Anirban Basu

ORCID: 0000-0002-5200-2054
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About
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Research Areas
  • Mosquito-borne diseases and control
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Viral Infections and Vectors
  • interferon and immune responses
  • Immune Response and Inflammation
  • COVID-19 Clinical Research Studies
  • Virology and Viral Diseases
  • MicroRNA in disease regulation
  • Infectious Encephalopathies and Encephalitis
  • HIV Research and Treatment
  • Tryptophan and brain disorders
  • RNA regulation and disease
  • GaN-based semiconductor devices and materials
  • Semiconductor materials and devices
  • Research on Leishmaniasis Studies
  • SARS-CoV-2 and COVID-19 Research
  • Neurogenesis and neuroplasticity mechanisms
  • Software Testing and Debugging Techniques
  • Long-Term Effects of COVID-19
  • Inflammasome and immune disorders
  • Immune Cell Function and Interaction
  • Respiratory viral infections research
  • Neonatal and fetal brain pathology
  • Malaria Research and Control
  • Advanced MEMS and NEMS Technologies

National Brain Research Centre
2016-2025

University of Washington
2019-2025

National Bureau of Economic Research
2024-2025

Post Graduate Institute of Medical Education and Research
2023-2025

Royal Holloway University of London
2020-2022

RMIT University
2021

Cornell University
2020

New York Hospital Queens
2012-2019

National Chemical Laboratory
2019

PES University
2018

Diabetes leads to vascular leakage, glial dysfunction, and neuronal apoptosis within the retina. The goal of studies reported here was determine role that retinal microglial cells play in diabetic retinopathy assess whether minocycline can decrease activation alleviate complications. Immunohistochemical analyses showed microglia are activated early diabetes. Furthermore, mRNAs for interleukin-1β tumor necrosis factor-α, proinflammatory mediators known be released from microglia, also...

10.2337/diabetes.54.5.1559 article EN Diabetes 2005-05-01

Abstract While a number of studies have documented the importance microglia in central nervous system (CNS) response to injury, infection and disease, little is known regarding its role viral encephalitis. We therefore, exploited an experimental model Japanese Encephalitis, better understand played by Encephalitis Virus (JEV) infection. Lectin staining performed assess microglial activation indicated robust increase reactive following A difference topographic distribution activated, resting,...

10.1002/glia.20474 article EN Glia 2007-01-03

Japanese encephalitis (JE) is the leading form of viral in Asia. It caused by JE virus (JEV), which belongs to family Flaviviridae. JEV endemic many parts Asia, where periodic outbreaks take hundreds lives. Despite catastrophes it causes, has remained a tropical disease uncommon West. With rapid globalization and climatic shift, started emerge areas threat was previously unknown. Scientific evidence predicts that will soon become global pathogen cause worldwide pandemics. Although some...

10.1371/journal.pntd.0000437 article EN cc-by PLoS neglected tropical diseases 2009-09-28

Rosmarinic acid (RA) reduced the mortality of mice infected with Japanese encephalitis virus (JEV). Significant decreases in viral loads (P < 0.001) and proinflammatory cytokine levels were observed JEV-infected animals treated RA compared to without treatment, at 8 9 days postinfection.

10.1128/aac.00041-07 article EN Antimicrobial Agents and Chemotherapy 2007-06-19

Abstract Minocycline is broadly protective in neurological disease models featuring inflammation and cell death being evaluated clinical trials. Japanese encephalitis virus (JEV) one of the most important causes viral worldwide. There no specific treatment for (JE) effective antiviral drugs have been discovered. Studies indicate that JE involves profound neuronal loss as well secondary caused because death. a semisynthetic second‐generation tetracycline exerts anti‐inflammatory antiapoptotic...

10.1111/j.1471-4159.2008.05238.x article EN Journal of Neurochemistry 2008-01-18

Background Japanese Encephalitis virus (JEV) is a common cause of acute and epidemic viral encephalitis. JEV infection associated with microglial activation resulting in the production pro-inflammatory cytokines including Interleukin-1 β (IL-1β) Interleukin-18 (IL-18). The Pattern Recognition Receptors (PRRs) underlying mechanism by which microglia identify particle leading to these unknown. Methodology/Principal Findings For our studies, we have used murine model as well BV-2 mouse cell...

10.1371/journal.pone.0032270 article EN cc-by PLoS ONE 2012-02-29

Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, is the leading cause of viral in Southeast Asia with potential to become global pathogen. Here, we identify glucose-regulated protein 78 (GRP78) as an important host for entry and replication. Using plasma membrane fractions from mouse neuronal (Neuro2a) cells, mass spectroscopy analysis identified GRP78 interacting recombinant JEV envelope domain III. was found be expressed on membranes Neuro2a primary neurons, human epithelial...

10.1128/jvi.02274-16 article EN Journal of Virology 2017-01-05

ABSTRACT MicroRNAs (miRNAs) are single-stranded small RNA molecules that regulate various cellular processes. miRNA 155 (miR-155) regulates aspects of innate and adaptive immune responses plays a key role in viral infections the resulting neuroinflammation. The present study evaluated involvement miR-155 modulating Japanese encephalitis virus (JEV)-induced We observed expression was upregulated during JEV infection mouse primary microglia, BV-2 microglia cell line, both human brains. In...

10.1128/jvi.02979-13 article EN Journal of Virology 2014-02-13

Flavivirus-mediated inflammation causes neuronal death, but whether the infected neurons can evoke an innate immune response to elicit their own protection, is unknown. In earlier study we have shown that RIG-I, play a significant role in inducing production and release of molecules are related inflammation. this study, using cell line, show RIG-I acts with STING concerted manner following its interaction Japanese encephalitis viral RNA induce type 1 interferon response. Knock-down showed...

10.1038/srep00347 article EN cc-by-nc-sa Scientific Reports 2012-04-02

Japanese encephalitis virus (JEV) is the causative agent of which more prevalent in South and Southeast Asia. JEV a neurotropic infiltrates into brain through vascular endothelial cells. infects neurons microglial cells causes neuronal damage inflammation. However, also evades cellular immune response to survive host Viruses are known modulate expression microRNAs, turn by targeting antiviral genes. The aim this study understand anti-inflammatory role miR-146a during infection, facilitates...

10.1186/s12974-015-0249-0 article EN cc-by Journal of Neuroinflammation 2015-02-17

IL-1β, also known as "the master regulator of inflammation", is a potent pro-inflammatory cytokine secreted by activated microglia in response to pathogenic invasions or neurodegeneration. It initiates vicious cycle inflammation and orchestrates various molecular mechanisms involved neuroinflammation. The role IL-1β has been extensively studied neurodegenerative disorders; however, underlying induced are still poorly understood. objective our study the comprehensive identification circuitry...

10.1186/s12974-016-0486-x article EN cc-by Journal of Neuroinflammation 2016-02-02

Interleukin-1β (IL-1β) is one of the most important cytokine secreted by activated microglia as it orchestrates vicious cycle inflammation inducing expression various other pro-inflammatory cytokines along with its own production. Microglia-mediated IL-1β production a tightly regulated mechanism which involves activation nucleotide-binding oligomerization domain leucine-rich repeat and pyrin domain-containing 3 (NLRP3) inflammasome pathway. Our previous study suggests critical role heat...

10.1186/s12974-018-1214-5 article EN cc-by Journal of Neuroinflammation 2018-06-09

Interleukin-1 (IL-1) is induced immediately after insults to the brain, and elevated levels of IL-1 have been strongly implicated in neurodegeneration that accompanies stroke, Alzheimer's disease, multiple sclerosis. In animal models, antagonizing has shown reduce cell death; however, basis for this protection not elucidated. Here we analyzed response penetrating brain injury mice lacking type 1 receptor (IL-1R1) determine which cellular molecular mediators tissue damage require signaling....

10.1523/jneurosci.22-14-06071.2002 article EN cc-by-nc-sa Journal of Neuroscience 2002-07-15

OBJECTIVES; To evaluate therapeutic efficacy of arctigenin in an experimental model Japanese encephalitis (JE).Four- to 5-week-old BALB/c mice either sex were infected intravenously with lethal dose 3 x 10(5) pfu virus (JEV). By the 9th day post-infection, all untreated animals succumbed infection. Arctigenin was dissolved DMSO at a concentration 0.5 mg/mL and stored 4 degrees C. After one following inoculation, given intraperitoneally, twice daily (10 mg/kg body weight) for next 7...

10.1093/jac/dkm503 article EN Journal of Antimicrobial Chemotherapy 2008-01-29

Abstract Background Activation of microglia, the resident macrophages central nervous system (CNS), is hallmark neuroinflammation in neurodegenerative diseases and other pathological conditions associated with CNS infection. The activation microglia often bystander neuronal death. Nuclear factor-κB (NF-κB) one important transcription factors known to be microglial which upregulates expression inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (Cox-2) pro-inflammatory cytokines. Recent...

10.1186/1742-2094-7-68 article EN cc-by Journal of Neuroinflammation 2010-10-15

J. Neurochem. (2010) 115 , 537–549. Abstract Japanese encephalitis virus (JEV), the leading cause of acute in South‐East Asia is a neurotropic infecting various CNS cell types. Most Flaviviruses including JEV get internalised into cells by receptor‐mediated endocytosis, which involve clathrin and membrane cholesterol. The cholesterol‐enriched microdomains referred to as lipid rafts act portals for entry number enveloped viruses, Flavivirus. However, precise role played internalisation neural...

10.1111/j.1471-4159.2010.06951.x article EN Journal of Neurochemistry 2010-08-13

Background Neuroinflammation associated with Japanese encephalitis (JE) is mainly due to the activation of glial cells subsequent release proinflammatory mediators from them. The recognition viral RNA, in part, by pattern receptor retinoic acid-inducible gene I (RIG-I) has been indicated have a role such processes. Even though neurons are also known express this receptor, its after JE virus (JEV) infections yet be elucidated. Methodology/Principal Findings Upon infecting murine neuroblastoma...

10.1371/journal.pone.0021761 article EN cc-by PLoS ONE 2011-06-30

Japanese encephalitis virus (JEV), a single-stranded RNA (ssRNA) virus, is the leading cause of in Asia. Microglial activation one key events JEV-induced neuroinflammation. Although various microRNAs (miRNAs) has been shown to regulate microglia during pathological conditions including neuroviral infections, till date, involvement miRNAs JEV infection not evaluated. Hence, we sought evaluate possible role mediating activation. Initial screening revealed significant up-regulation miR-29b...

10.1111/jnc.12609 article EN Journal of Neurochemistry 2013-11-16
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