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. 2026 Jul 3;66:296–304. doi: 10.1016/j.bioactmat.2026.06.030

Rapid inactivation kinetics of a broad range of viruses on a continuously self-cleaning polymer surface

Kacie M Wells a,1, Daniela Silva-Ayala b,1,2, Sarah J Dejarnette c, Jeremy P Faircloth d, Padraic O'Reilly e, Reza A Ghiladi f, Lee-Ann Jaykus d, Frank Scholle c, Anthony Griffiths b,⁎,2, Richard J Spontak h,g,f,⁎⁎
PMCID: PMC13355433  PMID: 42436955

Abstract

Infections arising from a broadening variety of viruses are becoming increasingly widespread due to greater zoonotic transmission, with the COVID-19 pandemic exemplifying a global event that claimed the lives of millions worldwide. While targeted vaccines are being developed to thwart the spread of viral infections, they often become available to the public in response to an (expected) outbreak and must be repeatedly adjusted to account for mutations. An alternative to this strategy instead focuses on infection prevention by inactivating viruses prior to human exposure. In this study, we examine the inactivation kinetics of a broad range of infectious viruses on a self-cleaning polymer that functions by a surface pH-drop mechanism upon hydration. Photo-induced surface microscopy confirms that the sulfonic acid groups responsible for proton transport initially reside on the polymer surface, where protons lower the pH of the aqueous layer in contact with the polymer to below unity. This additive-free mechanism results in pH-driven inactivation of three coronaviruses (including SARS-CoV-2), human adenovirus, Tulane virus (a human norovirus surrogate), and four high-consequence viruses (Sudan virus, Marburg virus, Lassa virus, and Nipah virus), often reaching the limit of detection in 10 min or less.

Graphical abstract

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Highlights

  • •

    Photo-induced force microscopy confirms the presence of sulfonic acid groups on the surface of an anionic polymer with antimicrobial properties.

  • •

    Several coronaviruses, including the SARS-CoV-2 virus, are inactivated on the surface of an anionic polymer in minutes due to a pH-drop mechanism.

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    Two non-enveloped viruses exhibit greater resistance to acid-driven inactivation on the same anionic block polymer over the same time frame.

  • •

    Electron microscopy reveals that the morphologies of non-enveloped and enveloped viruses change significantly when exposed to an anionic block polymer.

  • •

    Four viruses belonging to risk group 4 are inactivated to the limit of detection within ∼10 min when subjected to pH-driven surface inactivation.

  • •

    A modified kinetics model discerns if the inactivation results reported here follow first-order kinetics or a more complex inactivation pathway.

  • •

    pH-driven surface inactivation is a broadly-reactive preventative tactic that should not be susceptible to immune escape and antiviral resistance.

1. Introduction

In conjunction with a rapidly changing environment, microbial infections constitute one of the fastest growing and most worrisome global challenges, especially in light of the recent COVID-19 pandemic [1] and ongoing antimicrobial resistance (AMR) of bacteria and fungi [2]. According to predictions from a British study [3], annual deaths due to microbial infections will increase to over 39 million, surpassing the death toll due to all forms of cancer combined, by 2050. The COVID-19 pandemic, for example, is responsible for over 7 million fatalities and over 770 million infections worldwide [4]. Additionally, CDC-designated serious and urgent threats, along with nosocomial infections caused primarily by bacteria belonging to the ESKAPE family [5], currently account for over 1.2 million fatalities annually [6]. While antibiotics have long existed to kill bacteria such as Staphylococcus aureus (S. aureus) and fungi such as Candida auris (C. auris), microbes such as these exhibit signs of increasing AMR [7] and are becoming increasingly difficult to kill due primarily to overuse of conventional antibiotics [8] (with methicillin-resistant S. aureus, MRSA, and antifungal-resistant C. auris designated as serious and urgent threats, respectively, by the CDC [9]). For viruses, these concerns are further compounded by the continuous emergence of viral mutations, which can contribute to reduced susceptibility to antiviral therapeutics, escape from antibody-based interventions [10], and the ongoing evolution of viral variants with altered transmissibility or pathogenicity.

In recent decades, several viruses that pose significant public health risks have appeared within new populations or are swiftly increasing in both incidence and geographic range. Many of these viruses have emerged following zoonotic transmission, crossing species barriers from animal reservoirs and subsequently spreading within human populations [11,12]. Notable examples of high-consequence viruses include the hemorrhagic fever viruses — Sudan virus (SUDV) [13], Marburg virus (MARV) [14] and Lassa virus (LASV) [15] — and the neurovirulent Nipah virus (NiV) [16]. In addition, three distinct coronaviruses have triggered the spread of highly contagious respiratory syndromes — Middle East respiratory syndrome (MERS-CoV), severe acute respiratory syndrome (SARS-CoV) and SARS-CoV-2 (the causative agent of COVID-19) [17] — while other coronaviruses are relatively ubiquitous and responsible for typically self-limiting diseases including the common cold. The hemorrhagic-fever, neurovirulent and respiratory syndrome viruses considered here constitute particularly important threats to public health due to their high pandemic potential and lack of adequate medical countermeasures. Importantly, their impact on public health can be mitigated through early detection, intervention, and control measures. Seasonal infections, such the ones caused by some human coronaviruses, remain an ongoing and intermittent concern for human health.

Both SUDV and MARV belong to the Filoviridae family, whereas NiV and LASV belong to the Paramyxoviridae and Arenaviridae families, respectively. (Other human pathogens in the Paramyxoviridae family include mumps and measles, the latter of which is responsible for an outbreak this year of nearly 2100 reported cases in 39 U S. states as of June 12, 2026 [18]) Infections caused by hemorrhagic fever viruses can result in high human mortality rates. Collectively, they are responsible for sporadic outbreaks resulting in large emerging events to pandemics that threaten millions of people around the world [19], and the World Health Organization (WHO) has prioritized these viruses for research and development in the context of public health emergencies. Coronaviruses such as SARS-CoV, MERS-CoV, SARS-CoV-2, HCoV-OC43 and HCoV-229E belong to the Coronaviridae family, and resulting respiratory infections can range from mild to severe. While high mortality rates tend to accompany infections with SARS-CoV and MERS-CoV, SARS-CoV-2 is able to cause a disease spectrum ranging from asymptomatic to fatal. Even though all of these enveloped RNA viruses consist of highly organized proteins and lipids, the structure of their infectious viral particles varies widely: filoviruses can measure up to 1.4 μm in length, whereas paramyxoviruses and arenaviruses are ∼300 nm in diameter and coronaviruses are ∼140 nm in diameter [[14], [15], [16], [17]]. In addition, two non-enveloped viruses of interest here because of their high transmissibility include (i) human adenovirus-5 (HAd-5), which possesses a double-stranded DNA genome, belongs to the Adenoviridae family and measures ∼100 nm in diameter, and (ii) Tulane virus, a surrogate for human norovirus [20] (HuNoV) and a member of the Caliciviridae family, possessing a single-stranded, positive-sense RNA genome and measuring 30-35 nm in diameter. The latter of these viruses is the leading cause of acute viral gastroenteritis worldwide [21].

Destabilization and degradation of the components comprising viral particles constitute an effective virus-agnostic approach to ensure viral inactivation and inability to proceed with productive infection [[22], [23], [24]]. Due to the potential of some of the viruses listed above to cause severe diseases, outbreaks, and even pandemics, sanitary countermeasures must be developed to offer broad-spectrum inactivation, serving as barriers to infection and preventing disease dissemination. While vaccines remain the primary antiviral recourse, they can be accompanied by unexpected complications (e.g., the Sweet Syndrome induced by SARS-CoV-2 vaccines [25]). For this reason, efforts have begun to focus increasingly on additional and promising antiviral strategies [26]. This can be achieved through the use of novel compounds such as flavonoid glycosides [27] or the development of models capable of accurately predicting both in vivo and in vitro activities on the basis of intracellular properties [28]. Alternatively, we have previously demonstrated [24] that a nanostructured anionic block polymer inherently (without any additives) behaves as a continuously self-cleaning antimicrobial surface capable of rapidly and effectively inactivating the SARS-CoV-2 and HCoV-229E viruses, in addition to most of the bacteria in the ESKAPE family [29] (including MRSA), Clostridioides difficile in the vegetative state and two types of Candida fungi [30]. As described further below, the mechanism of action of this polymer surface is proton-driven pH disruption of a wide range of microorganisms. In this study, we report on the inactivation kinetics of various viruses on surfaces of this polymer possessing different morphologies, which govern proton diffusion. Experimental details regarding viruses and cell lines, inactivation measurements and polymer preparation are provided in the Supporting Information.

2. Inactivation mechanism and TESET polymer surface properties

The polymer used here is a poly[tert-butylstyrene-b-(ethylene-alt-propylene)-b-(styrene-co-styrenesulfonate)-b--(ethylene-alt-propylene)-b-tert-butylstyrene] (TESET) pentablock polymer, and its broadly-reactive antimicrobial surface property capable of inactivating viruses, vegetative bacteria and fungi derives from the release and subsequent mobility of protons from sulfonic acid groups within the polymer upon hydration [24]. Viruses are commonly spread by coughs and sneezes or gastrointestinal excretions. Transmission occurs by infectious droplets generated from one host that either enter directly into the respiratory system of another host or deposit as fomites on a surface, where they can remain viable for hours to days [[31], [32], [33]]. Fig. 1a illustrates this scenario and the inactivation of coronaviruses when they come into contact with the water-activated TESET polymer. The aqueous contact layer becomes enriched with protons and its pH level falls rapidly to below 1 [29], thereby inactivating a broad range of microbes after relatively short exposure times on the order of minutes. To confirm that the hydrophilic moieties of the TESET polymer reside on the surface to permit migration of protons to the aqueous contact layer, we have performed infrared photo-induced force microscopy (IR-PiFM), which is an atomic force microscopy (AFM) technique wherein the AFM is coupled with an infrared laser to facilitate simultaneous acquisition of surface topography and the corresponding chemical map with ca. 3 nm spatial resolution [34,35]. Representative topography and chemistry IR-PiFM images are displayed in Fig. 1b, and the full spectrum is described in Fig. S1 of the Supporting Information.

Fig. 1.

Fig. 1

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(a) Artistic rendition of the mechanism wherein viruses are transmitted within coughs and sneezes from one host to another. The pH of virus-containing water droplets deposited on the TESET polymer quickly plummets so that virus particles are completely inactivated in minutes. (b) Complementary topography (left) and chemistry (right) IR-PiFM images confirming the existence of sulfonic acid groups (colored according to the spectra included in Fig. S1 of the Supporting Information) on the surface of the TESET polymer cast from THF and subjected to SVA.

3. Time-dependent inactivation of a broad range of viruses on the TESET polymer

Inactivation results acquired for SARS-CoV-2 and HCoV-OC43 viruses, quantified by plaque assays (PFU/mL) and generated at the National Emerging Infectious Diseases Laboratories (NEIDL), are presented in Fig. 2 on different variations of the TESET polymer surface. Since the internal nanoscale morphology of the polymer dictates proton diffusivity, we have prepared several TESET morphologies. The two compared in each panel reflect solvent templating [36,37]: films cast from tetrahydrofuran (THF) possess contiguous hydrophilic pathways, whereas those cast from a toluene/isopropanol (TIPA) cosolvent exhibit ionic dispersions in a hydrophobic matrix. In addition, we have considered the effect of polymer post-treatment in each figure: as-cast (AC) polymer films are compared to those subjected to (i) solvent-vapor annealing with THF vapor (SVA, which promotes equilibration to a lamellar morphology [38]) and (ii) hydrothermal annealing with deionized liquid water (HTA, which promotes nonequilibrium channel formation [39]), both at ambient temperature. Measurements that are not statistically significant according to the unpaired student's two-tailed t-test are identified by an asterisk. The solid lines displayed in this and later figures are regressed fits of a pseudo-first-order kinetic model originally proposed [40] for the inactivation of MRSA and ampicillin-resistant Escherichia coli. The model and results are summarized in Table S1 of the Supporting Information. In all cases, the time required to reach the limit of detection (LOD), designated here as tLOD, ranged from 2 to 5 min.

Fig. 2.

Fig. 2

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Inactivation profiles of the SARS-CoV-2 and HCoV-OC43 coronaviruses examined at the NEIDL upon exposure to the TESET polymer prepared under different conditions to alter the internal nanoscale morphology and proton diffusive pathways. Films are produced by casting from THF (filled circles) or TIPA cosolvent (open circles), and they are tested as-cast (black), as well as after solvent-vapor annealing in THF (SVA, red) and hydrothermal annealing in deionized water (HTA, blue), both at ambient temperature. Solid lines correspond to regressed fits of a pseudo-first-order kinetic model to the data (see the Supporting Information for details). The limit of detection (LOD) and the time to reach the LOD (tLOD) are both labeled, and dashed lines are explained in Table S1 in the Supporting Information. Asterisks identify data that are not statistically significant. All experiments were performed in quadruplicate, with each condition evaluated using three technical replicates.

Inactivation profiles of enveloped HCoV-229E and non-enveloped HAd-5 and Tulane viruses, measured in a BSL-2 facility and quantified by monitoring cytopathic effects (TCID50/mL), are displayed in Fig. 3 and likewise confirm that all the TESET variants examined here are effective at inactivating these viruses to different degrees. While tLOD for the HCoV-229E virus is typically 30 min, application of SVA to the TIPA-cast polymer reduces tLOD to 10 min due to an increase in the connected pathways associated with the lamellar morphology. The two non-enveloped viruses, however, never quite reach the LOD over the exposure time interval selected (30 min). It is noteworthy that, while the TIPA-cast film after SVA significantly improves the inactivation of the HAd-5 virus, it leads to an unexpected plateau in the case of the Tulane virus.

Fig. 3.

Fig. 3

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Inactivation profiles of the enveloped HCoV-229E coronavirus and two non-enveloped viruses (HAd-5 and Tulane, yellow background). The format of the figure is detailed in the caption of Fig. 2. The dashed line for the Tulane virus exposed to the TIPA-cast TESET film subjected to SVA serves to connect the data beyond the pseudo-first-order kinetic model regression. All experiments were performed in triplicate, with each condition evaluated using three technical replicates.

4. Severe morphological changes of viral particles after exposure to the TESET polymer

The transmission electron microscopy (TEM) images provided in Fig. 4 reveal the morphological changes that occur to the HCoV-229E (Fig. 4a) and HAd-5 (Fig. 4b) viruses upon exposure to the TIPA-cast (SVA) TESET polymer surface for 20 and 30 min, respectively. In both instances, the unexposed viruses appear as-expected based on previous virus studies [41,42] but appear completely damaged upon inactivation by the TESET-induced acidolysis. Interestingly, the HCoV-229E virus particles exposed to the TESET polymer surface in Fig. 4a substantially aggregate, while the 1% uranyl acetate stain employed to enhance contrast in these images is no longer effective for the exposed HAd-5 virus, which may suggest a change in its classic icosahedral symmetry in Fig. 4b.

Fig. 4.

Fig. 4

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TEM images of the (a) HCoV-229E and (b) HAd-5 viruses before and after exposure for 20 and 30 min, respectively, to the TESET polymer cast from TIPA and subjected to SVA in THF vapor at ambient temperature. The scalebars in the insets correspond to 50 nm. Details regarding specimen preparation are provided in the Supporting Information.

5. Successful inactivation of viruses belonging to the dangerous risk Group-4 RG4

The time-dependent inactivation of the four high-consequence viruses (SUDV, LASV, MARV, and NiV), quantified by plaque assays (PFU/mL), is presented for comparison in Fig. 5 and reveals that tLOD is consistently reached between 5 and 10 min, with model results listed in Table S2 in the Supporting Information. There is generally little difference between THF- and TIPA-cast films, and post treatments have relatively little impact on the antimicrobial properties of the TESET films, suggesting that these viruses, along with the beta coronaviruses, are particularly susceptible to high-acid environments [43,44].

Fig. 5.

Fig. 5

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Inactivation profiles of four high-consequence viruses — Sudan virus (SUDV), Lassa virus (LASV), Marburg virus (MARV), and Nipah virus (NiV) — examined at the NEIDL. The format of the figure is detailed in the caption of Fig. 2. All experiments were independently performed in quadruplicate, with each condition evaluated using three technical replicates.

6. Discussion

The results reported in this work demonstrate that a wide range of both enveloped and non-enveloped viruses possessing significant potential for large-scale outbreaks and compromising public health and safety can be quickly and effectively inactivated by exposure to the hydrated TESET block polymer. Since a previous study likewise established that a chemically different anionic polymer also containing sulfonic acid groups is capable of inactivating microbes (but more slowly because of smaller hydrophilic channels) on the basis of the same mechanism [24], we expect that this design paradigm extends to other form-stable anionic polymers that swell, but do not dissolve, upon exposure to aqueous media due to the presence of strongly acidic groups. Moreover, a recent study has established [45] that the efficacy of the antimicrobial mechanism can be independently controlled by systematic variation of either (i) the degree of sulfonation (DOS) at constant film thickness (L) or (ii) L at constant DOS, both of which govern the proton reservoir needed for contact layer acidification via proton diffusion. Adding to the arsenal of strategies that focus on overcoming the spread of diseases due to drug resistance [46], block polymers such as TESET can be safely used alone as dense cast films or lightly modified and sprayed for coating applications in high-transmission venues such as permanent/mobile hospitals, assisted-living facilities and schools especially in resource-poor areas that accounted for 8.5% of the global population in 2024 [47].

The materials-oriented preventative strategy discussed here is intended to augment, not replace, existing medical approaches strategically designed to prevent or treat viral infections by targeting specific chemical functionalities on viral particles. Viruses can escape vaccination strategies through antigenic variation and may develop resistance to antiviral agents as they evolve and mutate [48,49]. In contrast, the non-specific pH-driven inactivation mechanism of the TESET polymer should not be susceptible to conventional mechanisms of immune escape or viral resistance. As a tool to mitigate the impact of fomites, this polymer surface provides rapid and effective viral inactivation (often reaching the limit of detection) after relatively short exposure times typically less than 10 min. Additionally, the TESET polymer is a thermoplastic elastomer suitable for either thermal or solvent recycling, and it is fully rechargeable through the introduction of an aqueous acid [29]. Lastly, as life-saving antiviral agents or vaccines become increasingly unavailable in resource-poor communities around the world, distrusted due to popular beliefs in industrialized societies [50] or ineffective (if they even exist) against specific viral strains (e.g., the Bundibugyo strain of Ebola in the current Congo-Uganda outbreak [51]), the virucidal approach described in this study provides an effective non-drug countermeasure to combat the transmission of viruses via fomites, an important exposure route for a wide range of infections.

Forreasons such as these, new technologies focused on the development of effective and eco-friendly self-cleaning surfaces [[52], [53], [54]] play a critical role in preventing the spread of disease. Continuously-disinfecting, self-disinfecting or self-cleaning surfaces offer several advantages over conventional episodic cleaning approaches that routinely rely on disinfecting sprays, wipes and UV radiation, all of which can be harmful to those using them and/or the environment (most notably as solid waste) after long-term repeated use. The on-going pathogen-inactivating action of self-cleaning surfaces provides continuous protection between routine cleaning events, particularly in high-touch environments, thereby reducing surface degradation caused by corrosive agents or disinfecting chemicals that can gradually become detrimental. Importantly, their material-specific mechanism of action promotes the inactivation of diverse microorganisms and thus helps to reduce fomite-mediated transmission, as well as the environmental reseeding, of pathogens [52]. In this regard, it is important to recognize that viruses can remain stable on various surfaces for relatively long periods of time [32,33]. Innovations in functionalization intended to improve orthogonal properties (e.g., abrasion resistance to minimize surface damage incurred by repeated touching [55]) of self-cleaning materials without compromising microbiocidal efficacy are anticipated to expedite their introduction into real-world applications. The additive-free TESET polymer, acting through a unique proton-driven physicochemical inactivation mechanism involving substantial surface acidification upon hydration, has already been field-tested as a broadly-reactive self-cleaning surface on ticketing kiosks and counters at U.S. airports during the COVID-19 pandemic [24]. As reported [29] in a previous study and observed in practice, the microbiocidal efficacy of the polymer not only remains effective after repeated cycling but also can be fully restored upon short-term exposure to an aqueous acid.

In addition to demonstrating the effectiveness of the TESET polymers against a broad variety of viruses, the results reported in this study reveal several interesting outcomes that warrant discussion. First, the inactivation of the beta coronaviruses (SARS-CoV-2 and HCoV-OC43) and the four high-consequence viruses (SUDV, LASV, MARV, and NiV) display rapid and near log-linear inactivation kinetics, although not many obey a first-order kinetics mechanism. In marked contrast, the HCoV-229E, HAd-5 and Tulane viruses generally appear slower (more difficult) to inactivate, and several datasets exhibit significant tailing effects. Relative to the beta coronaviruses, alpha coronaviruses such as HCoV-229E are reported [56] to be more stable under acidic conditions. Sučec et al. [57] attribute this characteristic distinguishing alpha and beta coronaviruses to structural differences in the envelope proteins, particularly with regard to how the transmembrane domains respond to pH-induced hydration changes. As seen in the TEM images in Fig. 4a, the protein spikes on the HCoV-229E virus particles are completely gone upon inactivation. Second, of the two non-enveloped viruses examined here, Tulane virus is likewise stable in relatively acidic conditions (at pH levels as low as ∼3.0) [58]. Human adenovirus 5 is also known [59] to be acid-resistant, although the degree of resistance is dependent on ionic conditions, decreasing with decreasing pH. The TEM images displayed in Fig. 4b confirm that the adenovirus appears to lose all capsid integrity after exposure to the TESET polymer. As a general rule of thumb, non-enveloped viruses are usually more acid-resistant and environmentally stable than enveloped viruses. The lipid-rich outer layer of enveloped viruses contains embedded host cell receptors and can be vulnerable to acidic conditions, whereas the outer protein capsid of non-enveloped viruses (which also houses host receptors) is more resistant to environmental stressors, including pH extremes. Collectively, the inactivation data acquired for these three viruses — HCoV-229E, HAd-5 and Tulane — are consistent with what would be expected on the basis of their structural characteristics.

7. Abbreviated methods

7.1. Viruses and exposure to polymer films

The human coronavirus strain HCoV-OC43 was obtained from the Biodefense and Emerging Infections Research Resources Repository (BEI Resources, NR-52725), and the SARS-CoV-2 variant XBB.1.5 was obtained from BEI Resources (NR-59105), courtesy of Dr. William Florence at the National Institutes of Health. Mink cells from the American Type Culture Collection (ATCC [Manassas, VA]; Mv 1 Lu, CCL-64) were used for OC43 plaque assays, and Vero E6 cells (African Green Monkey, BEI Resources, NR-596) were used for the SARS-CoV-2 variant XBB.1.5 plaque assays. All work with the SARS-CoV-2 variant XBB.1.5 was performed in the containment facilities at the National Emerging Infectious Diseases Laboratories (NEIDL). Polymer films were trimmed into 2 cm2 squares and individually placed into sterile 6-well plates. To evaluate virucidal activity and further inactivation comparison, all the virus stocks used were diluted to achieve an exposure dose of 104 PFU in 50 μL total volume. To preserve the biological matrix associated with virus propagation, viral inocula were prepared directly from cell culture stocks. The HCoV-OC43, SARS-CoV-2 XBB.1.5, SUDV, MARV, LASV, and NiV series were diluted in Dulbecco's Modified Eagle Medium (DMEM) supplemented with 2% fetal bovine serum (FBS), whereas HCoV-229E and HAd-5 were maintained in DMEM containing 10% FBS and Tulane virus was maintained in M199 medium with 10% FBS. Briefly, five 10 μL droplets of virus inoculum were carefully deposited directly onto the surface of each polymer film, ensuring uniform contact between the viral suspension and the material surface. Virus-containing droplets remained in direct contact with the polymer for exposure times ranging from 1 to 30 min at ambient temperature. At the end of each exposure period, the virus–polymer interaction was immediately quenched by the addition of 2 mL of DMEM supplemented with 2% FBS. The resulting suspension was gently resuspended to recover remaining viral particles from the polymer surface, and 1 mL was transferred into a sterile 1.5 mL microcentrifuge tube. Samples were vortexed for 2–3 s and centrifuged at 1000 RCF for 2 min to remove debris prior to downstream analysis. The recovered suspensions were immediately processed for infectious virus quantification by plaque-forming unit (PFU) assay. For plaque assays, cells were seeded one day prior to infection at a density of 8 × 105 cells per well in 6-well plates to generate confluent monolayers. Samples recovered from the virus inactivation step, as well as controls, were serially diluted in 10-fold increments from 10−1 to 10−6, and 200 μL of each dilution were added to the corresponding cell monolayers. As a negative control, DMEM supplemented with 2% FBS alone was used, while 104 PFU in 50 μL total volume of virus not exposed to polymer and processed the same as exposed doses (addition of 2 μL of DMEM supplemented with 2% FBS previous to plaque assay) served as the positive infectivity control. Infectious viral titers were calculated as PFU/mL. The limit of detection for the assay was 200 infectious particles/mL. All experiments were independently performed in quadruplicate, with each condition evaluated using three technical replicates. More specifics are available in the Supporting Information. The human coronavirus strain HCoV-229E was obtained from the ATCC (VR-740) and was propagated on a human hepato-carcinoma cell line (Huh-7) in cell growth media (DMEM, 1% antibiotics, 10% FBS) at 35 °C. Polymer films were cut to fit the bottom of a 96-well plate, and 25 mL of virus suspension (stock concentration ranging from 106 to 108 TCID50/mL) were placed on polymer films for desired exposure times. Viral infectivity was determined by TCID50 assay, detailed in the Supporting Information. The non-enveloped human adenovirus, HAd-5 virus, was obtained from Dr. Scott Laster (North Carolina State University) and was propagated on the lung cancer cell line (A549) in cell growth media (DMEM, 1% antibiotics, 10% FBS) at 35 °C. Polymer films were cut to fit the bottom of a 96-well plate, and 25 μL of virus suspension (stock concentration ranging from 106 to 108 TCID50/mL) were placed on polymer films for desired exposure times. Virus titers were calculated as described above. Tulane virus stock, another non-enveloped virus, was provided courtesy of Dr. Jason Jiang, Cincinnati Children's Hospital, Cincinnati, OH. Here, LLC-MK2 cells (ATCC CCL-7) were used for culturing and titering the virus, and were grown as previously described by Farkas et al. [60] using complete M199 medium (Thermo Fisher, Waltham, MA) supplemented with 10% FBS (Thermo Fisher, Waltham, MA) and 1% penicillin-streptomycin (Thermo Fisher, Waltham, MA), with incubation at 5% CO2 and 37 °C. Tulane virus stock solutions in cell culture lysate were generated by passaging in LLC-MK2 cells grown to 90% confluence and infected at an MOI of 0.1 in M199 with 2% FBS. At 80-100% CPE, the virus was released from infected cells using three sequential freeze-thaw cycles (−80 °C) followed by centrifugation at 2500g for 10 min to remove cellular debris. Tulane virus infectivity was determined as described above. For the high-consequence risk group-4 RG4 viruses, Sudan virus (SUDV) and Marburg virus (MARV) were provided by Dr. Thomas Ksiazek at the World Reference Center for Emerging Viruses and Arboviruses at the University of Texas Medical Branch. Lassa virus (LASV) was provided by BEI Resources/NIH, and Nipah virus (NiV) was provided by BEI Resources (NR-50799). Vero E6 cells (African Green Monkey, BEI Resources, NR-596) were used for SUDV, MARV, NiV, and LASV plaque assays. All work with infectious viruses was performed in the BSL-4 facilities at the NEIDL. Polymer films were trimmed to 2 cm2 squares and placed in a sterile 6-well plate. Five drops of 10 μL (50 μL total) of virus were added to the surface of each film square and exposed for different times ranging from 1 to 30 min, plaque counting to calculate the viral titer (PFU/mL), detailed further in the Supporting Information.

7.2. Polymer film preparation

The TESET polymer, manufactured as Nexar™ by the Kraton Corporation (Houston, TX) was provided in sheet form. Its number-average molecular weight after 52 mol% midblock sulfonation was 89 kDa, and the TESET acronym reflects the molecular architecture of the polymer consisting of 33.7 wt% T, 22.5 wt% E and 43.8 wt% S (sulfonated) sequences ("blocks"). Films of the TESET polymer were produced by first dissolving a predetermined mass of the polymer in either THF or TIPA cosolvent at ambient temperature to obtain a 4% w/v polymer solution, which was subsequently cast into Teflon molds and slowly dried over the course of either 7 (THF) or 14 (TIPA) days under glass cover positioned in a fume hood. Resultant films were further dried under vacuum for 18 h under ambient conditions and typically measured ca. 500 μm thick. Some films were further treated with solvent-vapor annealing (SVA) or hydrothermal annealing (HTA). Films subjected to SVA were exposed to THF vapor at ambient temperature for 24 h in a glass chamber, and then further dried under ambient conditions for 24 h and vacuum-dried for 18 h, whereas HTA films were suspended in DI water for 24 h, then dried under ambient conditions for 24 h and vacuum-dried for 18 h.

7.3. Infrared photo-induced force microscopy

Infrared photo-induced force microscopy (IR-PiFM) is a multi-modal atomic force microscopy (AFM) technique that integrates an IR laser with an AFM microscope, allowing for the simultaneous collection of both topographic and chemical data at sub-5 nm resolution [12]. All IR-PiFM measurements included in Fig. 1b were conducted on a Vista 75 microscope (Molecular Vista Inc., San Jose, CA), paired with a quantum cascade laser (QCL) with a tuning wavenumber range from 1840 to 780 cm−1, with a spectral line width of 0.5 cm−1. Here, 2 μm2 images were captured at a scan speed of 0.5 Hz, while 1 μm2 images were acquired at 1 Hz. The corresponding PiF-IR spectra were power-normalized and collected with a sweep time of ∼20 s. Platinum-iridium-coated NCH 300 kHz non-contact cantilevers from Nanosensors (Neuchatel, Switzerland) were used for all measurements, and image and data processing was performed with the SurfaceWorks software package.

7.4. Transmission electron microscopy

After the HCoV-229E virus was grown in Huh-7 cells and subsequently harvested when the cytopathic effect exceeded 50%, the virus suspension was clarified by pelleting the cell debris at 3,000g for 10 min. The virus-containing supernatant was first filtered through a 0.22 μm polyethersulfone membrane and then further purified through a 15% and 45% CsCl in tris-NaCl-EDTA (TNE) buffer in a SW40 Ti rotor operated at 21,000 rpm for 3 h at 4 °C. The virus was pelleted through a 20% sucrose cushion in TNE buffer at 35,000 rpm for 2 h at 4 °C. The virus pellet was resuspended in TNE buffer (pH 7.4) for a minimum of 12 h at 4 °C, and the purified virus was used as-is or applied to the TESET polymer film for a desired exposure time before analysis by TEM. Human adenovirus- 5 virus was grown in A549 cells and then prepared as above. After pelleting the cell debris and filtering the supernatant, the virus suspension was purified through a “heavy” (1.45 g/mL) and “light” (1.25 g/mL) CsCl gradient in tris-Cl (pH 7.90) buffer in a SW28 rotor operated at 20,000 rpm for 2.5 h at 4 °C. The virus was resuspended in tris-Cl and subsequently concentrated through a MWCO 300 kDa centrifugal concentrator (Vivaspin 20) at 3,000g for 5 min at 4 °C. For each specimen, a carbon-coated 300-mesh grid from Ted Pella Inc. (Redding, CA) was placed on a 10 μL drop of either purified virus suspension for 1 min, and the grid was then wicked with filter paper. Afterwards, it was placed on a 10 μL drop of 1% uranyl acetate from Electron Microscopy Sciences (Hatfield, PA) for 10 s and wicked again with filter paper, after which the grid was dried under ambient conditions for at least 12 h prior to examination. Images were acquired on a Thermo Fisher Titan electron microscope operated at an accelerating voltage of 80 kV.

Ethics approval and consent to participate

Not applicable. This study only involves in vitro virus inactivation experiments using commercial cell lines and laboratory viral strains, without human participants, human biological samples or live animal in vivo tests.

Funding

This work was financially supported by the Center for Applied Virus Experimentation, part of the Comparative Medicine Institute, and the Global One Health Academy, as well as Kraton Corporation, at North Carolina State University. Start-up funding was also provided to A.G. at Boston University. We thank Dr. A.J. Bell for technical assistance.

CRediT authorship contribution statement

Kacie M. Wells: Data curation, Formal analysis, Investigation, Methodology, Writing – original draft, Writing – review & editing. Daniela Silva-Ayala: Data curation, Formal analysis, Investigation, Methodology, Writing – original draft, Writing – review & editing. Sarah J. Dejarnette: Data curation, Investigation, Methodology, Writing – review & editing. Jeremy P. Faircloth: Data curation, Investigation, Methodology. Padraic O'Reilly: Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Writing – original draft, Writing – review & editing. Reza A. Ghiladi: Conceptualization, Funding acquisition, Project administration, Resources, Writing – original draft, Writing – review & editing. Lee-Ann Jaykus: Funding acquisition, Methodology, Project administration, Resources, Supervision, Writing – original draft, Writing – review & editing. Frank Scholle: Conceptualization, Formal analysis, Funding acquisition, Methodology, Project administration, Supervision, Writing – original draft, Writing – review & editing. Anthony Griffiths: Conceptualization, Formal analysis, Funding acquisition, Project administration, Resources, Supervision, Writing – original draft, Writing – review & editing. Richard J. Spontak: Conceptualization, Formal analysis, Funding acquisition, Project administration, Resources, Supervision, Writing – original draft, Writing – review & editing.

Declaration of competing interest

The authors declare the following personal relationships which may be considered as potential competing interests: Padraic O'Reilly is currently employed by Molecular Vista.

Acknowledgments

This work was financially supported by the Center for Applied Virus Experimentation, part of the Comparative Medicine Institute, and the Global One Health Academy, as well as Kraton Corporation, at North Carolina State University. Start-up funding was also provided to A.G. at Boston University. We thank Dr. A.J. Bell for technical assistance.

Footnotes

Peer review under the responsibility of editorial board of Bioactive Materials.

Appendix A

Supplementary data to this article can be found online at https://doi.org/10.1016/j.bioactmat.2026.06.030.

Contributor Information

Anthony Griffiths, Email: agriffiths@missouri.edu.

Richard J. Spontak, Email: spontak@ncsu.edu.

Appendix A. Supplementary data

The following is the Supplementary data to this article:

Multimedia component 1
mmc1.pdf (3MB, pdf)

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