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Anirban Basu

Anirban Basu

· Stergachis Family Endowed Director & Professor of Health EconomicsVerified

University of Washington · Pharmacy

Active 1964–2026

h-index54
Citations9.1k
Papers26041 last 5y
Funding
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About

Anirban Basu, PhD, MS, is a health economist and statistician who specializes in research on comparative and cost-effectiveness analyses, causal inference methods, program evaluation, and outcomes research. He directs The Comparative Health Outcomes, Policy, and Economics (CHOICE) Institute at the University of Washington, Seattle, with appointments in the departments of Pharmacy, Health Services, and Economics. He is a Faculty Research Fellow at the National Bureau of Economic Research and a Fellow of the American Statistical Association. His research focuses on heterogeneity in clinical and economic outcomes, micro behavior with respect to heterogeneous information, and the value of individualized care. He teaches topics in health economics, decision analysis, cost-effectiveness analysis, and health services research methods. Basu received his PhD in Public Policy with a specialization in Health Economics from The University of Chicago and an MS in Biostatistics from the University of North Carolina at Chapel Hill.

Research topics

  • Biology
  • Neuroscience
  • Immunology
  • Biochemistry
  • Medicine
  • Computational biology
  • Genetics
  • Pathology
  • Microbiology
  • Bioinformatics
  • Virology

Selected publications

  • From sensing to shaping: microglial responses in the pathogenesis of viral encephalitis

    Current Opinion in Immunology · 2026-04-27

    articleSenior authorCorresponding
  • Do for-profit hospitals cream-skim patients? Evidence from inpatient psychiatric care in California

    Journal of Health Economics · 2025-06-21 · 1 citations

    article
  • Kawasaki Disease Can Come Calling as Aphon(e)ia: Laryngeal Weakness as the Presentation of Myositis in Kawasaki Disease

    International Journal of Rheumatic Diseases · 2025-01-01

    letter

    Myositis is an under-recognized atypical manifestation of Kawasaki disease (KD) with ill-defined treatment guidelines. We write to highlight a case where potentially life-threatening laryngeal weakness was the presentation of myositis in KD. An 18-month-old boy presented with acute fever, redness of oral mucosa, tongue, dorsal swelling of the hands, and diffuse rash. Investigations showed anemia (hemoglobin 79 g/L), thrombocytopenia (34 × 109/L), hyponatremia (129 mmol/L), hypoalbuminemia (29 g/L), and elevated CRP 36 mg/L. Echocardiography showed normal coronaries. With the diagnosis of complete KD, he was treated with intravenous immunoglobulin (IVIg) (2 g/kg) and aspirin on day 9 of illness [1]. He had prompt fever defervescence and periungual desquamation started on day 10 (Figure 1). However, on day 12, he developed difficulty in getting up, progressive aphonia with cough during deglutition. He had reduced power of both proximal lower limbs (grade 2/5) with normal deep tendon reflexes and cranial nerve examination. A vocal cord ultrasonogram (USG) showed equal bilateral cord movement, ruling out recurrent laryngeal nerve palsy [2, 3] (Figure 1). Creatine kinase (CK) level was significantly increased (4155 U/L). With complete aphonia and difficult deglutition, a normal gag reflex, equal vocal cord movement demonstrated in USG, and highly elevated CK levels, a possibility of myositis in KD was considered with laryngeal and proximal limb muscle involvement. Due to impending respiratory failure, he was started on nasogastric tube feeds and given second dose of IVIg. As the symptoms persisted, he was given intravenous methylprednisolone followed by oral steroids tapered and stopped over 6 weeks. Limb weakness and aphonia significantly improved in a few days, with normalization of voice intensity and muscle power at 4-week follow-up (Figure 2). Myositis in KD was first reported in 1980 [4]. Although the exact etiology remains an enigma, published literature suggests that immune-complex deposits in KD may induce weakness [5]. The onset of muscle weakness followed the diagnosis of KD in 78% of the reported cases, as seen in the index patient [4-8]. Previous studies show that the median time between the symptom onset and the development of myositis was 9 days (range: 36 h to 35 days) [5]. Literature also suggests that muscle enzyme levels are directly proportional to the degree of weakness [6]. To the best of our knowledge, this is only the second case to be reported so far with laryngeal weakness causing potential respiratory failure [6]. This case report underscores that, even with prompt diagnosis and treatment, children with KD remain at risk of developing myositis. They need careful clinical monitoring through the subacute phase to look for evidence of myositis. The subset of patients with substantially higher CK values are more susceptible to respiratory failure as severity is directly proportional to the enzyme levels. It also highlights that myositis may require adjuvant therapy like corticosteroids to avoid potentially life-threatening complications. C.V.G., A.B. writing – original draft, figures, writing – review and editing. C.V.G., P.B., R.A. literature search, editing of the manuscript. R.K.P. conceptualisation, overall supervision, critical editing of the manuscript at each step and final approval. The authors declare no conflicts of interest. All the data underlying this article are available in the manuscript.

  • Climate change and neurotropic vector-borne viruses: addressing emerging threats through a One Health approach

    mBio · 2025-09-22 · 1 citations

    reviewOpen accessSenior author

    Vector-borne diseases are mainly transmitted through the bites of infected arthropods. They are a major public health concern as they account for more than 700,000 deaths annually. Among many vector-borne pathogens, the neurotropic viruses have been contributing to the increased number of deaths across the globe due to severe neurological complications. Despite the advancement of vector control strategies, the prevalence and severity of neurotropic viral infections have not been alleviated till date. Anthropogenic activities cause persistent fluctuations in temperature and weather trends. This plays a major part in shaping the fate of transmission dynamics and pathogenesis of such diseases. Changes in climatic factors, such as global warming and delayed withdrawal of monsoon, have had huge impacts on stretching the window of disease transmission worldwide. The abundance, survival, feeding activity, and vectorial competence of the arthropods are expected to increase with rising temperatures. This review aims to discuss how climate change affects ecosystems, thereby influencing vectors and the associated neurotropic viruses. It also highlights the urgent need for the "One Health" strategy. It is a concept that recognizes that humans and animals do not exist in isolation and are part of a larger ecosystem where their activity and health are interconnected to one another. This holistic approach is essential in addressing the emerging threats posed by climate change, rising rates of infection, and epidemics across the globe.

  • FROM DORMANT TO DANGEROUS: TUBERCULOSIS REACTIVATION WITH ADALIMUMAB USE

    CHEST Journal · 2025-10-01

    articleOpen accessSenior author
  • Home‐Based Care Outcomes: Does the Care Provider Matter?

    Health Economics · 2025-04-28 · 2 citations

    articleOpen access

    Long-term services in the home are predominately provided by family or friends, with a growing proportion of individuals receiving formal care, or paid care by a professional, or a combination of both. However, the relative benefits to the care recipient of who provides the care are largely unknown. A person's use of formal and family care is affected by factors that also may affect their outcomes, complicating the estimation of any causal relationship. Using the 2002-2018 Health and Retirement Study (HRS), we examine three types of home-based care combinations: family only, formal only, and both formal and family care. We use an instrumental variables strategy, using family structure as instruments for both formal care and the combination of formal and family care, to estimate the plausibly causal impact of the care provider on self-reported mental and physical health outcomes. We find that, once the endogeneity of the care provider is accounted for, having both formal and family care leads to better self-rated health, mobility and lower depression compared to people receiving family care only. Receiving formal care only does not affect care recipient outcomes compared to receiving family care only. These results are robust to several sensitivity analyses, including different instrument specifications, subsamples of care recipients that do not have a spouse/partner, among women care recipients, and changing the timing of the measurement of the outcomes. These findings are important to consider as we strive to best meet the growing demand for person-centered, high-quality long-term care in the least restrictive setting possible.

  • LncRNA <i>JINR1</i> regulates <i>miR-216b-5p/</i> GRP78 and <i>miR-1-3p/</i> DDX5 axis to promote JEV infection and cell death

    Journal of Virology · 2025-04-24 · 6 citations

    articleOpen access

    ABSTRACT Japanese encephalitis virus (JEV) infection in the central nervous system (CNS) leads to neuroinflammation and neuronal cell death. Several long non-coding RNAs (lncRNAs) are differentially expressed during viral infection and regulate multiple aspects of viral pathogenesis. Previously, we have shown that JEV/West Nile virus (WNV) infection promotes JEV-induced non-coding RNA 1 ( JINR1 ) expression in SH-SY5Y cells, and it interacts with RNA-binding motif protein 10 (RBM10) to enhance cell death and viral replication. In this study, we show that JEV or WNV infection of the SH-SY5Y cells inhibits the expression of microRNAs (miRNAs) miR-216b-5p and miR-1-3p . These miRNAs bind to the JEV/WNV genome, and their overexpression during JEV/WNV infection reduces viral replication and cell death. Depleting JINR1 or RBM10 during viral infection prevents the downregulation of miR-216b-5p and miR-1-3p . In addition, JINR1 or RBM10 knockdown during JEV/WNV infection enhances the binding of RNA Pol II and H3K4me3 at the promoters of miR-216b-5p and miR-1-3p. JINR1 or RBM10 depletion also prevents the binding of H3K27me3 at the promoters of these miRNAs, suggesting that JINR1 and RBM10 are involved in their transcription repression. Interestingly , JINR1 also acts as a competing endogenous RNA (ceRNA) that directly binds to miR-216b-5p and miR-1-3p, resulting in the upregulation of their targets glucose-regulated protein 78 (GRP78) and DEAD-Box Helicase 5 (DDX5), respectively, which are involved in regulating viral replication. Our findings suggest that JINR1 uses multiple mechanisms to promote JEV and WNV infection in neuronal cells. IMPORTANCE Infection of the central nervous system (CNS) by Japanese encephalitis virus (JEV) or West Nile virus (WNV) leads to neuroinflammation and neuronal cell death. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) regulate viral infection by regulating the expression of host genes. However, knowledge about the interplay between lncRNAs and miRNAs during JEN/WNV infection is limited. We show that JEV/WNV infection inhibits the expression of anti-viral host miRNAs miR-216b-5p and miR-1-3p . These miRNAs inhibit the JEV and WNV replication by directly binding with their genome. JINR1 and its interacting protein, RBM10, inhibit the transcription of miR-216b-5p and miR-1-3p . Interestingly, JINR1 also binds and sequesters miR-216b-5p and miR-1-3p , resulting in upregulation of their targets GRP78 and DDX5, respectively, which promote viral infection. Our findings suggest that lncRNA JINR1 is a potential target for developing anti-virals against JEV/WNV infection.

  • PARP-16 regulates the PERK and IRE-1α Mediated Unfolded Protein Response in Japanese Encephalitis Virus–Infected Neural Stem/Progenitor Cells

    Molecular Neurobiology · 2025-02-20 · 1 citations

    articleSenior author
  • Low-density Lipoprotein Receptor is an important host factor in flaviviral entry and replication in neurons

    Biochemical and Biophysical Research Communications · 2024-12-10 · 7 citations

    articleSenior authorCorresponding
  • Correction: Bispidine-Amino Acid Conjugates Act as a Novel Scaffold for the Design of Antivirals That Block Japanese Encephalitis Virus Replication

    PLoS neglected tropical diseases · 2024-01-25

    erratumOpen access

    [This corrects the article DOI: 10.1371/journal.pntd.0002005.].

Frequent coauthors

  • Sourish Ghosh

    89 shared
  • Surajit Chakraborty

    Indian Institute of Social Welfare and Business Management

    49 shared
  • Steven W. Levison

    37 shared
  • Kallol Dutta

    31 shared
  • J. Kyle Krady

    Pennsylvania State University

    29 shared
  • Sriparna Mukherjee

    24 shared
  • Deepak Kaushik

    Maharshi Dayanand University

    23 shared
  • Kanhaiya Lal Kumawat

    National Brain Research Centre

    23 shared

Labs

Education

  • Ph.D., Public Policy (Health Economics)

    University of Chicago

    2004
  • M.S., Biostatistics

    UNC-Chapel Hill

    1999
  • M.S., Industrial Pharmacy

    University of Toledo

    1997
  • B.S., Pharmaceutical Technology

    Jadavpur University India

Awards & honors

  • Fellow of the American Statistical Association
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