Back to first-pass browser

First-pass extracted concept

ICAM-1-targeted receptor antagonism for rhinovirus prevention

Candidate: concept label1 source documents3 linked claims
Jump to explainersJump to evidenceJump to sourcesJump to claims
Live refresh every 5sNext refresh in 5s

Extracted Explainers

What the tool is doing

This review centers on therapeutic strategies that block ICAM-1 to prevent rhinovirus adhesion to airway epithelium. The intended use is reduction of virus-induced exacerbations in chronic respiratory disease.

Source 1DOIPubMed

Resources required

An implementable version would require a modality capable of antagonizing ICAM-1 at the respiratory epithelium. The abstract does not specify the exact therapeutic format.

Source 1DOIPubMed

What problem it solves

It addresses the problem that HRV uses ICAM-1 to enter the host lung epithelium and trigger exacerbations. This is presented as especially relevant in smoking-related COPD where ICAM-1 is upregulated.

Source 1DOIPubMed

What it does not solve

The abstract does not show that ICAM-1 blockade addresses all causes of exacerbation or all respiratory pathogens. It also does not establish a complete therapy for COPD itself.

Source 1DOIPubMed

Alternatives

The abstract contrasts this approach mainly against the current lack of robust therapies for COPD rather than naming specific alternative antiviral strategies.

Source 1DOIPubMed

Evidence Snippets

However, the lack of robust therapies for COPD in particular has triggered a renewed interest in assessing receptor antagonism-based anti-viral strategies for treatment of intercurrent viral infections in those with pre-existing chronic lung diseases... the review also sheds light specifically on evolving precision therapeutic strategies in blocking ICAM-1 for preventing viral adhesion and exacerbations of COPD.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1disease associationsupports2022Source 1DOIPubMed

Airway ICAM-1 protein is increased in asthmatics, smokers, and smoking-related COPD according to the literature summarized by the review.

Quoted textsource-backed
Multiple observations of increased airway ICAM-1 protein in asthmatics, smokers and smoking-related COPD have been recorded in the literature.
Claim 2mechanistic rolesupports2022Source 1DOIPubMed

Human rhinovirus entry into host lung epithelium is facilitated primarily by ICAM-1.

Quoted textsource-backed
The rhinoviral entry into the host lung epithelium is facilitated primarily by the adhesion site ("receptor") intercellular adhesion molecule-1 (ICAM-1)
Claim 3therapeutic rationalesupports2022Source 1DOIPubMed

Blocking ICAM-1 is presented as a precision therapeutic strategy for preventing viral adhesion and COPD exacerbations.

Quoted textsource-backed
the review also sheds light specifically on evolving precision therapeutic strategies in blocking ICAM-1 for preventing viral adhesion and exacerbations of COPD.