Clinical Focus

  • Fellow

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)

Professional Education

  • Doctor of Medicine, Stanford University, MED-MD (2013)
  • Master of Science, Stanford University, EPIDM-MS (2009)
  • Bachelor of Science, Massachusetts Institute of Technology, Brain and Cognitive Sciences (2002)
  • Doctor of Philosophy, UC-Berkeley School of Public Health, Epidemiology (2013)

Stanford Advisors

Research & Scholarship

Research Projects

  • Phylogeographic Surveillance of California HIV Transmission Networks (Dissertation)

    Start Date



    Stanford, CA


    Stanford University; UC Berkeley School of Public Health; San Mateo Medical Center; Santa Clara Valley Medical Center; UCSF AIDS Research Institute

  • Virologic and clinical impact of single-dose nevirapine on nevirapine-containing HAART among HIV-positive women in rural Zimbabwe. (Scholarly Concentration Project)

    Start Date



    Stanford, CA; Harare, Zimbabwe


    Stanford University; University of Zimbabwe Medical School; Zimbabwe AIDS Prevention Programme

  • Diversity, Evolution, and Pathogenesis of HIV-1 Subtype C in southern Africa (Dissertation)

    Start Date



    Stanford, CA


    Stanford University; UC Berkeley School of Public Health


All Publications

  • Placental Malaria and Mother-to-Child Transmission of Human Immunodeficiency Virus-1 in Rural Rwanda AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE Bulterys, P. L., Chao, A., Dalai, S. C., Zink, M. C., Dushimimana, A., Katzenstein, D., Saah, A. J., Bulterys, M. 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

  • Viral Sequence Analysis from HIV-Infected Mothers and Infants: Molecular Evolution, Diversity, and Risk Factors for Mother-To-Child Transmission CLINICS IN PERINATOLOGY Bulterys, P. L., Dalai, S. C., Katzenstein, D. A. 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

  • 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 Benn, C. L., Luthi-Carter, R., Kuhn, A., Sadri-Vakili, G., Blankson, K. L., Dalai, S. C., Goldstein, D. R., Spires, T. L., Pritchard, J., Olson, J. M., van Dellen, A., Hannan, A. J., Cha, J. J. 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 Dalai SC, Dyal J, Salari K, Kassaye S, Levy V, Israelski D, Katzenstein D 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 Balamane, M., Winters, M. A., Dalai, S. C., Freeman, A. H., Traves, M. W., Israelski, D. M., Katzenstein, D. A., Klausner, J. D. 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

  • Evolution and molecular epidemiology of subtype C HIV-1 in Zimbabwe AIDS Dalai, S. C., de Oliveira, T., Harkins, G. W., Kassaye, S. G., Lint, J., Manasa, J., Johnston, E., Katzenstein, D. 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

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