# Inhibitory Activity of Hydroxypropyl Methylcellulose on Rhinovirus and Influenza A Virus Infection of Human Nasal Epithelial Cells

## TL;DR

This study shows that hydroxypropyl methylcellulose can protect nasal cells from rhinovirus and influenza A virus infections, even in acidic conditions.

## Contribution

The study demonstrates HPMC's protective effects against respiratory viruses in human nasal epithelial cells under acidic and neutral pH conditions.

## Key findings

- HPMC significantly reduced viral loads for both rhinovirus and influenza A virus in nasal epithelial cells.
- HPMC treatment before or after infection did not harm nasal cell integrity or ciliary function.
- Protective effects of HPMC were observed regardless of acidic or neutral pH conditions.

## Abstract

The nasal epithelium is the primary site for entry of respiratory viruses. In comparison to oral administration, nasal drug applications directed locally to the site of infection can serve as early interventional barriers against respiratory virus pathogenesis by limiting viral spread in the upper airway. Experiments on the diffusion of methylene blue and nanoparticles in both water and low pH conditions revealed that hydroxypropyl methylcellulose (HPMC) can act as an effective physical barrier. This study also evaluated the activity of HPMC as a barrier against common respiratory viruses, i.e., rhinovirus (RV) and influenza A virus (IAV) using the in vitro human nasal epithelial cell (hNEC) model. Utilizing the hNEC infection model, we assessed the protective effects of HPMC in pH 3.5 and pH 7 buffers against RV and IAV. Acidic and pH-neutral buffers and HPMC dissolved in acidic and pH-neutral buffers were administered for 4 h prior to virus infection and at 4 h post-infection (hpi). The apical supernatant was harvested at 24 hpi to determine the viral loads of RV and IAV (H1N1 and H3N2). HPMC was demonstrated to exert protective effects in the infected hNECs independent of acidic pH. Pre-treatment with HPMC in acidic buffer significantly diminished viral loads for both RV and IAV infections of hNECs. Similarly, direct treatment of HPMC in acidic buffer after infection (4 hpi) also effectively decreased viral loads of both RV and IAV. Moreover, treatment using HPMC in acidic buffer before or after infection did not affect the epithelial integrity and ciliary function of hNECs. This study demonstrates the protective effects of HPMC in acidic buffer against RV and IAV infections of the human nasal epithelium.