Yellow Ferry Resident Takes on Covid-19

Dr. Jay Lalezari  |  photo from Bing  |  post by Maria Finn

Dr. Jay Lalezari lives at Yellow Ferry Harbor. You might see him walking his dog Kaya on the nearby spit, dancing at Silent Disco, or unloading his dusty van post Burning Man. He’s not your typical doctor and you won’t find him with a stethoscope. Rather, he’s been on the front lines of developing drugs to stop deadly viruses since the 80s. He’s the founder of Quest Clinical Research, a small, independent clinic in San Francisco that was at the epicenter of the AIDS crisis and has conducted clinical trials for antiviral medications and vaccines for HIV, Hepatitis B and C, HPV, influenza, and other illnesses. He had been testing a drug called Leronlimab for patients with HIV and women with breast cancer. It has also demonstrated early exciting results at treating COVID-19 though it is still in clinical trials. I sat down with Dr. Jay to learn more about viruses and their findings on this medication, Leronlimab.

How did you become involved with clinical trials for viruses?

I came to SF in 1986 during the throes of the AIDS epidemic. My mom survived the Holocaust. My dad is a founding father of modern immunology. I myself was a failed homosexual. I was drawn to AIDS like a moth to a flame.

What did you learn from the AIDS virus?

I witnessed unspeakable suffering as well as the presence of Grace as antiviral drug development scored a huge victory and HIV became a chronic manageable disease. I also found that AIDS made people wary of physical intimacy. I was deeply offended by that. Life affords us a few pleasures to compensate for all the rest. Having sex become unsafe for so many including young people seemed utterly unfair.

When did you move to the houseboats?

My ex-wife actually relocated me in September of 2010. I moved onto Issaquah Dock and began my post-divorce recovery. I was miserable at first and hardly anyone would even speak to me. But moving onto the houseboats saved my life. When a houseboat became available on Yellow Ferry Dock in spring of 2011, I jumped on it.

How did AIDS change the pharmaceutical industry?

Treating viral infections is different and more complicated than dealing with other infections. Viruses are simpler pathogens and harder to distinguish from the human host. Exploiting those differences is tricky. Up until now, the two great successes in clinical virology have been HIV and Hepatitis C— and soon, I believe, COVID-19.

You were testing Leronlimab on cancer cells when COVID-19 hit. Why did you think it might work for this virus?

Leronlimab is an antibody that blocks a cell receptor called CCR5. The CCR5 receptor just happens to be a key doorway HIV uses to get inside a cell so that’s why we developed it as an HIV treatment. But the actual function of CCR5 inside our body is to direct cell movement and function. Breast, prostate, and a few other cancers co-opt the immune system to support their growth by using the CCR5 receptor to control cell movement and function. We were targeting that role of CCR5 to support cancer cell growth when COVID-19 hit. Our early signals of success in breast cancer led us to believe we could impact the inflammation, or cytokine storm, that is killing patients with Covid-19 since it is the same cell movement and function controlled by CCR5 that is involved. And, as incredible as it sounds, I believe we got very lucky and that  Leronlimab will be shown to work better than anyone could ever have imagined.

How did you first know this drug would work on COVID-19?

It’s a peculiar situation where the drug demonstrated its efficacy before we ever got to randomized, placebo-controlled, clinical studies. Leronlimab has been given on an emergency basis to over 60 individuals in the US who were in dire condition due to COVID-19. What we saw in a group of those patients at day three after a single dose is reversal of severe immune exhaustion, calming of the cytokine storm and even decreases in viral load. There is nothing subtle or ambiguous about these amazing results and we’ve seen this in every patient we’ve treated and evaluated. We were also fortunate to identify the cytokine that appears to be driving the whole inflammatory mess. It’s called RANTES. COVID-19 is a RANTES disease—RANTES is an immune protein whose whole job is to bind CCR5 and drive inflammation. By blocking CCR5, we just happened to shut down the key driver of the whole inflammatory cascade.

Where is the drug now?

We are still waiting for the results of randomized, placebo-controlled studies. In the meantime, the FDA has been distracted by the foolishness around hydroxychloroquine and Remdesivir. I believe the former is more harmful than helpful, and the latter is at best marginally helpful and only if started very early. I believe the time and energy those two drugs have taken up has prevented the FDA from seeing or understanding what’s happening with Leronlimab.

So what are your plans with Leronlimab for now?

We’ll have initial randomized, placebo-controlled data by early July. We’ll see what happens then. I should also mention that the drug has now been given to over 900 patients without a discernible safety issue. The drug is extremely safe. And I believe very soon we’ll have the clinical data to show the world just how well it works in Covid-19.