Honors & Awards

  • Stanford SIGF Bio-X Interdisciplinary Graduate Fellowship Award, Stanford University (2014-2017)
  • SPARK/Spectrum Innovation Accelerator Seed Grant Award in Therapeutics, Stanford University, SPARK Program (2014-2015)
  • NIAID Merit Award for achievements associated with research on 2009 H1N1 pandemic influenza virus, National Institutes of Allergy & Infectious Diseases (2009)
  • Research Fellowship Training Award, National Institutes of Health (2008-2010)
  • WELCH Chemistry Undergraduate Research Grant, The WELCH Foundation (2005-2006)
  • Honor Society Member, Alpha Sigma Lambda (2005-)

Membership Organizations

  • Microbiology & Immunology Department, M&I graduate student co-president
  • Alpha Sigma Lambda Honor Society, Member
  • Association for Women in Science, Member of mentoring program

Education & Certifications

  • Bachelor of Arts, St Edwards University, Philosophy (2006)
  • Bachelor of Science, St Edwards University, Biochemistry (2006)

Stanford Advisors

Research & Scholarship

Current Research and Scholarly Interests

My primary research focus is in translational molecular virology, with a special interest in uncovering and characterizing RNA structure-function relationships and their role in RNA virus life cycles. Just as many current antibiotics target RNA secondary structures, I envisage a completely new class of antivirals that will similarly target critical RNA secondary structures within viral genomes (such as packaging, translation, or replication signals). To pursue these goals, my research combines molecular virology and genetic tools with emerging high-throughput RNA structure-probing technologies to uncover new classes of conserved viral, non-protein targets for the development of much needed antiviral therapies.

Lab Affiliations


Journal Articles

  • The Natural History of Influenza Infection in the Severely Immunocompromised vs Nonimmunocompromised Hosts. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America Memoli, M. J., Athota, R., Reed, S., Czajkowski, L., Bristol, T., Proudfoot, K., Hagey, R., Voell, J., Fiorentino, C., Ademposi, A., Shoham, S., Taubenberger, J. K. 2014; 58 (2): 214-24


    Introduction. Medical advances have led to an increase in the world's population of immunosuppressed individuals. The most severely immunocompromised patients are those who have been diagnosed with a hematologic malignancy, solid organ tumor, or who have other conditions that require immunosuppressive therapies and/or solid organ or stem cell transplants. Materials and methods. Medically attended patients with a positive clinical diagnosis of influenza were recruited prospectively and clinically evaluated. Nasal washes and serum were collected. Evaluation of viral shedding, nasal and serum cytokines, clinical illness, and clinical outcomes were performed to compare severely immunocompromised individuals to nonimmunocompromised individuals with influenza infection. Results. Immunocompromised patients with influenza had more severe disease/complications, longer viral shedding, and more antiviral resistance while demonstrating less clinical symptoms and signs on clinical assessment. Conclusions. Immunocompromised patients are at risk for more severe or complicated influenza induced disease, which may be difficult to prevent with existing vaccines and antiviral treatments. Specific issues to consider when managing a severely immunocompromised host include the development of asymptomatic shedding, multi-drug resistance during prolonged antiviral therapy, and the potential high risk of pulmonary involvement. Clinical trials registration, identifier NCT00533182.

    View details for DOI 10.1093/cid/cit725

    View details for PubMedID 24186906

  • MultiDrug-Resistant 2009 Pandemic Influenza A(H1N1) Viruses Maintain Fitness and Transmissibility in Ferrets JOURNAL OF INFECTIOUS DISEASES Memoli, M. J., Davis, A. S., Proudfoot, K., Chertow, D. S., Hrabal, R. J., Bristol, T., Taubenberger, J. K. 2011; 203 (3): 348-357


    The 2009 influenza A(H1N1) pandemic called attention to the limited influenza treatment options available, especially in individuals at high risk of severe disease. Neuraminidase inhibitor-resistant seasonal H1N1 viruses have demonstrated the ability to transmit well despite early data indicating that resistance reduces viral fitness. 2009 H1N1 pandemic viruses have sporadically appeared containing resistance to neuraminidase inhibitors and the adamantanes, but the ability of these viruses to replicate, transmit, and cause disease in mammalian hosts has not been fully characterized.Two pretreatment wild-type viruses and 2 posttreatment multidrug-resistant viruses containing the neuraminidase H275Y mutation collected from immunocompromised patients infected with pandemic influenza H1N1 were tested for viral fitness, pathogenicity, and transmissibility in ferrets.The pretreatment wild-type viruses and posttreatment resistant viruses containing the H275Y mutation all demonstrated significant pathogenicity and equivalent viral fitness and transmissibility.The admantane-resistant 2009 pandemic influenza A(H1N1) virus can develop the H275Y change in the neuraminidase gene conferring resistance to both oseltamivir and peramivir without any loss in fitness, transmissibility, or pathogenicity. This suggests that the dissemination of widespread multidrug resistance similar to neuraminidase inhibitor resistance in seasonal H1N1 is a significant threat.

    View details for DOI 10.1093/infdis/jiq067

    View details for Web of Science ID 000286611800012

    View details for PubMedID 21208927

  • Rapid Selection of Oseltamivir- and Peramivir-Resistant Pandemic H1N1 Virus during Therapy in 2 Immunocompromised Hosts CLINICAL INFECTIOUS DISEASES Memoli, M. J., Hrabal, R. J., Hassantoufighi, A., Eichelberger, M. C., Taubenberger, J. K. 2010; 50 (9): 1252-1255


    Pandemic 2009 H1N1 virus isolates containing the neuraminidase inhibitor resistance mutation H275Y have been reported. We describe rapid selection for the H275Y resistance mutation during therapy in 2 immunocompromised individuals at 9 and 14 days of therapy, as well as the first described case of clinically significant resistance to peramivir.

    View details for DOI 10.1086/651605

    View details for Web of Science ID 000276248300008

    View details for PubMedID 20345239

  • Prior infection with classical swine H1N1 influenza viruses is associated with protective immunity to the 2009 pandemic H1N1 virus INFLUENZA AND OTHER RESPIRATORY VIRUSES Kash, J. C., Qi, L., Dugan, V. G., Jagger, B. W., Hrabal, R. J., Memoli, M. J., Morens, D. M., Taubenberger, J. K. 2010; 4 (3): 121-127


    The 2009 H1N1 pandemic emerged even though seasonal H1N1 viruses have circulated for decades. Epidemiological evidence suggested that the current seasonal vaccine did not offer significant protection from the novel pandemic, and that people over the age of 50 were less susceptible to infection.In a mouse challenge study with the 2009 pandemic H1N1 virus, we evaluated protective immune responses elicited by prior infection with human and swine influenza A viruses.Mice infected with A/Mexico/4108/2009 (Mex09) showed significant weight loss and 40% mortality. Prior infection with a 1976 classical swine H1N1 virus resulted in complete protection from Mex09 challenge. Prior infection with either a 2009 or a 1940 seasonal H1N1 influenza virus provided partial protection and a >100-fold reduction in viral lung titers at day 4 post-infection.These findings indicate that in experimental animals recently induced immunity to 1918-derived H1N1 seasonal influenza viruses, and to a 1976 swine influenza virus, afford a degree of protection against the 2009 pandemic virus. Implications of these findings are discussed in the context of accumulating data suggesting partial protection of older persons during the 2009 pandemic.

    View details for DOI 10.1111/j.1750-2659.2010.00132.x

    View details for Web of Science ID 000276356100003

    View details for PubMedID 20409208

  • Rapid Selection of a Transmissible Multidrug-Resistant Influenza A/H3N2 Virus in an Immunocompromised Host JOURNAL OF INFECTIOUS DISEASES Memoli, M. J., Hrabal, R. J., Hassantoufighi, A., Jagger, B. W., Sheng, Z., Eichelberger, M. C., Taubenberger, J. K. 2010; 201 (9): 1397-1403


    The overall impact of influenza virus infection in immunocompromised patients is largely unknown. Antigenic drift and genetic variations during prolonged influenza infection have been demonstrated. In this report we describe a multidrug-resistant H3N2 influenza virus isolated from an immunocompromised patient after 5 days of therapy.Multiple nasal wash samples were collected from an infected patient, and viral isolates were characterized. Sensitivity to antiviral agents was evaluated. Fitness and transmissibility were assessed in ferrets and tissue culture.An in-frame 4-amino acid deletion emerged in the neuraminidase (NA) gene of an H3N2 virus after 5 days of oseltamivir therapy. No other changes in the NA or hemagglutinin genes were noted. Drug sensitivity assays revealed resistance to oseltamivir (>10-fold increase in 50% inhibitory concentration [IC(50)]) and reduction in sensitivity to zanamivir (3-7-fold increase in IC(50) or 50% effective concentration). No change in fitness or transmissibility was observed.An in-frame NA gene deletion was rapidly selected for in an immunocompromised patient, resulting in decreased sensitivity of the isolate to available NA inhibitors without a change in fitness or transmissibility. This finding has implications for our understanding of the emergence of antiviral resistance and treatment of patients with influenza A infection, especially those who are immunocompromised.

    View details for DOI 10.1086/651610

    View details for Web of Science ID 000276248400017

    View details for PubMedID 20350163

  • The PB2-E627K Mutation Attenuates Viruses Containing the 2009 H1N1 Influenza Pandemic Polymerase MBIO Jagger, B. W., Memoli, M. J., Sheng, Z., Qi, L., Hrabal, R. J., Allen, G. L., Dugan, V. G., Wang, R., Digard, P., Kash, J. C., Taubenberger, J. K. 2010; 1 (1)


    The swine-origin H1N1 influenza A virus emerged in early 2009 and caused the first influenza pandemic in 41 years. The virus has spread efficiently to both the Northern and the Southern Hemispheres and has been associated with over 16,000 deaths. Given the virus's recent zoonotic origin, there is concern that the virus could acquire signature mutations associated with the enhanced pathogenicity of previous pandemic viruses or H5N1 viruses with pandemic potential. We tested the hypothesis that mutations in the polymerase PB2 gene at residues 627 and 701 would enhance virulence but found that influenza viruses containing these mutations in the context of the pandemic virus polymerase complex are attenuated in cell culture and mice.

    View details for DOI 10.1128/mBio.00067-10

    View details for Web of Science ID 000284716600010

    View details for PubMedID 20689744

Stanford Medicine Resources: