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Ahram Online
Dr. Ashraf Ibrahim, a lead investigator at Lundquist Institute and Professor of Infectious Diseases at UCLA, explains to Ahram Online the causes behind the spread of Mucormycosis (black fungus) across India, and the precautionary measures to reduce infection.
Born and raised in Kuwait to Arab Expatriate parents, Dr. Ibrahim spent 30 years of his career in microbial physiology and pathogenesis in the US.
Over the last seven years, Dr. Ibrahim has been developing antibody that stems the spread of the black fungus.
Based on the animal trials, the new therapy showed promising effects. Still, more studies and trials on humans should be pursued before the drug wins clinical approval.
What is the efficacy of the new black fungus drug on which you have been working, compared to other approved therapies?
We are developing a humanized monoclonal antibody (immunotherapy) to treat black mould infection, which is better known in the scientific community as Mucormycosis. It is a lethal infection with 50-100% lethality (depending on the site of infection and the status of the patient). In mice, the immunotherapy outperforms any antifungal drug currently approved for treating the infection.
More important, the combination therapy of antifungal drug and immunotherapy is highly superior to antifungal therapy in mice. We get almost complete protection against the disease with the combination therapy vs. 10-40% protection with antifungal drug therapy alone. With such a lethal disease, it is important to realize that the immunotherapy is not intended to be administered alone but rather as a combination of the therapy with antifungal drugs.
What are the causes behind the spread of the black and the white fungus in India?
India has been known to have a very high number of Mucormycosis cases prior to COVID-19. One population-based study estimated the number of Mucormycosis cases at more than 200,000 patients per year. Compare this to few thousand cases in the US or Europe. The increased number of cases in India is probably due to the large number of uncontrolled diabetic cases among Indian citizens.
Another important factor predisposing for black fungus is immunosuppression with cortisone. In COVID-19 patients, the combination of uncontrolled diabetes with high dose cortisone to control the exuberant inflammatory immune response resulting from COVID-19 infection represents a perfect storm for black fungus infection and worst outcome.
Another thing to keep in mind is the tropical environment present in India with high humidity. Fungi in general thrives in humid environment and this make for high load of fungal spores in the environment including those causing black fungal infection.
Some health authorities in India have called for declaring the rise of black fungus an epidemic. What is your comment on that?
With more than 7000 confirmed cases in two months, this is absolutely an epidemic and genuinely concerning. I hear that they are running into shortage of critical antifungal drugs to treat the infection. This is a disease which, if not attended to immediately with a combination of surgical removal of infected tissues when possible and antifungal therapy, is often 100% lethal.
Which measures should be taken to avoid black fungus and white fungus infection?
Controlled diabetes is a must and caution in administering corticosteroids (cortisone in dosing and duration) is advisable. Trying to figure out the source of infection in these patients is also important. It could be happening from humidifiers or contaminated air cylinders. It is hard to tell what the source of infection is, but this needs to be looked at since the numbers are alarming.
Would you explain the mechanism of the new antibody?
The antibody is designed to target a cell surface protein that is critical in allowing the fungus to bind and invade human cells. In other words, the antibody prevents the fungus from invading human tissues and cause widespread infection. The antibody also allow human immune cells –white blood cells — to better recognize the invading fungus and attack it.
Could other infectious diseases be treated by this new drug; ie, the white fungus (aspergillosis)?
This is a monoclonal antibody specific to (black fungus) since the target molecule is only present in fungi that cause Mucormycosis. However, we are working on another antibody, that is in an animal model, which is effective in treating white fungus.
When do you expect the human clinical trials to start? and be approved medically by drug regulators?
It all depends on how soon we can raise US $5-10 Million. If we are reliant on NIH funding, I expect it would take another 4 years to finish manufacturing and start Phase I clinical trial. It will be another 4-5 years to finish a Phase II clinical trial and approval (again due to funding issues). If we have the money upfront, we can be in Phase I clinical trial within one year and another 2 years for a Phase II and approval.
