Stephen E. Hawes
· ProfessorVerifiedUniversity of Washington · Epidemiology
Active 1975–2026
About
Dr. Stephen E. Hawes is a professor and former chair of the Department of Epidemiology at the University of Washington's School of Public Health. He holds adjunct appointments in the Departments of Global Health and Health Services. His primary research interests include human papillomavirus (HPV), other sexually transmitted diseases (STDs), cervical and anal cancer and precursor lesions, and HIV-1 and HIV-2. With over 25 years of research experience, he has conducted cohort studies in Senegal, West Africa, as well as in Seattle. Dr. Hawes is the Director of the UW Strategic Analysis, Research and Training (START) Center and has led global mentoring and scientific research workshops in countries such as Kenya, Namibia, Peru, Vietnam, and Cambodia.
Research topics
- Internal medicine
- Medicine
- Gynecology
- Demography
- Family medicine
- Immunology
- Nursing
- Gender studies
- Environmental health
Selected publications
medRxiv · 2026-03-02
articleOpen accessBackground: )-based regimens. We evaluated PWID taking DTG to assess longitudinal rates of viral non-suppression and emergence of drug resistance mutations in Kenya. Methods: ) every 6 months for 2 years. We used univariable Cox proportional hazards to assess longitudinal risk for viremia (VL >200 copies/ml). Plasma specimens with viremia were genotyped for HIV drug resistance, including minority variants, using a lab-developed PacBio sequencing assay, and referenced by the Stanford HIVdb program. Results: Among 250 participants, 125 were receiving methadone, 199 (79.6) reported heroin use, 70% were male, and median age was 39 years. 194 (77.6%) participants completed all five study visits, 41 (16.4%) were lost to follow-up and 15 (6.0%) died. Across all study visits, 166 (66.0%) of the 250 participants were always suppressed, and 84 (33.6%) were viremic at least once during follow-up, including 8 (3.2%) who were always viremic and 76 (30.4%) who were intermittently suppressed. Living in an improvised shelter or outdoors was significantly associated with a higher risk of viremia (HR=4.35, 95% CI: 1.52-12.53). 93 specimens had drug resistance genotyping, 27 (29%) of which were from participants with incomplete follow-up. NNRTI resistance was frequent (37-41% across visits), whereas major resistance mutations were infrequent to tenofovir (4.3%), lamivudine (7.5%), and DTG (1%, minority variant S153F detected at 1% frequency). Accessory DTG mutations, which do not independently reduce susceptibility, were more common, observed in 41% (38/93) of genotyped specimens, most often T97A, E138K, and L74M. Conclusion: Among PWID living with HIV on TLD in Kenya, one-third had intermittent or sustained viral non-suppression across two years of follow-up. While NNRTI resistance was common, DTG resistance mutations were rare. Improving viral suppression among PWID living with HIV will reduce transmission risks and improve clinical outcomes.
PLOS Global Public Health · 2026-02-04
articleOpen accessCompared to HIV-1, HIV-2 infection is characterized by lower viral loads and slower decline in CD4 cells, however the majority of people living with HIV-2 (PLWH2) progress to AIDS and will benefit from antiretroviral therapy. Mutations leading to protease inhibitor (PI) resistance in HIV-2 are poorly characterized, but have important implications for second-line therapy. We evaluated the phenotypic drug susceptibility impacts of HIV-2 protease changes which are identified in genotypic resistance tools. We generated a library of 54 full length HIV-2ROD9 clones that included 21 individual protease mutations, alone or in various combinations. We generated eight additional clones containing combinations of changes observed in PI-treated PLWH2. We tested the clones in a single-cycle PI assay to determine darunavir (DRV) and lopinavir (LPV) EC50, and calculated fold change resistance relative to wild-type HIV-2ROD9. Four of the 21 amino acid changes tested alone conferred PI resistance: V47A and T56V conferred 4.1 and 2.9-fold resistance, respectively, to LPV, I50V conferred 4.6-fold resistance to DRV, and I54M conferred 5.5-fold resistance to DRV and 2.2-fold resistance to LPV. Other changes either lowered the EC50 or caused no change. Some combinations including V47A, I50V, I54M, or T56V also conferred resistance, with EC50 values 4.4 to 17-fold higher than wild-type. Six of eight PLWH2-derived strains were replication-competent: five exhibited resistance to LPV (>8.8-fold resistance), and three exhibited resistance to DRV (>4.7-fold). HIV-1 and HIV-2 are not equivalently susceptible to all antiretroviral agents and do not utilize identical pathways to resistance. We provide phenotypic evidence supporting the resistance role of changes in HIV-2 protease which do not have HIV-1 analogues, as well as evidence that analogues of "major" resistance changes in HIV-1 may have no resistance impacts in HIV-2, despite apparent treatment selection. These results should inform the HIV-2 genotypic resistance tools and help improve treatment for PLWH2.
Scoping review of levonorgestrel pharmacokinetic data in special populations
Faculty of 1000 Research Ltd · 2025-01-01
otherOpen accessSenior authorHIV Resistance to Dolutegravir Varies With Coadministered Agents
Clinical Infectious Diseases · 2025-08-30 · 2 citations
articleOpen accessWe hypothesized that HIV-dolutegravir resistance is more frequent when coadministered with nucleos(t)ides with shorter intracellular half-lives. Multivariable analysis of 183 viremic (≥200 c/mL) participants from 4 cohorts (N = 660 participants) found dolutegravir resistance in 21 (11.5%). Dolutegravir resistance was greater with dolutegravir + lamivudine + zidovudine/(1 on stavudine) (odds ratio [OR] = 19.4, 95% confidence interval [CI]: 5.1-74.3) or dolutegravir + lamivudine +abacavir (OR = 5.4, 95% CI: 1.1-25.8), compared with dolutegravir + lamivudine + tenofovir.
PLoS ONE · 2025-12-22
articleOpen accessSenior authorBACKGROUND: Concerns regarding the effects of non-tampon menstrual products on reproductive and urogenital health, particularly the risk of infections, is an area of ongoing investigation. We conducted an updated systematic review to assess the methodological quality of current evidence assessing associations between menstrual product use and reproductive and urogenital tract infections (RUTIs), and offer recommendations for future research. METHODS: Three databases (PubMed, Web of Science, United States Food and Drug Administration Manufacturer User Facility Device Experience) were searched for relevant published studies or product safety reports up to October 13, 2024. We included studies on menstruators of any age and geography assessing for any reusable/disposable menstrual pads, menstrual cups, or homemade alternatives worn only for menstrual absorbency compared to other menstrual products or no product use, with outcomes centered on RUTIs. Protocols, reviews, and studies assessing only tampons or non-menstrual absorbents were excluded. Results were evaluated and synthesized using tabular methods according to measures of association, and assessed across four criteria categories 1) product definition, 2) comparator definition, 3) outcome definition, and 4) confounder consideration. RESULTS: Thirty-one studies were included in this review. Most studies clearly defined outcomes and considered necessary confounders. In contrast, studies with well-defined products (6.5%) and comparator products (9.7%) were uncommon. Just 3.2% and 9.7% of studies fully defined products and comparators, respectively. Ten studies (32.2%) reported some data on four or more confounders, and seventeen (54.8%) defined their infectious outcomes and included laboratory confirmation. A meta-analysis was not possible due to data heterogeneity across product, comparator, and outcome definitions. Overall, associations between menstrual products and RUTIs are inconclusive. CONCLUSION: Future studies should 1) clearly define product and comparator type, material, frequency of change, and washing, drying, and storage practices for reusable products, 2) prioritize laboratory or clinician-confirmed outcomes over self-reported symptoms, and 3) adjust for relevant confounders.
HIV-1 3΄ polypurine tract mutations and integrase inhibitor resistance
AIDS · 2025-10-30 · 1 citations
articleThe WHO recommends the use of the integrase strand transfer inhibitor (INSTI) dolutegravir for first-line antiretroviral therapy (ART) in all adults living with HIV infection. Although dolutegravir-based ART is well tolerated and effective, mutations in the integrase-encoding region of HIV-1 pol that confer resistance to dolutegravir can undermine treatment efficacy. An alternative pathway to dolutegravir resistance has also been described involving mutations in the 3΄ polypurine tract (3΄PPT), an RNA sequence element known to be important for retroviral reverse transcription and integration. The possible emergence of dolutegravir resistance mutations outside of integrase carries important ramifications for people receiving INSTI-based interventions. In this review, we assess the state of the literature pertaining to mutations in the 3΄PPT of HIV-1 and the potential of such mutations to confer INSTI resistance. We interpret these findings within the larger background of work that informs our understanding of reverse transcription, integration, and the expression of unintegrated DNA (uDNA) in HIV-1-infected cells. We also discuss technical complications that arise as a result of uDNA expression in culture-based drug susceptibility assays, and critically evaluate the supporting evidence for current models of 3΄PPT mutant replication. We conclude by proposing additional studies to determine the role of the 3΄PPT in clinical HIV-1 drug resistance.
2025-09-02
articleOpen access<p>Supplementary Table S1 shows HPV subtypes detected with HRA HSIL disease extent</p>
Cancer Epidemiology Biomarkers & Prevention · 2025-07-11
articleOpen accessBACKGROUND: Molecular biomarkers could enhance anal cancer screening accuracy in people living with human immunodeficiency virus. We assessed the performance of human papillomavirus (HPV) 16/18 E6 oncoprotein in detecting anal high-grade squamous intraepithelial lesions (HSIL) in men living with human immunodeficiency virus. METHODS: We analyzed clinical data from 125 clinic visits of 82 men living with human immunodeficiency virus who underwent high-resolution anoscopy in Seattle, Washington (2015-2016), including the presence and extent of HSIL. Anal brush specimens were tested for high-risk HPV DNA, with HPV-16/18-positive samples further tested for E6 oncoprotein. Sensitivity, specificity, positive predictive value, and negative predictive value of HPV-16/18 E6 oncoprotein for HSIL were calculated, along with prevalence ratios with 95% confidence intervals. RESULTS: Forty-eight (38.4%) samples were HPV-16/18 positive, including three E6 positive. Forty-nine (39.2%) samples had corresponding HSIL. Specificity and positive predictive value of HPV-16/18 E6 for HSIL was 100%, and the prevalence ratio was 7.33 (95% confidence interval, 2.44-22.07) for HPV-16/18 E6-positive versus high-risk HPV-negative samples. Sensitivity for HSIL, however, was only 6.1%, with a moderate negative predictive value (62.3%). Two of four persons with HSILs with >75% disease extent had corresponding HPV-16/18 E6-positive samples, whereas none of 30 persons with <25% extent did. CONCLUSIONS: The HPV-16/18 E6 oncoprotein has potential utility as a triage biomarker for identifying and prioritizing lesions at the highest risk for progression. IMPACT: People living with human immunodeficiency virus are at an increased risk of anal cancer and would benefit from improved screening methods. Further research may elucidate the role of HPV-16/18 E6 oncoprotein in anal cancer prevention, alone or combined with other biomarkers.
2025-09-02
articleOpen access<p>Supplementary Figure S1 is a flowchart Flowchart showing participant enrollment, sample inclusion, and clinical outcomes.</p>
medRxiv · 2025-09-02
preprintOpen accessSenior authorAbstract Background Concerns regarding the effects of non-tampon menstrual products on reproductive and urogenital health, particularly the risk of infections, is an area of ongoing investigation. We conducted an updated systematic review to assess methodological quality of the current evidence assessing associations between menstrual product use and reproductive and urogenital infections (RUTIs), and offer recommendations for future research. Methods Three databases (PubMed, Web of Science, United States Food and Drug Administration Manufacturer User Facility Device Experience) were searched for relevant published studies or product safety reports up to October 13, 2024. We included studies on menstruators of any age and geography assessing for any reusable/disposable menstrual pads, menstrual cups, or homemade alternatives worn only for menstrual absorbency compared to other menstrual products or no product use, with outcomes centered on RUTIs. Protocols, reviews, and studies assessing only tampons or non-menstrual absorbents were excluded. Results were evaluated and synthesized using tabular methods according to measures of association, and across four criteria categories 1) product definition, 2) comparator definition, 3) outcome definition, and 4) confounder consideration. Results Thirty-one studies were included in this review. Most studies clearly defined outcomes and considered necessary confounders. In contrast, studies with well-defined products (6.5%) and comparator products (9.7%) were uncommon. Ten studies (32.2%) reported some data on four or more confounders, and seventeen (54.8%) defined their infectious outcomes and included laboratory confirmation. A meta-analysis was not possible due to data heterogeneity across product, comparator, and outcome definitions. Overall, associations between menstrual products and RUTIs are inconclusive. Conclusion Future studies should 1) clearly define product and comparator type, material, frequency of change, and washing, drying, and storage practices for reusable products, 2) prioritize laboratory or clinician-confirmed outcomes over self-reported symptoms, and 3) adjust for relevant confounders.
Recent grants
NIH · $1.6M · 2005
Frequent coauthors
- 95 shared
Nancy B. Kiviat
- 94 shared
Qinghua Feng
Ningbo University
- 85 shared
Cathy W. Critchlow
Amgen (United States)
- 75 shared
Papa Salif Sow
- 63 shared
Joshua Stern
University of Washington
- 55 shared
Geoffrey S. Gottlieb
- 53 shared
Linda O. Eckert
University of Washington
- 53 shared
Papa Souleymane Touré
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