Intranasal antivirals against respiratory syncytial virus: the current therapeutic development landscape

Oti, Victor Baba; Idris, Adi; McMillan, Nigel A.J.

doi:10.1080/14787210.2024.2378185

Expert Review of Anti-infective Therapy

2024

DOI: 10.1080/14787210.2024.2378185

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Intranasal antivirals against respiratory syncytial virus: the current therapeutic development landscape

Victor Baba Oti,

Adi Idris,

Nigel A.J. McMillan

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Cited by 2 publications

References 38 publications

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Hypothetical molecular mechanism of a novel class of bacteriocin-based antivirals for the inhibition of respiratory Syncytial Virus (RSV)

Molina,

Yamasqui Padilla,

Aguaiza Pichazaca

et al. 2025

Medical Hypotheses

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Hypothetical molecular mechanism of a novel class of bacteriocin-based antivirals for the inhibition of respiratory Syncytial Virus (RSV)

Molina,

Yamasqui Padilla,

Aguaiza Pichazaca

et al. 2025

Medical Hypotheses

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Interaction Between the Matrix Protein and the Polymerase Complex of Respiratory Syncytial Virus

Atchison,

Croft,

Mathew

et al. 2024

Viruses

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The global burden of respiratory syncytial virus (RSV) and severe associated disease is prodigious. RSV-specific vaccines have been launched recently but there is no antiviral medicine commercially available. RSV polymerase (L) protein is one of the promising antiviral targets, along with fusion and nucleocapsid proteins. During medicinal chemistry campaigns, two potent L-protein inhibitors (PC786 and PC751) were identified. Both compounds inhibited the RSV A/B-induced cytopathic effect in HEp-2 cells equally, but PC786 was more potent than PC751 in bronchial epithelial cells. Repeated treatment with escalating concentrations on RSV A2-infected HEp-2 cells revealed both inhibitors led to a Y1631H mutation in the L protein, but only PC786 induced a mutation in the M protein (V153A). By L protein fragment and M protein binding analysis, we showed that the M protein interacts with the 1392–1735 amino acid region of the L protein, where PC786 potentially binds. In addition, PC786 treatment or PC786-induced mutant RSV was found to increase M-protein nuclear localisation later in infection, concomitant with delayed fusion protein localisation at the budding viral filaments. As M protein is known to play a key role in virus assembly and budding late in infection, our data suggests that disrupting the interaction between the M and L proteins could provide a novel target for antiviral development.

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Intranasal antivirals against respiratory syncytial virus: the current therapeutic development landscape

Cited by 2 publications

References 38 publications

Hypothetical molecular mechanism of a novel class of bacteriocin-based antivirals for the inhibition of respiratory Syncytial Virus (RSV)

Hypothetical molecular mechanism of a novel class of bacteriocin-based antivirals for the inhibition of respiratory Syncytial Virus (RSV)

Interaction Between the Matrix Protein and the Polymerase Complex of Respiratory Syncytial Virus

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