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Related Experiment Video

Updated: Oct 27, 2025

A Precision Medicine Tool for Measurement and Monitoring of Hemoglobin S in Sickle Cell Disease Patients Receiving Transfusion Therapy

A Precision Medicine Tool for Measurement and Monitoring of Hemoglobin S in Sickle Cell Disease Patients Receiving Transfusion Therapy

COULD COVID-19 BE A HEMOGLOBINOPATHY?

Tania Ahmed Shakoori¹, Muhammad Mansoor Hafeez¹, Arif Malik¹

¹Institute of Molecular Biology and Biotechnology (IMBB), University of Lahore, New Campus, Defense Road 1, KM off Raiwind Road, Lahore, Pakistan.

Acta Clinica Croatica

|July 21, 2021

Summary

This summary is machine-generated.

COVID-19 may damage red blood cells via CD147, causing hemoglobinopathy and high-altitude pulmonary edema-like lung injury. This novel mechanism suggests exchange transfusion and anti-CD147 drugs as potential therapies for COVID-19 related acute respiratory distress syndrome.

Keywords:

Acute respiratory distress syndrome CD147 COVID-19 High altitude pulmonary edema, pathophysiology High altitude pulmonary embolism

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A Precision Medicine Tool for Measurement and Monitoring of Hemoglobin S in Sickle Cell Disease Patients Receiving Transfusion Therapy

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Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry

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Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload

Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload

Published on: March 14, 2017

Area of Science:

Pathophysiology
Hematology
Pulmonology

Background:

The COVID-19 pandemic highlights the need for understanding disease mechanisms to develop effective therapies.
Current understanding of COVID-19 related acute respiratory distress syndrome (ARDS) is incomplete.
Radiological findings in COVID-19 ARDS resemble high altitude pulmonary edema (HAPE), prompting investigation into shared pathophysiological pathways.

Purpose of the Study:

To propose a novel physiological mechanism for COVID-19 pathogenesis.
To explain the development of COVID-19 related ARDS.
To identify potential therapeutic targets based on the proposed mechanism.

Main Methods:

Review of recent research and clinical observations.
Analysis of bioinformatics prediction models.
Hypothesizing a novel mechanism involving red blood cell infection and hemoglobinopathy.

Main Results:

COVID-19 may infect red blood cells via CD147, leading to hemoglobin damage and hypoxemia.
Hypoxemia may induce pulmonary hypoxic vasoconstriction, causing HAPE-like lung lesions.
A vicious cycle of alveolar hypoxia and exaggerated hypoxemia is proposed.

Conclusions:

The proposed mechanism suggests COVID-19 ARDS may stem from hemoglobinopathy and HAPE-like pathophysiology.
Laboratory experiments are recommended to validate these hypotheses.
Potential adjunct therapies include exchange transfusion and anti-CD147 drugs.