV infection. Vaginal delivery and natural breastfeeding are advised.


2016 ◽  
Vol 22 (12) ◽  
pp. 2228-2230 ◽  
Author(s):  
Emanuele Nicastri ◽  
Concetta Castilletti ◽  
Pietro Balestra ◽  
Simonetta Galgani ◽  
Giuseppe Ippolito

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