Dr. Sudeb Dalai, MD PhD is an Infectious Disease Physician at Stanford University School of Medicine and the Palo Alto Medical Foundation. Currently a Clinical Assistant Professor (Teaching) at Stanford, he has taught courses and conducted research in academia/industry for over 18 years.
Dr. Dalai completed his undergraduate degree at MIT, MD and MS at Stanford, PhD in Epidemiology at UC Berkeley School of Public Health, Internal Medicine Residency at UCSD, and Fellowship in Infectious Diseases at Stanford. He has received numerous teaching and leadership awards and research grants and has co-authored multiple peer-reviewed publications. His work has been supported by the Infectious Diseases Society of America, the Howard Hughes Medical Institute, the Paul and Daisy Soros Foundation, and the National Institutes of Health. Dr. Dalai is an internationally-invited speaker and has been featured in multiple media outlets including ABC, NBC, Good Morning America, US News & World Report, Buzzfeed, and The Huffington Post. In 2003 he was elected to the MIT Board of Trustees and in 2020 he was voted as a Board Member of the MIT Club of Northern California.
- Infectious Disease
- HIV Medicine
- Internal Medicine
Honors & Awards
Gores Teaching Award, Stanford University (2009)
Clinical and Translational Science Award (CTSA) Seed Grant, Stanford Office of Community Health (2010-2012)
Peninsula AIDS Research Consortium (PARC) Research Grant, PARC (2009)
Paul and Daisy Soros Fellowship for New Americans, The Paul and Daisy Soros Foundation (2008-2010)
Infectious Disease Society of America (IDSA) Research Fellowship, IDSA (2005)
California HIV Research Program (CHRP) Dissertation Grant, CHRP (2010-2012)
Howard Hughes Medical Institute (HHMI) Research Fellowship, HHMI (2006-2008)
Medical Education: Stanford University School of Medicine (2013) CA
Board Certification: American Board of Internal Medicine, Infectious Disease (2019)
Fellowship: Stanford University Infectious Disease Fellowships (2018) CA
Residency: UCSD Internal Medicine Residency (2015) CA
Board Certification, American Board of Internal Medicine (2017)
Fellowship, Stanford University, Infectious Disease (2018)
Residency, University of California, San Diego, Internal Medicine (2015)
Internship, University of California, San Diego, Internal Medicine (2014)
PhD, University of California, Berkeley School of Public Health, Epidemiology (2013)
MD, Stanford University School of Medicine (2013)
MS, Stanford University School of Medicine, Epidemiology (2010)
BS, Massachusetts Institute of Technology, Brain and Cognitive Sciences (2002)
Liquid biopsy for invasive mold infections in hematopoietic cell transplant recipients with pneumonia through next-generation sequencing of microbial cell-free DNA in plasma.
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
BACKGROUND: Non-invasive diagnostic options are limited for invasive mold infections (IMI). We evaluated the performance of a plasma microbial cell-free DNA sequencing (mcfDNA-Seq) test for diagnosing pulmonary IMI after hematopoietic cell transplant (HCT).METHODS: We retrospectively assessed the diagnostic performance of plasma mcfDNA-Seq NGS in 114 HCT recipients with pneumonia after HCT who had stored plasma obtained within 14 days of diagnosis of Proven/Probable Aspergillus IMI (n=51), Proven/Probable non-Aspergillus IMI (n=24), Possible IMI (n=20), and non-IMI controls (n=19). Sequences were aligned to a database including >400 fungi. Organisms above a fixed significance threshold were reported.RESULTS: Among 75 patients with Proven/Probable pulmonary IMI, mcfDNA-Seq detected ≥1 pathogenic mold in 38 patients (sensitivity, 51%; 95% CI, 39%-62%). When restricted to samples obtained within 3 days of diagnosis, sensitivity increased to 61%. McfDNA-Seq had higher sensitivity for Proven/Probable non-Aspergillus IMI (sensitivity, 79%; 95% CI, 56%-93%) compared to Aspergillus IMI (sensitivity, 31%; 95% CI, 19%-46%). McfDNA-Seq also identified non-Aspergillus molds in an additional 7 patients in the Aspergillus subgroup and Aspergillus in 1 patient with Possible IMI. Among 19 non-IMI pneumonia controls, mcfDNA-Seq was negative in all samples suggesting a high specificity (95% CI, 82%-100%) and up to 100% positive predictive value (PPV) with estimated negative predictive values (NPV) of 81%-99%. The mcfDNA-seq assay was complementary to serum GMI testing; in combination, they were positive in 84% of individuals with Proven/Probable pulmonary IMI.CONCLUSIONS: Non-invasive mcfDNA-Seq had moderate sensitivity and high specificity, NPV, and PPV for pulmonary IMI after HCT, particularly for non-Aspergillus.
View details for DOI 10.1093/cid/ciaa1639
View details for PubMedID 33119063
Next-generation sequencing of microbial cell-free DNA for rapid noninvasive diagnosis of infectious diseases in immunocompromised hosts.
2019; 8: 1194
Background: Cell-free DNA (cfDNA) sequencing has emerged as an effective laboratory method for rapid and noninvasive diagnosis in prenatal screening testing, organ transplant rejection screening, and oncology liquid biopsies but clinical experience for use of this technology in diagnostic evaluation of infections in immunocompromised hosts is limited. Methods: We conducted an exploratory study using next-generation sequencing (NGS) for detection of microbial cfDNA in a cohort of ten immunocompromised patients with febrile neutropenia, pneumonia or intra-abdominal infection. Results: Pathogen identification by cfDNA NGS demonstrated positive agreement with conventional diagnostic laboratory methods in 7 (70%) cases, including patients with proven/probable invasive aspergillosis, Pneumocystis jirovecii pneumonia, Stenotrophomonas maltophilia bacteremia, Cytomegalovirus and Adenovirus viremia. NGS results were discordant in 3 (30%) cases including two patients with culture negative sepsis who had undergone hematopoietic stem cell transplant in whom cfDNA testing identified the potential etiological agent of sepsis; and one kidney transplant recipient with invasive aspergillosis who had received >6 months of antifungal therapy prior to NGS testing. Conclusion: These observations support the clinical utility of measurement of microbial cfDNA sequencing from peripheral blood for rapid noninvasive diagnosis of infections in immunocompromised hosts. Larger studies are needed.
View details for DOI 10.12688/f1000research.19766.4
View details for PubMedID 31814964
View details for PubMedCentralID PMC6883395
Diagnosis and Genotyping of Coxiella burnetii Endocarditis in a Patient with Prosthetic Pulmonary Valve Replacement Using Next-Generation Sequencing of Plasma Microbial Cell-Free DNA.
Open forum infectious diseases
2019; 6 (6): ofz242
Determining the causative etiology of culture-negative endocarditis can be challenging. We performed next-generation sequencing of plasma microbial cell-free DNA to facilitate rapid diagnosis and genotyping of Coxiella burnetii in a patient with culture-negative endocarditis of a prosthetic pulmonary valve, enabling early targeted treatment prior to valve replacement surgery.
View details for DOI 10.1093/ofid/ofz242
View details for PubMedID 31249846
View details for PubMedCentralID PMC6580995
Combining Phylogenetic and Network Approaches to Identify HIV-1 Transmission Links in San Mateo County, California.
Frontiers in microbiology
2018; 9: 2799
The HIV epidemic in San Mateo County is sustained by multiple overlapping risk groups and is an important hub for HIV transmission in northern California. Limited access to care has led historically to delayed clinical presentation, higher rates of opportunistic infections, and an increased prevalence of antiretroviral drug resistance. The virologic and clinical consequences of treatment within these multiple ethnic and behavioral groups are poorly understood, highlighting the need for efficient surveillance strategies that are able to elucidate transmission networks and drug resistance patterns. We obtained sequence data from a group of 316 HIV-positive individuals in the San Mateo AIDS Program over a 14-year period and integrated epidemiologic, phylogenetic, and network approaches to characterize transmission clusters, risk factors and drug resistance. Drug resistance mutations were identified using the Stanford HIV Drug Resistance Database. A maximum likelihood tree was inferred in RAxML and subjected to clustering analysis in Cluster Picker. Network analysis using pairwise genetic distances was performed in HIV-TRACE. Participants were primarily male (60%), white Hispanics and non-Hispanics (32%) and African American (20.6%). The most frequent behavior risk factor was male-male sex (33.5%), followed by heterosexual (23.4%) and injection drug use (9.5%). Nearly all sequences were subtype B (96%) with subtypes A, C, and CRF01_AE also observed. Sequences from 65% of participants had at least one drug resistance mutation. Clustered transmissions included a higher number of women when compared to non-clustered individuals and were more likely to include heterosexual or people who inject drugs (PWID). Detailed analysis of the largest network (N = 47) suggested that PWID played a central role in overall transmission of HIV-1 as well as bridging men who have sex with men (MSM) transmission with heterosexual/PWID among primarily African American men. Combined phylogenetic and network analysis of HIV sequence data identified several overlapping risk factors in the epidemic, including MSM, heterosexual and PWID transmission with a disproportionate impact on African Americans and a high prevalence of drug resistance.
View details for PubMedID 30574123
Placental Malaria and Mother-to-Child Transmission of Human Immunodeficiency Virus-1 in Rural Rwanda
AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
2011; 85 (2): 202-206
We conducted a nested case-control study of placental malaria (PM) and mother-to-child transmission (MTCT) of human immunodeficiency virus-1 (HIV-1) within a prospective cohort of 627 mother-infant pairs followed from October 1989 until April 1994 in rural Rwanda. Sixty stored placentas were examined for PM and other placental pathology, comparing 20 HIV-infected mother-infant (perinatal transmitter) pairs, 20 HIV-uninfected pairs, and 20 HIV-infected mothers who did not transmit to their infant perinatally. Of 60 placentas examined, 45% showed evidence of PM. Placental malaria was associated with increased risk of MTCT of HIV-1 (adjusted odds ratio [aOR] = 6.3; 95% confidence interval [CI] = 1.4-29.1), especially among primigravidae (aOR = 12.0; 95% CI = 1.0-150; P < 0.05). Before antiretroviral therapy or prophylaxis, PM was associated with early infant HIV infection among rural Rwandan women living in a hyper-endemic malaria region. Primigravidae, among whom malaria tends to be most severe, may be at higher risk.
View details for DOI 10.4269/ajtmh.2011.10-0589
View details for Web of Science ID 000293613000004
View details for PubMedID 21813835
View details for PubMedCentralID PMC3144813
Viral Sequence Analysis from HIV-Infected Mothers and Infants: Molecular Evolution, Diversity, and Risk Factors for Mother-To-Child Transmission
CLINICS IN PERINATOLOGY
2010; 37 (4): 739-?
Great progress has been made in understanding the pathogenesis, treatment, and transmission of HIV and the factors influencing the risk of mother-to-child transmission (MTCT). Many questions regarding the molecular evolution and genetic diversity of HIV in the context of MTCT remain unanswered. Further research to identify the selective factors governing which variants are transmitted, how the compartmentalization of HIV in different cells and tissues contributes to transmission, and the influence of host immunity, viral diversity, and recombination on MTCT may provide insight into new prevention strategies and the development of an effective HIV vaccine.
View details for DOI 10.1016/j.clp.2010.08.003
View details for Web of Science ID 000285485400005
View details for PubMedID 21078447
View details for PubMedCentralID PMC3175486
Environmental Enrichment Reduces Neuronal Intranuclear Inclusion Load But Has No Effect on Messenger RNA Expression in a Mouse Model of Huntington Disease
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
2010; 69 (8): 817-827
Huntington disease (HD) is a fatal neurodegenerative disease with no effective treatment. In the R6/1 mouse model of HD, environmental enrichment delays the neurologic phenotype onset and prevents cerebral volume loss by unknown molecular mechanisms. We examined the effects of environmental enrichment on well-characterized neuropathological parameters in a mouse model of HD. We found a trend toward preservation of downregulated neurotransmitter receptors in striatum of environmentally enriched mice and assessed possible enrichment-related modifications in gene expression using microarrays. We observed similar gene expression changes in R6/1 and R6/2 transgenic mice but found no specific changes in enrichment-related microarray expression profiles in either transgenic or wild-type mice. Furthermore, specific corrections in transprotein-induced transcriptional dysregulation in R6/1 mice were not detected by microarray profiling. However, gene-specific analyses suggested that long-term environmental enrichment may beneficially modulate gene expression dysregulation. Finally, environmental enrichment significantly decreased neuronal intranuclear inclusion load, despite unaffected transgene expression levels. Thus, the therapeutic effects of environmental enrichment likely contribute to decreasing aggregated polyglutamine protein levels without exerting strong effects on gene expression.
View details for DOI 10.1097/NEN.0b013e3181ea167f
View details for Web of Science ID 000280478800005
View details for PubMedID 20613636
- HIV-1 evolution and drug resistance among patients receiving antiretroviral therapy in San Mateo County, California, 1997-2006 Retrovirology 2010; 7 (Suppl 1): 20
Detection of HIV-1 in Saliva: Implications for Case-Identification, Clinical Monitoring and Surveillance for Drug Resistance.
The open virology journal
2010; 4: 88-93
Saliva tests that detect antibodies are used to diagnose HIV infection. The goal of this study was to determine whether saliva could be used for nucleic acid-based tests to measure HIV-1 virus load (VL) and detect drug resistance.69 HIV infected individuals provided 5-10 ml of saliva and blood samples. Viral RNA was isolated from saliva and dried blood spots using the Nuclisens extraction. Saliva VL was measured using a modified Amplicor assay, and genotyping was performed using an in-house RT-PCR/sequencing protocol. Plasma VLs were obtained from concurrently drawn clinical tests.Thirty-six of 47 (77%) plasma viremic patients had measurable saliva HIV-1 RNA. Paired plasma and saliva HIV RNA levels were significantly correlated (Spearman's correlation = .6532, p<.0001), but saliva VL was typically lower. Three of 22 patients with undetectable plasma VL (<50 copies/ml) had detectable saliva HIV RNA. Eleven of 30 patients with undetectable saliva RNA had detectable plasma HIV-1 RNA. Comparison of the protease and reverse transcriptase gene sequences from paired saliva and plasma of 20 patients showed less than 1% difference overall, and few resistance-related amino acid differencesMost patients with plasma virus >50 copies/mL had detectable saliva HIV RNA, and the genotypic data was highly concordant between saliva and plasma. In patients with high levels of plasma HIV RNA, saliva might be useful in identifying viremia and evaluating drug resistance.
View details for DOI 10.2174/1874357901004010088
View details for PubMedID 21673840
View details for PubMedCentralID PMC3111737
Evolution and molecular epidemiology of subtype C HIV-1 in Zimbabwe
2009; 23 (18): 2523-2532
To investigate the origins and evolutionary history of subtype C HIV-1 in Zimbabwe in a context of regional conflict and migration.HIV-1C pol sequence datasets were generated from four sequential cohorts of antenatal women in Harare, Zimbabwe sampled over 15 years (1991-2006).One hundred and seventy-seven HIV-1C pol sequences were obtained from four successive cohorts in Zimbabwe. Maximum-likelihood methods were used to explore phylogenetic relationships between Zimbabwean HIV-1C sequences and subtype C strains from other regions. A Bayesian coalescent-based framework was used to estimate evolutionary parameters for HIV-1C in Zimbabwe, including origin and demographic growth patterns.Zimbabwe HIV-1C pol demonstrated increasing sequence divergence over the 15-year period. Nearly all Zimbabwe sequences clustered phylogenetically with subtype C strains from neighboring countries. Bayesian evolutionary analysis indicated a most recent common ancestor date of 1973 with three epidemic growth phases: an initial, slow phase (1970s) followed by exponential growth (1980s), and a linearly expanding epidemic to the present. Bayesian trees provided evidence for multiple HIV-1C introductions into Zimbabwe during 1979-1981, corresponding with Zimbabwean national independence following a period of socio-political instability.The Zimbabwean HIV-1C epidemic likely originated from multiple introductions in the late 1970s and grew exponentially during the 1980s, corresponding to changing political boundaries and rapid population influx from neighboring countries. The timing and phylogenetic clustering of the Zimbabwean sequences is consistent with an origin in southern Africa and subsequent expansion. HIV-1 sequence data contain important epidemiological information, which can help focus treatment and prevention strategies in light of more recent political volatility in Zimbabwe.
View details for DOI 10.1097/QAD.0b013e3283320ef3
View details for Web of Science ID 000272135800017
View details for PubMedID 19770693
View details for PubMedCentralID PMC2923658