About

Samuel Campos is an Associate Professor in the Department of Immunobiology at the University of Arizona. His professional contact email is skcampos@arizona.edu. The university acknowledges its location on the land and territories of Indigenous peoples, including the O’odham and the Yaqui, and emphasizes building sustainable relationships with Native Nations and Indigenous communities through education, partnerships, and community service.

Research topics

• Biology
• Virology
• Medicine
• Immunology
• Cell biology
• Pathology
• Genetics
• Political Science
• Biochemistry
• Chemistry
• Cancer research

Selected publications

• Cell-based high-content approach for SARS-CoV-2 neutralization identifies unique monoclonal antibodies and PI3K pathway inhibitors

  Frontiers in Cell and Developmental Biology · 2025-05-22

  articleOpen access

  The sudden rise of the SARS-CoV-2 virus and the delay in development of effective therapeutics for mitigation made evident a need for ways to screen compounds that can block infection and prevent further pathogenesis and spread. However, identifying effective drugs that are efficacious against viral infection and replication with minimal toxicity for the patient can be difficult. Monoclonal antibodies were shown to be effective, but as the SARS-CoV-2 mutated, these antibodies became ineffective. Small-molecule antivirals were identified using pseudovirus constructs to recapitulate infection in nonhuman cells, such as Vero E6 cells. However, the impact was limited due to poor translation of these compounds in the clinical setting. This is partly due to the lack of similarity of screening platforms to the in vivo physiology of the patient and partly because drugs effective in vitro showed dose-limiting toxicities. In this study, we performed two high-throughput screens in human lung adenocarcinoma cells with authentic SARS-CoV-2 virus to identify both monoclonal antibodies that neutralize the virus and clinically useful kinase inhibitors to block the virus and prioritize minimal host toxicity. Using high-content imaging combined with single-cell and multidimensional analysis, we identified antibodies and kinase inhibitors that reduce viral infection without affecting the host. Our screening technique uncovered novel antibodies and overlooked kinase inhibitors (i.e., PIK3i, mTORi, and multiple RTKi) that could be effective against the SARS-CoV-2 virus. Further characterization of these molecules will streamline the repurposing of compounds for the treatment of future pandemics and uncover novel mechanisms viruses use to hijack and infect host cells.

  PublisherOA PDFDOI

• Human Papillomavirus Infection Blunts STING Signaling and Alters Downstream Response

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-11-06

  preprintOpen access

  Abstract The cGAS/STING pathway is an important innate immune pathway that senses and responds to foreign DNA or damaged host DNA. cGAS recognizes DNA and generates the second messenger cGAMP which activates STING. STING then creates a platform for IRF3 to be phosphorylated before pIRF3 induces a type I interferon response resulting in transcription of anti-viral genes. We examined how HPV18 infection modulates cGAS/STING activation following DNA stimulation in primary human foreskin keratinocytes from three different donors. Following exogenous activation, HPV(+) cells produced higher levels of cGAMP compared to patient-matched HPV(-) cells yet phosphorylation of STING and IRF3 was reduced in the HPV(+) cells. The reduced STING and IRF3 activation corresponded with a selective dampening of type I interferon driven antiviral genes and pro-inflammatory cytokines in HPV(+) cells. Simultaneously, HPV(+) cells had a baseline increase in genes associated with epithelial proliferation and skin development, which remained elevated following cGAMP treatment. We demonstrate that both E6 and E7 are required and sufficient to drive increased cGAMP levels and attenuate STING activation. Our results characterize cGAS/STING pathway activation across time in HPV positive and negative cells and demonstrate that the HPV oncogenes cooperate to suppress early STING activation despite higher levels of cGAMP in these HPV(+) cells. These findings indicate that HPV modulates cGAS/STING signaling to blunt antiviral defenses without impacting other arms of the cGAS/STING pathway response. Importance In this study, we used primary human keratinocytes from multiple donors to track cGAS/STING activity over time following stimulation. We found that although HPV(+) cells produced more cGAMP, these cells showed reduced early activation of STING and IRF3. Downstream of cGAS/STING, many antiviral genes were suppressed by HPV however, epithelial proliferation-related genes had an HPV-mediated increase in baseline expression which remained higher than uninfected cells following cGAMP stimulation. We identified the HPV oncogenes E6 and E7 work together to enhance cGAMP levels and suppress parts of the downstream STING signaling response. These findings reveal that HPV attenuates cGAS/STING signaling and downstream events, selectively suppressing antiviral genes without inhibiting other parts of the pathway. Our results provide new insights into how HPV modulates innate immune responses.

  PublisherDOI

• Characterization of natural product inhibitors of quorum sensing in <em>Pseudomonas aeruginosa</em> reveals competitive inhibition of RhlR by <em>ortho</em>-vanillin

  2024-05-22

  preprint1st authorCorresponding
  PublisherDOI

• Correction for Rasmussen et al., “Virology—the path forward”

  Journal of Virology · 2024-02-09 · 4 citations

  erratumOpen access

  7: "elevating SARS-CoV-1 to a select agent in 2009" should read "elevating SARS-CoV-1 to a select agent in 2012."The CDC proposed adding SARS-CoV-1 to the Select Agent registry in a federal notice on 13 July 2009 (https://www.federalregister.gov/documents/2009/07/13/E9-16536/posses sion-use-and-transfer-of-select-agents-and-toxins-proposed-addition-of-sars-associ ated).This notice of proposed rulemaking explicitly states that compliance with the proposed amendment would require anyone possessing SARS-CoV-1 to obtain current or amended registration with the HHS Select Agent Program and acknowledged that registration is a time-consuming and potentially costly process.Contemporaneous sources demonstrate that the research impact was anticipated in 2009 (https://absa.org/wpcontent/uploads/2017/01/090911DHHS_SARS_Select_Agent_Comments.pdf and https:// www.cidrap.umn.edu/sars/cdc-proposes-list-sars-virus-select-agent) and had already had a negative impact on SARS-CoV-1 research (S.

  PublisherOA PDFDOI

• A Peptide Derived from Sorting Nexin 1 Inhibits HPV16 Entry, Retrograde Trafficking, and L2 Membrane Spanning

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-05-25

  preprintOpen accessSenior authorCorresponding

  High risk human papillomavirus (HPV) infection is responsible for 99% of cervical cancers and 5% of all human cancers worldwide. HPV infection requires the viral genome (vDNA) to gain access to nuclei of basal keratinocytes of epithelium. After virion endocytosis, the minor capsid protein L2 dictates the subcellular retrograde trafficking and nuclear localization of the vDNA during mitosis. Prior work identified a cell-permeable peptide termed SNX1.3, derived from the BAR domain of sorting nexin 1 (SNX1), that potently blocks the retrograde and nuclear trafficking of EGFR in triple negative breast cancer cells. Given the importance of EGFR and retrograde trafficking pathways in HPV16 infection, we set forth to study the effects of SNX1.3 within this context. SNX1.3 inhibited HPV16 infection by both delaying virion endocytosis, as well as potently blocking virion retrograde trafficking and Golgi localization. SNX1.3 had no effect on cell proliferation, nor did it affect post-Golgi trafficking of HPV16. Looking more directly at L2 function, SNX1.3 was found to impair membrane spanning of the minor capsid protein. Future work will focus on mechanistic studies of SNX1.3 inhibition, and the role of EGFR signaling and SNX1- mediated endosomal tubulation, cargo sorting, and retrograde trafficking in HPV infection.

  PublisherOA PDFDOI

• Virology—the path forward

  Journal of Virology · 2024-01-03 · 9 citations

  articleOpen access

  In the United States (US), biosafety and biosecurity oversight of research on viruses is being reappraised. Safety in virology research is paramount and oversight frameworks should be reviewed periodically. Changes should be made with care, however, to avoid impeding science that is essential for rapidly reducing and responding to pandemic threats as well as addressing more common challenges caused by infectious diseases. Decades of research uniquely positioned the US to be able to respond to the COVID-19 crisis with astounding speed, delivering life-saving vaccines within a year of identifying the virus. We should embolden and empower this strength, which is a vital part of protecting the health, economy, and security of US citizens. Herein, we offer our perspectives on priorities for revised rules governing virology research in the US.

  PublisherOA PDFDOI

• A peptide derived from sorting nexin 1 inhibits HPV16 entry, retrograde trafficking, and L2 membrane spanning

  Tumour Virus Research · 2024-06-21

  articleOpen accessSenior author

  High risk human papillomavirus (HPV) infection is responsible for 99 % of cervical cancers and 5 % of all human cancers worldwide. HPV infection requires the viral genome (vDNA) to gain access to nuclei of basal keratinocytes of epithelium. After virion endocytosis, the minor capsid protein L2 dictates the subcellular retrograde trafficking and nuclear localization of the vDNA during mitosis. Prior work identified a cell-permeable peptide termed SNX1.3, derived from the BAR domain of sorting nexin 1 (SNX1), that potently blocks the retrograde and nuclear trafficking of EGFR in triple negative breast cancer cells. Given the importance of EGFR and retrograde trafficking pathways in HPV16 infection, we set forth to study the effects of SNX1.3 within this context. SNX1.3 inhibited HPV16 infection by both delaying virion endocytosis, as well as potently blocking virion retrograde trafficking and Golgi localization. SNX1.3 had no effect on cell proliferation, nor did it affect post-Golgi trafficking of HPV16. Looking more directly at L2 function, SNX1.3 was found to impair membrane spanning of the minor capsid protein. Future work will focus on mechanistic studies of SNX1.3 inhibition, and the role of EGFR signaling and SNX1-mediated endosomal tubulation, cargo sorting, and retrograde trafficking in HPV infection.

  PublisherDOI

• Cell-based high-content approach for SARS-CoV-2 neutralization identifies unique monoclonal antibodies and PI3K pathway inhibitors

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-10-07 · 1 citations

  preprintOpen access

  The sudden rise of the SARS-CoV-2 virus and the delay in the development of effective therapeutics to mitigate it made evident a need for ways to screen for compounds that can block infection and prevent further pathogenesis and spread. Yet, identifying effective drugs efficacious against viral infection and replication with minimal toxicity for the patient can be difficult. Monoclonal antibodies were shown to be effective, yet as the SARS-CoV-2 mutated, these antibodies became ineffective. Small molecule antivirals were identified using pseudovirus constructs to recapitulate infection in non-human cells, such as Vero E6 cells. However, the impact was limited due to poor translation of these compounds in the clinical setting. This is partly due to the lack of similarity of screening platforms to the in vivo physiology of the patient and partly because drugs effective in vitro showed dose-limiting toxicities. In this study, we performed two high-throughput screens in human lung adenocarcinoma cells with authentic SARS-CoV-2 virus to identify both monoclonal antibodies that neutralize the virus and clinically useful kinase inhibitors to block the virus and prioritize minimal host toxicity. Using high-content imaging combined with single-cell and multidimensional analysis, we identified antibodies and kinase inhibitors that reduce virus infection without affecting the host. Our screening technique uncovered novel antibodies and overlooked kinase inhibitors (i.e. PIK3i, mTORi, multiple RTKi) that could be effective against SARS-CoV-2 virus. Further characterization of these molecules will streamline the repurposing of compounds for the treatment of future pandemics and uncover novel mechanisms viruses use to hijack and infect host cells.

  PublisherOA PDFDOI

• The harms of promoting the lab leak hypothesis for SARS-CoV-2 origins without evidence

  Journal of Virology · 2024-08-01 · 12 citations

  articleOpen access

  Science is humanity's best insurance against threats from nature, but it is a fragile enterprise that must be nourished and protected. The preponderance of scientific evidence indicates a natural origin for SARS-CoV-2. Yet, the theory that SARS-CoV-2 was engineered in and escaped from a lab dominates media attention, even in the absence of strong evidence. We discuss how the resulting anti-science movement puts the research community, scientific research, and pandemic preparedness at risk.

  PublisherOA PDFDOI

• Virology under the Microscope—a Call for Rational Discourse

  mBio · 2023-01-26 · 4 citations

  articleOpen access

  Viruses have brought humanity many challenges: respiratory infection, cancer, neurological impairment and immunosuppression to name a few. Virology research over the last 60+ years has responded to reduce this disease burden with vaccines and antivirals. Despite this long history, the COVID-19 pandemic has brought unprecedented attention to the field of virology. Some of this attention is focused on concern about the safe conduct of research with human pathogens. A small but vocal group of individuals has seized upon these concerns - conflating legitimate questions about safely conducting virus-related research with uncertainties over the origins of SARS-CoV-2. The result has fueled public confusion and, in many instances, ill-informed condemnation of virology. With this article, we seek to promote a return to rational discourse. We explain the use of gain-of-function approaches in science, discuss the possible origins of SARS-CoV-2 and outline current regulatory structures that provide oversight for virological research in the United States. By offering our expertise, we - a broad group of working virologists - seek to aid policy makers in navigating these controversial issues. Balanced, evidence-based discourse is essential to addressing public concern while maintaining and expanding much-needed research in virology.

  PublisherDOI

Recent grants

• Mechanisms and Consequences of L2-Dependent Subcellular Trafficking of the HPV Genome.

  NIH · $1.3M · 2020–2024

• Mechanisms of L2-Mediated Membrane Translocation of the Papillomaviral Genome

  NIH · $1.8M · 2014–2020

• NIH Grant F32CA123842

  NIH · $95k · 2008

Frequent coauthors

• Michael A. Barry

  Mayo Clinic in Arizona

  52 shared

• Shuaizhi Li

  University of Arizona

  16 shared

• Koenraad Van Doorslaer

  University of Arizona

  9 shared

• James C. Alwine

  University of Pennsylvania

  9 shared

• Michelle A. Ozbun

  9 shared

• Curtis A. Thorne

  9 shared

• Janice A. Chapman

  University of Arizona

  8 shared

• Carly R. Cabel

  University of Arizona

  8 shared

Education

• Ph.D., Biochemistry & Cell Biology

  Rice University

  2005

• B.S., Biology

  Virginia Polytechnic Institute and State University

  1999