About

Erle S. Robertson, Ph.D., is the Harry P. Schenck Professor in Otorhinolaryngology at the University of Pennsylvania's Perelman School of Medicine. He is also the Program Leader of the Tumor Virology Training Program within the Department of Microbiology. His research focuses on mechanisms of oncogenesis by gammaherpesviruses, particularly Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), which are associated with various human malignancies including lymphomas, nasopharyngeal carcinoma, and Kaposi's sarcoma. Dr. Robertson investigates how these viruses induce cell-mediated growth transformation using genetics, genomics, and biochemical approaches to elucidate unknown pathways involved in cellular transformation and cancer development. His work includes studying viral gene functions, such as EBNA3C in EBV, and understanding how KSHV persists and contributes to oncogenesis. He has contributed to identifying cellular targets involved in cell division, metastasis, apoptosis, and other processes relevant to human cancers.

Research topics

• Biology
• Virology
• Cell biology
• Cancer research
• Molecular biology

Selected publications

• Lactate-induced miR-7-5p/TRIM33 reprograms metabolic flux to suppress tumor growth and viral reactivation

  Molecular Therapy · 2026-02-01

  article
  PublisherDOI

• HPV profiles in Botswana: An analysis of healthy women, cervical intraepithelial neoplasia, and invasive cervical cancer

  Gynecologic Oncology Reports · 2025-10-18

  articleOpen accessSenior author

  • Widespread HIV and HPV in Sub-Saharan Africa contributes to the growing burden of cervical cancer. • Compared to healthy students, women with CIN or invasive cervical cancer have a higher prevalence of high-risk (HR) HPV. • Compared to women with CIN, women with invasive cervical cancer have higher prevalence of HR HPV. • Cellular HPV viral burden remains unchanged between healthy students, women with CIN, and women with cervical cancer. • Regardless of viral burden, further acquisition of HR HPV in those with CIN is important in progression to cervical cancer. High prevalence of HPV and HIV contribute to the high rate of cervical cancer (CaCx) in Botswana. HPV subtypes in healthy, unvaccinated students (Cohort 1), women with CIN II/III (Cohort 2), and women with invasive CaCx (Cohort 3) were compared. The Ipabalele study in Gaborone, Botswana enrolled patients between 2016–2020. Demographics, clinical characteristics, and HPV cervical swabs were collected. PathoChip quantified prevalence of HPV subtypes. Overall 414 patients enrolled. Cohort 1: 43; Cohort 2; 212; Cohort 3: 159. Median age was 19, 39, and 46 years. Women living with HIV (WLWH) accounted for 0 %, 76 %, and 72 %. High-risk (HR) HPV prevalence in Cohort 1 increased 34 % to 57 % over 20 months. HPV profiles did not differ by HIV status. The prevalence of all HR HPV subtypes in Cohorts 2 and 3 is increased compared to Cohort 1. The prevalence of HPV HR subtypes except for HPV 53 is increased in Cohort 3 compared to Cohort 2. Among WLWH, Cohort 3 had a higher prevalence of HPV 16, 18, and 34 compared to Cohort 2. Among women without HIV, Cohort 3 had a higher prevalence of HPV 16 and 18 compared to Cohort 2. Compared to healthy women, HPV subtype representation is higher among women with CIN and CaCx. This suggests the presence of multiple HR HPV strains may impact transformation from pre-cancerous lesions to CaCx, highlighting the importance of CIN detection and primary prevention of HR HPV to decrease the incidence of CaCx in Botswana.

  PublisherDOI

• Supplementary Tables 1-5 from Patients with Cervical Cancer with and without HIV Infection Have Unique T-cell Activation Profiles despite Similar Survival Outcomes after Chemoradiation

  2025-05-13

  supplementary-materialsOpen accessSenior author

  <p>Supplementary Tables 1-5</p>

  PublisherOA PDFDOI

• Supplementary Figure 4 from Patients with Cervical Cancer with and without HIV Infection Have Unique T-cell Activation Profiles despite Similar Survival Outcomes after Chemoradiation

  2025-05-13

  preprintOpen accessSenior author

  <p>Supplementary Figure 4</p>

  PublisherOA PDFDOI

• Supplementary Figure 3 from Patients with Cervical Cancer with and without HIV Infection Have Unique T-cell Activation Profiles despite Similar Survival Outcomes after Chemoradiation

  2025-05-13

  preprintOpen accessSenior author

  <p>Supplementary Figure 3</p>

  PublisherOA PDFDOI

• Data from Patients with Cervical Cancer with and without HIV Infection Have Unique T-cell Activation Profiles despite Similar Survival Outcomes after Chemoradiation

  2025-05-13

  preprintOpen accessSenior author

  <div>Abstract<p>The global burden of cervical cancer is highest in low- and middle-income countries. Women living with human immunodeficiency virus (HIV) infection are particularly affected by cervical cancer despite availability and adherence to antiretroviral therapy. Immune profile correlates of survival and treatment response have not been widely explored in patients with and without HIV infection. This study recruited women with cervical cancer undergoing definitive chemoradiation (CRT) in Botswana. Clinical characteristics and blood samples were collected. Flow cytometry was performed on samples prior to initiation, at completion, and 3 months after CRT. Logistic regression analysis identified immune markers that differed by HIV status and correlated with overall survival (OS). The study enrolled 131 consecutive women (HIV+ <i>N</i> = 89 and HIV− <i>N</i> = 42). From initiation to 3 months after CRT, a significant decrease in CD4 frequency (72%–60.55%, <i>P</i> < 0.001) and an increase in CD8 frequency (20.9%–31.5%, <i>P</i> < 0.001) were seen in women without HIV, whereas no significant changes in CD4 frequency (52.5%–50.9%) or CD8 frequency (39.9%–41.4%) were observed in those with HIV. Peripheral T cells underwent similar activation across the cohort regardless of HIV status. Improved OS was associated with reduced frequency of IL-2–expressing CD4 T-cell subsets. In women living with HIV, enhanced OS was associated with the presence of proinflammatory CD8 T cells. CRT induces peripheral T-cell activation and distinct cytokine profiles that differ by HIV status. Despite similar OS, HIV infection may differentially affect immune response to CRT in women with well-managed HIV.</p>Significance:<p>Chemoradiation affects the immune system of patients with cervical cancer with well-controlled HIV infection differently than those without HIV, yet their survival does not differ. This finding is an important step in understanding how management of HIV infection can modify cancer outcomes, particularly in settings with a high burden of HIV.</p></div>

  PublisherDOI

• R9AP is a common receptor for EBV infection in epithelial cells and B cells

  Nature · 2025-06-18 · 16 citations

  articleOpen access

  Epstein–Barr virus (EBV) persistently infects more than 90% of the human population, causing infectious mononucleosis1, susceptibility to autoimmune diseases2 and multiple malignancies of epithelial or B cell-origin3. EBV infects epithelial cells and B cells through interaction between viral glycoproteins and different host receptors4, but it has remained unknown whether a common receptor mediates infection of its two major host cell targets. Here, we establish R9AP as a crucial EBV receptor for entry into epithelial and B cells. R9AP silencing or knockout, R9AP-derived peptide and R9AP monoclonal antibody each significantly inhibit, whereas R9AP overexpression promotes, EBV uptake into both cell types. R9AP binds directly to the EBV glycoprotein gH/gL complex to initiate gH/gL–gB-mediated membrane fusion. Notably, the interaction of R9AP with gH/gL is inhibited by the highly competitive gH/gL-neutralizing antibody AMMO1, which blocks EBV epithelial and B cell entry. Moreover, R9AP mediates viral and cellular membrane fusion in cooperation with EBV gp42–human leukocyte antigen class II or gH/gL–EPHA2 complexes in B cells or epithelial cells, respectively. We propose R9AP as the crucial common receptor of B cells and epithelial cells and a potential prophylactic and vaccine target for EBV. R9AP is a key receptor for entry of Epstein–Barr virus into human epithelial and B cells, and interacts directly with the viral glycoprotein gH/gL complex to mediate virus–host membrane fusion.

  PublisherOA PDFDOI

• Figure 1 from Patients with Cervical Cancer with and without HIV Infection Have Unique T-cell Activation Profiles despite Similar Survival Outcomes after Chemoradiation

  2025-05-13

  preprintOpen accessSenior author

  <p>Changes in the CD4:CD8 ratio before and after CRT. Frequency of CD4 and CD8 T-cell subsets by flow cytometry. Box plots overlay individual patient data points for CD4 frequency divided by CD8 frequency (CD4:CD8 ratio) over three longitudinal study time points (Initial, EOT, and M3) in the (<b>A</b>) total cohort and (<b>B</b>) cohort stratified by HIV status. Significance (<i>P</i> < 0.05) indicated by *; blue and green lines indicate statistical comparison between Initial and M3 time points for the cohorts with and without HIV, respectively. ns, not significant.</p>

  PublisherDOI

• Figure 4 from Patients with Cervical Cancer with and without HIV Infection Have Unique T-cell Activation Profiles despite Similar Survival Outcomes after Chemoradiation

  2025-05-13

  preprintOpen accessSenior author

  <p>Correlation of the CD4:CD8 ratio with patient OS. Kaplan–Meier curves show OS probabilities by peripheral CD4:CD8 ratio for the total analyzed cohort and by HIV status. Ratios are designated as those lower than the mean (blue) vs. higher than the mean (red).</p>

  PublisherDOI

• Figure 2 from Patients with Cervical Cancer with and without HIV Infection Have Unique T-cell Activation Profiles despite Similar Survival Outcomes after Chemoradiation

  2025-05-13

  preprintOpen accessSenior author

  <p>Changes in T-cell subsets before and after CRT by HIV status. <b>A,</b> CD8 T cells and (<b>B</b>) CD4 T cells were stratified into four major subsets by two additional markers (CCR7 and CD45RA) to identify naïve (CD45RA<sup>+</sup>CCR7<sup>+</sup>), central memory (CD45RA<sup>−</sup>CCR7<sup>+</sup>), effector memory (CD45RA<sup>−</sup>CCR7<sup>−</sup>), and effector (CD45RA<sup>+</sup>CCR7<sup>−</sup>) subsets. Box plots overlay individual patient data points for subset frequencies over three longitudinal study time points (Initial, EOT, and M3).</p>

  PublisherDOI

Recent grants

• NIH Grant R01CA171979

  NIH · $1.5M · 2019

• NIH Grant R01CA091792

  NIH · $3.4M · 2013

• NIH Grant R29CA072150

  NIH · $538k · 2001

• NIH Grant R01DE017338

  NIH · $811k · 2009

• NIH Grant R01AI067037

  NIH · $1.6M · 2013

Frequent coauthors

• Ke Lan

  Zhongnan Hospital of Wuhan University

  45 shared

• Qiliang Cai

  Shanghai Medical College of Fudan University

  43 shared

• Subhash C. Verma

  University of Nevada, Reno

  43 shared

• Masanao Murakami

  36 shared

• Hem Chandra Jha

  36 shared

• Abhik Saha

  Presidency University

  30 shared

• Yonggang Pei

  University of Science and Technology of China

  22 shared

• Jie Lu

  20 shared

Labs

• Robertson LabPI

Education

• PhD, Microbiology and Molecular Genetics

  Wayne State University

  1992

Awards & honors

• Dean's list for entire period, 1987
• Honorary MS (Honorary Masters) University of Pennsylvania, 2…