Monocytes and NK Cells Activity in Covid-19 Patients
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|ClinicalTrials.gov Identifier: NCT04375176|
Recruitment Status : Recruiting
First Posted : May 5, 2020
Last Update Posted : May 5, 2020
SARS-CoV-2 belong to beta-coronavirus family and its transmission route and symptoms follow those of all community-acquired coronaviruses. The main difference of the novel Coronavirus is the higher mortality rate, that is around 3%.
Death rate is over 1% only for patients over 50 years old, whereas until 40 years old is under 0,4%. No fatalities are declared among children under 10 years old to date. Death rate is almost double for male rather than female. This distribution of mortality rate according to age of infected patients could be only partially ascribed to other comorbidities in addition to great age. In fact, patients with no pre-existing conditions have however a case fatality rate of 0,9%.
The almost null rate of severe illness in children and generally in patients younger than 40 years old is quite un-explicable. Infant, children and young people could be infected but infection is rapidly self-limited or without symptoms. Older patients undergo severe lung injury as consequence of an immune response that is late in coming.
Possible explanation of these phenomena could be something, which assure ability to prompt response to SARS-CoV-2 in younger people independently from the novelty of the virus itself.
It would seem to be that younger people are already sensitized to the antigens of the virus without a previous contact.
This immunity is not really specific, but "partially specific" for many antigens of the virus, however able to limit the infection in the organism. Something stimulated the immune system and it scattered immunity against more and more antigens present. Children are the age group mostly exposed to all community-circulating viruses.
This immunity is not persistent but progressively fade out. It protects from the age of two, when the hypothetical stimulation occurs, to the fifth decade because of its slow decrease.
The only external stimulation, which healthy people receive are vaccines. All vaccinations and especially tetanic, diphtheria toxoids and inactivated bacteria as pertussis could stimulate immune system. They develop the specific immunity but generate also a sprouting immunity against antigens in transit, as coronaviruses and other community-circulating viruses.
The developed immunity gives some protection against multiple viral infection for years until the natural fade out.
After the fifth decade, that immunity is slower to be recall and reactivated. Additionally, transplant recipients and HIV infected patients, which have an immune system inhibited, unexpectedly, do not seem to suffer the worst complications of SARS-CoV-2 infection. An immune system imbalance could be play a pivotal role during the reaction to the virus, limiting destructive consequences of excessive inflammation.
According to the medical hypothesis on which the protocol is based on, young people could benefit from a functional adaptation of innate immune cells induced through epigenetic reprogramming and, especially, a pre-existing "partially specific" immunity to the community viruses caused by "bystander effect" of preceding vaccinations. In this study, we will explore the main differences existing among patients infected by SARS-CoV-2 who experience the illness at different degree of severity. We suppose to recognize different populations of patients, each one with a specific immunological pattern. It could differ in terms of cytokines, soluble factors serum level and immune cells activity both of the innate compartment and of the acquired one. The proof of a role of these immunological phenomena in the pathogenesis of Covid-19 are bases for implementation of therapeutic immunomodulatory treatments. In addition, the definition of an immunological risk profile could tailor established therapies to each kind of patient.
|Condition or disease||Intervention/treatment|
|COVID-19 Severe Acute Respiratory Syndrome Coronavirus 2 Immunomodulation||Diagnostic Test: Study of immune-mediated mechanisms in patients tested positive for SARS-CoV-2|
|Study Type :||Observational|
|Estimated Enrollment :||150 participants|
|Official Title:||Study of Immune-mediated Mechanisms in Patients Tested Positive for SARS-CoV-2: Phenotypic and Functional Analysis of Monocytes and NK Cells in the Blood of Subjects Affected by Covid 19|
|Actual Study Start Date :||April 27, 2020|
|Estimated Primary Completion Date :||June 30, 2020|
|Estimated Study Completion Date :||October 31, 2020|
Tested positive for SARS-CoV-2
Patients, tested positive for SARS-CoV-2, will be recruited in E.R. of the "Ospedale Di Circolo - ASST Settelaghi" Teaching Hospital in Varese.
Diagnostic Test: Study of immune-mediated mechanisms in patients tested positive for SARS-CoV-2
Phenotypic and functional analysis of monocytes and NK cells
- Immune cells activity [ Time Frame: 6 months ]Scientists' hypothesis is that monocytes, NK, CD4 AND CD8 T cells, in patients with severe infection to SARS-CoV-2, show an impairment in their function: cells reveal an overpowering hyperactivity that provokes a pathologic inflammatory response with a massive production of proinflammatory cytokine, edema and pulmonary fibrosis.
- Protective factors and new therapeutic strategies [ Time Frame: 6 months ]The secondary objectives are to correlate clinical data and vaccination history with laboratory immune pattern to identify protective factors for Covid 19 and open paths for new therapeutic strategies.
Biospecimen Retention: Samples With DNA
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT04375176
|Contact: Giuseppe Ietto, M.D.||+firstname.lastname@example.org|
|Contact: Domenico Iovino, M.D.||+393407308867||domenico.iovino@ASST-Settelaghi.it|
|Varese, Italy, 21100|
|Contact: Giuseppe Ietto, M.D. +393398758024 email@example.com|
|Principal Investigator: Giuseppe Ietto, MD|
|Principal Investigator: Lorenzo Mortara, Professor|
|Sub-Investigator: Domenico Iovino, MD|
|Sub-Investigator: Daniela Dalla Gasperina, Professor|
|Principal Investigator: Giulio Carcano, Professor|
|Sub-Investigator: Andreina Baj, MD|
|Sub-Investigator: Walter Ageno, Professor|
|Sub-Investigator: Francesco Acquati, Professor|
|Sub-Investigator: Angelo Genoni, Dr|
|Sub-Investigator: Denisa Baci, PhD|
|Sub-Investigator: Matteo Gallazzi, PhD|
|Sub-Investigator: Annarosaria De Vito, PhD|
|Sub-Investigator: Elisa Monti, MD|
|Sub-Investigator: Andrea Vigezzi, MD|
|Sub-Investigator: Caterina Franchi, MD|
|Sub-Investigator: Valentina Iori, MD|
|Sub-Investigator: Federica Masci, MD|
|Study Chair:||Giulio Carcano, Professor||Università degli Studi dell'Insubria|
|Principal Investigator:||Giuseppe Ietto, M.D.||Università degli Studi dell'Insubria|
|Principal Investigator:||Lorenzo Mortara, Professor||Università degli Studi dell'Insubria|