Ignite Creation Date:
2024-05-06 @ 6:04 PM
Last Modification Date:
2024-10-26 @ 2:41 PM
Study NCT ID:
NCT05536219
Status:
RECRUITING
Last Update Posted:
2023-11-18
First Post:
2022-09-07
Brief Title:
Impact of the Presence of Anti-interferon Autoantibodies on the Viral Load in Severe Respiratory Infections
Sponsor:
Hospices Civils de Lyon
Organization:
Hospices Civils de Lyon
Study Overview
Official Title:
Impact of the Presence of Anti-interferon Autoantibodies on the Viral Load in Severe Respiratory Infections in Intensive Care
Status:
RECRUITING
Status Verified Date:
2023-11
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
INTERFERICUS
Brief Summary:
Type I interferons IFN-I production is induced by the detection of viral molecules such as RNA or DNA viral strands through pattern recognition receptors PRR present on many immune cell types Despite a minimal concentration IFN-I secretion activate the secretion by neighbouring cells of more than 700 proteins with antiviral properties inhibition of viral replication destabilization of virus membranes etc IFN-I constitute therefore one of the major first line of defence established by the immune system in response to viral infection Briefly during the Coronavirus disease COVID-19 pandemic several teams including ours highlighted a lack of IFN-I response in approximately one in five individuals presenting a severe form of COVID-19
Interestingly within a large part of them in vitro investigations revealed the presence of autoantibodies presenting neutralizing capacities against alpha andor omega interferons This finding confirms the deleterious role of anti-IFN-I autoantibodies on the antiviral immune response and the key role of IFN-I pathway regarding defences against COVID-19 infection Furthermore those observations pave the way to interesting research that would allow understanding the underlying pathophysiological mechanisms of severe viral respiratory infection
The research hypothesis are
i IFN-I deficiency could induce severe forms of viral infections which could lead to intensive care admission ii IFN-I deficiency could increase viral loads in nasopharyngeal samples and be associated with protracted viral clearance iii The frequency of viral co-infections may be higher in case of IFN-I antiviral pathway blockade iv severe forms of respiratory viruses infections could be induced by other anti-cytokine autoantibodies
In addition to confirming research hypotheses recently mentioned the aim of this clinical protocol will be to assess the impact of antiviral innate immune response alterations in severe respiratory infections
Interestingly within a large part of them in vitro investigations revealed the presence of autoantibodies presenting neutralizing capacities against alpha andor omega interferons This finding confirms the deleterious role of anti-IFN-I autoantibodies on the antiviral immune response and the key role of IFN-I pathway regarding defences against COVID-19 infection Furthermore those observations pave the way to interesting research that would allow understanding the underlying pathophysiological mechanisms of severe viral respiratory infection
The research hypothesis are
i IFN-I deficiency could induce severe forms of viral infections which could lead to intensive care admission ii IFN-I deficiency could increase viral loads in nasopharyngeal samples and be associated with protracted viral clearance iii The frequency of viral co-infections may be higher in case of IFN-I antiviral pathway blockade iv severe forms of respiratory viruses infections could be induced by other anti-cytokine autoantibodies
In addition to confirming research hypotheses recently mentioned the aim of this clinical protocol will be to assess the impact of antiviral innate immune response alterations in severe respiratory infections
Detailed Description:
None
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None