Valosin‐containing protein ATPase activity regulates the morphogenesis of Zika virus replication organelles and virus‐induced cell death

2021 ◽  
Author(s):  
Anaïs Anton ◽  
Clément Mazeaud ◽  
Wesley Freppel ◽  
Claudia Gilbert ◽  
Nicolas Tremblay ◽  
...  
Keyword(s):  
Cell Death ◽  
Atpase Activity ◽  
Virus Replication ◽  
Zika Virus

The P-MAPA immunomodulator partially prevents apoptosis induced by Zika virus infection in THP-1 cells

2020 ◽  
Vol 21 ◽  
Author(s):  
Morganna C. Lima ◽  
Elisa A. N. Azevedo ◽  
Clarice N. L. de Morais ◽  
Larissa I. O. de Sousa ◽  
Bruno M. Carvalho ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Virus Infection ◽  
Virus Replication ◽  
Zika Virus ◽  
Mammalian Cells ◽  
Caspase 3 ◽  
Neurological Complications ◽  
Zika Virus Infection

Background: Zika virus is an emerging arbovirus of global importance. ZIKV infection is associated with a range of neurological complications such as the Congenital Zika Syndrome and Guillain Barré Syndrome. Despite the magnitude of recent outbreaks, there is no specific therapy to prevent or to alleviate disease pathology. Objective: To investigate the role of P-MAPA immunomodulator in Zika-infected THP-1 cells. Methods: THP-1 cells were subjected at Zika virus infection (Multiplicity of Infection = 0.5) followed by treatment with P-MAPA for until 96 hours post-infection. After that, the cell death was analyzed by annexin+/ PI+ and caspase 3/ 7+ staining by flow cytometry. In addition, the virus replication and cell proliferation were accessed by RT-qPCR and Ki67 staining, respectively. Results: We demonstrate that P-MAPA in vitro treatment significantly reduces Zika virus-induced cell death and caspase-3/7 activation on THP-1 infected cells, albeit it has no role in virus replication and cell proliferation. Conclusions: Our study reveals that P-MAPA seems to be a satisfactory alternative to inhibits the effects of Zika virus infection in mammalian cells.

scholarly journals Combination Therapy with Reovirus and ATM Inhibitor Enhances Cell Death and Virus Replication in Canine Melanoma

2019 ◽  
Vol 15 ◽  
pp. 49-59 ◽  
Author(s):  
Masaya Igase ◽  
Shusaku Shibutani ◽  
Yosuke Kurogouchi ◽  
Noriyuki Fujiki ◽  
Chung Chew Hwang ◽  
...  
Keyword(s):  
Cell Death ◽  
Combination Therapy ◽  
Virus Replication ◽  
Canine Melanoma

scholarly journals Drug-Screening Strategies for Inhibition of Virus-Induced Neuronal Cell Death

Viruses ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2317
Author(s):  
Durbadal Ojha ◽  
Tyson A. Woods ◽  
Karin E. Peterson
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Zika Virus ◽  
Treatment Options ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Virus Production ◽  
Neuronal Stem Cell ◽  
Stem Cell Lines ◽  
Simplex Virus

A number of viruses, including Herpes Simplex Virus (HSV), West Nile Virus (WNV), La Crosse Virus (LACV), Zika virus (ZIKV) and Tick-borne encephalitis virus (TBEV), have the ability to gain access to the central nervous system (CNS) and cause severe neurological disease or death. Although encephalitis cases caused by these viruses are generally rare, there are relatively few treatment options available for patients with viral encephalitis other than palliative care. Many of these viruses directly infect neurons and can cause neuronal death. Thus, there is the need for the identification of useful therapeutic compounds that can inhibit virus replication in neurons or inhibit virus-induced neuronal cell death. In this paper, we describe the methodology to test compounds for their ability to inhibit virus-induced neuronal cell death. These protocols include the isolation and culturing of primary neurons; the culturing of neuroblastoma and neuronal stem cell lines; infection of these cells with viruses; treatment of these cells with selected drugs; measuring virus-induced cell death using MTT or XTT reagents; analysis of virus production from these cells; as well as the basic understanding in mode of action. We further show direct evidence of the effectiveness of these protocols by utilizing them to test the effectiveness of the polyphenol drug, Rottlerin, at inhibiting Zika virus infection and death of neuronal cell lines.

scholarly journals Zika virus has oncolytic activity against glioblastoma stem cells

2017 ◽  
Vol 214 (10) ◽  
pp. 2843-2857 ◽  
Author(s):  
Zhe Zhu ◽  
Matthew J. Gorman ◽  
Lisa D. McKenzie ◽  
Jiani N. Chai ◽  
Christopher G. Hubert ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Death ◽  
Brain Cancer ◽  
Zika Virus ◽  
Oncolytic Virus ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Neural Cells ◽  
Glioblastoma Stem Cells ◽  
Oncolytic Activity

Glioblastoma is a highly lethal brain cancer that frequently recurs in proximity to the original resection cavity. We explored the use of oncolytic virus therapy against glioblastoma with Zika virus (ZIKV), a flavivirus that induces cell death and differentiation of neural precursor cells in the developing fetus. ZIKV preferentially infected and killed glioblastoma stem cells (GSCs) relative to differentiated tumor progeny or normal neuronal cells. The effects against GSCs were not a general property of neurotropic flaviviruses, as West Nile virus indiscriminately killed both tumor and normal neural cells. ZIKV potently depleted patient-derived GSCs grown in culture and in organoids. Moreover, mice with glioblastoma survived substantially longer and at greater rates when the tumor was inoculated with a mouse-adapted strain of ZIKV. Our results suggest that ZIKV is an oncolytic virus that can preferentially target GSCs; thus, genetically modified strains that further optimize safety could have therapeutic efficacy for adult glioblastoma patients.

Antiviral activity of pinocembrin against Zika virus replication

2019 ◽  
Vol 167 ◽  
pp. 13-24 ◽  
Author(s):  
Jia Le Lee ◽  
Marcus Wing Choy Loe ◽  
Regina Ching Hua Lee ◽  
Justin Jang Hann Chu
Keyword(s):  
Antiviral Activity ◽  
Virus Replication ◽  
Zika Virus

scholarly journals Variable Inhibition of Zika Virus Replication by Different Wolbachia Strains in Mosquito Cell Cultures

2017 ◽  
Vol 91 (14) ◽  
Author(s):  
Michaela J. Schultz ◽  
Sharon Isern ◽  
Scott F. Michael ◽  
Ronald B. Corley ◽  
John H. Connor ◽  
...  
Keyword(s):  
Virus Replication ◽  
Zika Virus ◽  
Western Hemisphere ◽  
Mosquito Cell ◽  
Mosquito Vector ◽  
Viral Inhibition ◽  
Virus Growth ◽  
Content Type ◽  
Bacterial Endosymbiont ◽  
Mosquito Cells

ABSTRACT Mosquito-borne arboviruses are a major source of human disease. One strategy to reduce arbovirus disease is to reduce the mosquito's ability to transmit virus. Mosquito infection with the bacterial endosymbiont Wolbachia pipientis wMel is a novel strategy to reduce Aedes mosquito competency for flavivirus infection. However, experiments investigating cyclic environmental temperatures have shown a reduction in maternal transmission of wMel, potentially weakening the integration of this strain into a mosquito population relative to that of other Wolbachia strains. Consequently, it is important to investigate additional Wolbachia strains. All Zika virus (ZIKV) suppression studies are limited to the wMel Wolbachia strain. Here we show ZIKV inhibition by two different Wolbachia strains: wAlbB (isolated from Aedes albopictus mosquitoes) and wStri (isolated from the planthopper Laodelphax striatellus) in mosquito cells. Wolbachia strain wStri inhibited ZIKV most effectively. Single-cycle infection experiments showed that ZIKV RNA replication and nonstructural protein 5 translation were reduced below the limits of detection in wStri-containing cells, demonstrating early inhibition of virus replication. ZIKV replication was rescued when Wolbachia was inhibited with a bacteriostatic antibiotic. We observed a partial rescue of ZIKV growth when Wolbachia-infected cells were supplemented with cholesterol-lipid concentrate, suggesting competition for nutrients as one of the possible mechanisms of Wolbachia inhibition of ZIKV. Our data show that wAlbB and wStri infection causes inhibition of ZIKV, making them attractive candidates for further in vitro mechanistic and in vivo studies and future vector-centered approaches to limit ZIKV infection and spread. IMPORTANCE Zika virus (ZIKV) has swiftly spread throughout most of the Western Hemisphere. This is due in large part to its replication in and spread by a mosquito vector host. There is an urgent need for approaches that limit ZIKV replication in mosquitoes. One exciting approach for this is to use a bacterial endosymbiont called Wolbachia that can populate mosquito cells and inhibit ZIKV replication. Here we show that two different strains of Wolbachia, wAlbB and wStri, are effective at repressing ZIKV in mosquito cell lines. Repression of virus growth is through the inhibition of an early stage of infection and requires actively replicating Wolbachia. Our findings further the understanding of Wolbachia viral inhibition and provide novel tools that can be used in an effort to limit ZIKV replication in the mosquito vector, thereby interrupting the transmission and spread of the virus.

scholarly journals Human Sertoli cells support high levels of Zika virus replication and persistence

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Anil Kumar ◽  
Juan Jovel ◽  
Joaquin Lopez-Orozco ◽  
Daniel Limonta ◽  
Adriana M. Airo ◽  
...  
Keyword(s):  
Virus Replication ◽  
Sertoli Cells ◽  
Zika Virus
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