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In Vitro Evaluation of antivirals using airway tissues

MucilAir™, SmallAir™ and AlveolAir™ are efficient models to study respiratory virus pathogenesis and evaluate antivirals toxicity and efficacy

Respiratory viral infections cause mild to severe diseases worldwide, such as common cold, bronchiolitis and pneumonia and are associated with huge costs for society.

Relevant human models are mandatory to test new molecules for shortening and alleviating these diseases, or to develop new therapies.

MucilAir™, SmallAir™ and AlveolAir™, holds in vitro specific mechanisms to counter invaders comparable to the in vivo situation, such as mucus production, mucociliary clearance, and secretion of defensive molecules.

Contract us to evaluate the efficiency of your novel antiviral compound on the following clinical viral strains:

HRV-A 16
HRV-B 14
HRV-C 15

Influenza A (H1N1 and H3N2)
Influenza B


Coronavirus (OC 43, SARS-CoV-2)

Respiratory Syncytial Virus

Others :
Parainfluenza virus 3

Efficient Replication of difficult-to-grow viruses

A panel of clinical rhinovirus (RV), respiratory enterovirus (EV), influenza virus (Flu), respiratory syncytial virus (RSV) and coronavirus (HCoV) specimens are all capable of productive infection in MucilAir™. The virions enter and exit preferentially through the apical surface (Tapparel et al., Virology, 2013 Nov; 446:1-8). Thus, MucilAir™ is a relevant, reliable, and convenient tool for replicating respiratory viruses, including the most challenging ones.


Efficient replication of various clinical virus strains using MucilAir™ exponential phase, peak of infection.

Viral tropism

HRV-C15 is colocalized with ciliated cells

EV-68 is colocalized with ciliated cells

HRV-A49 is colocalized with ciliated cells

H3N2 is colocalized with goblet cells

In red: virus colocalization, in blue, nucleus, in green ciliated cells except for H3N2: goblet cells

Inhibition of virus replication

Inhibition of HRV-A16 by Rupintrivir and H1N1 by Oseltamivir

The replication of the HRV A16, B14, C15 and EV-D68 is inhibited by Rupintrivir in a dose dependent manner in the MucilAir™ cultures.

Remdesivir Dose-response on SARS-CoV-2

Remdesivir efficiently inhibits SARS-CoV-2 replication

Impaired barrier function restoration (TEER)

HRV C15, H3N2 and H1N1 induced transient decrease in TEER inhibition which can be prevented by Rupintrivir or Oseltamivir treatment.

Mucociliary function inhibition

All tested respiratory viruses block mucociliary clearance except rhinovirus B and coronavirus OC43 on MucilAir™

Impaired Mucociliary function restoration

EV-D68 induced impairment of mucociliary clearance is prevented by Rupintrivir at day 4


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