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The Dirty Dog Jazz Café will remain closed until our jazz family can again safely gather in an intimate setting to hear live jazz. What makes the Dirty Dog and jazz so important in our lives is its ability to bring us closer together. For the moment we will have to stay close by staying apart. This necessary intermission will end, and jazz will once again leak out the Dirty Dog’s front door and smiling people will pour in.

See you then.


It is difficult enough to be isolated, but it is really hard not to know how your friends are faring. I miss the ease with which the staff of the Dirty Dog went about their business in a tight space. I would watch them pause to take in the music and listen to the musicians talk admiringly about the staff. Mutual respect brought people together in a strong bond. A tiny virus has separated them.  How is that possible? I sure don’t have a clue how a virus can shut down the whole world. I also never could figure out  how jazz artists can seamlessly improvise. Life has many mysteries. To some people that is a welcome challenge. They will try to find a way to understand and describe the world that will lift them a little bit out of it. Right now we are asked to just stay in place.

To get rid of some of the mystery it is helpful to understand why social distancing is necessary. It is hard to avoid experts trying to explain to us why we should screw up our lives for the common good. They want us to live in a bubble until the all clear alarm goes off. I personally believe them but want to know more. After we figure out how to defeat the coronavirus, maybe we will learn how jazz musicians can improvise as an

ensemble. Hopefully they will remember how to play together in the same room.

And when the virus is no longer we will have a chance to look back at those in our  community who rose above the challenges. Here are two giants of jazz who certainly gave us examples of a life well lived.


I was with my Dad on the first day in April when he passed away. The jazz world has now lost two jazzmen who were well known for being world class dads. They both passed away on  April 1 2020. They were both victims of the coronavirus that is described below.

ELLIS MARSALIS (November 14, 1934 – April 1, 2020)

Photo courtesy Mark L Brown

“The cause of his death came from complications of Covid-19, the disease caused by the coronavirus”, his son Branford said.

Ellis Marsalis was a pianist and an educator whose own abilities were sometimes overshadowed by his well known four musician sons.The Marsalises were widely understood to be jazz’s royal family. Wynton had become the founding artistic director of Jazz at Lincoln Center in New York, the world’s pre-eminent nonprofit organization devoted to jazz, and he has won the Pulitzer Prize for music. Branford is a world-renowned saxophonist and bandleader with three Grammys to his name. Delfeayo is a trombonist, and Jason is a drummer and vibraphonist, boh are well established as bandleaders.  Delfeayo and Jason have played the Dirty Dog while Branford and Wynton have graced the Detroit Jazz Festival.

Ellis Marsalis spent decades as a working musician and teacher in New Orleans. He was a beloved musician,mentor, husband and father.

Branford Marsalis said

“My dad was a giant of a musician and teacher, but an even greater father,” “He poured everything he had into making us the best of what we could be.”

Wynton Marsalis said

“My daddy passed away last night. We now join the worldwide family who are mourning grandfathers and grandmothers, mothers and fathers, sisters and brothers— kinfolk, friends, neighbors, colleagues, acquaintances and others.

What can one possibly say about loss in a time when there are many people losing folks that mean so much to them? One of my friends lost both her mother AND father just last week. We all grieve and experience things differently, and I’m sure each of my five brothers are feeling and dealing in their own way.

My daddy was a humble man with a lyrical sound that captured the spirit of place–New Orleans, the Crescent City, The Big Easy, the Curve. He was a stone-cold believer without extravagant tastes.

Like many parents, he sacrificed for us and made so much possible. Not only material things, but things of substance and beauty like the ability to hear complicated music and to read books; to see and to contemplate art; to be philosophical and kind, but to also understand that a time and place may require a pugilistic-minded expression of ignorance.

His example for all of us who were his students (a big extended family from everywhere), showed us to be patient and to want to learn and to respect teaching and thinking and to embrace the joy of seriousness. He taught us that you could be conscious and stand your ground with an opinion rooted ‘in something’ even if it was overwhelmingly unfashionable. And that if it mattered to someone, it mattered.

I haven’t cried because the pain is so deep….it doesn’t even hurt. He was absolutely my man. He knew how much I loved him, and I knew he loved me (though he was not given to any type of demonstrative expression of it). As a boy, I followed him on so many underpopulated gigs in unglamorous places, and there, in the passing years, learned what it meant to believe in the substance of a fundamental idea whose only verification was your belief.

I only ever wanted to do better things to impress HIM. He was my North Star and the only opinion that really deep down mattered to me was his because I grew up seeing how much he struggled and sacrificed to represent and teach vital human values that floated far above the stifling segregation and prejudice that defined his youth but, strangely enough, also imbued his art with an even more pungent and biting accuracy.

But for all of that, I guess he was like all of us; he did the best he could, did great things, had blind spots and made mistakes, fought with his spouse, had problems paying bills, worried about his kids and other people’s, rooted for losing teams, loved gumbo and red beans, and my momma’s pecan pie. But unlike a healthy portion of us, he really didn’t complain about stuff. No matter how bad it was.

A most fair-minded, large-spirited, generous, philanthropic (with whatever he had), open-minded person is gone. Ironically, when we spoke just 5 or 6 days ago about this precarious moment in the world and the many warnings he received ‘to be careful, because it wasn’t his time to pass from COVID’, he told me, “Man, I don’t determine the time. A lot of people are losing loved ones. Yours will be no more painful or significant than anybody else’s”.

That was him, “in a nutshell”, (as he would say before talking for another 15 minutes without pause).

In that conversation, we didn’t know that we were prophesying. But he went out soon after as he lived—-without complaint or complication. The nurse asked him, “Are you breathing ok?” as the oxygen was being steadily increased from 3 to 8, to too late, he replied, ”Yeah. I’m fine.”

For me, there is no sorrow only joy. He went on down the Good Kings Highway as was his way, a jazz man, “with grace and gratitude.” And I am grateful to have known him.”

BUCKY PIZZARELLI (January 9, 1926 – April 1, 2020)

Photo courtesy of John Dunn

His son the guitarist and singer John Pizzarelli said the cause was the coronavirus.

A master of the subtle art of rhythm guitar as well as a gifted soloist, Bucky Pizzarelli  can be heard on hundreds of records in various genres. He toured with Benny Goodman and was a longtime member of the “Tonight Show” orchestra.

His unlikely nickname was bestowed on him by his father, who as a teenager had decided to explore the Wild West he knew only from movies. He left New Jersey to spent some time as a ranch hand in Odessa, Texas. He returned to New Jersey with a lot of memories and that would lead him to nickname his young son Buckskin. Shortened to Bucky, the name stuck.

Mr. Pizzarelli with his son John  Credit…Heidi Schumann for The New York Times


Family was important to Bucky so when Johnny Carson moved “The Tonight Show” to California from New York in 1972, he remained behind. He did not want to uproot his four school-age children from their New Jersey home. He continued to perform frequently in New York nightclubs as the leader of small groups, and as a sideman with leading jazz musicians like the saxophonists Zoot Sims, Bud Freeman,  Joe Venuti.and the violinist Stéphane Grappelli, Bucky Pizzarelli was a mainstay of the New York jazz scene where he often performed with his son. John. 

Bucky and John often would be joined by Mr. Pizzarelli’s other son, Martin, a bassist, and John’s wife, the vocalist Jessica Molaskey,. John Pizzarelli once described them as “the von Trapp family on martinis.”

Ellis’ and Bucky’s lives were full of twists, turns ups and downs, yet these two celebrated jazzmen gave more than they took, with class and grace. They gave us a blueprint of how we should be going forward.

These are not our easiest days. but from time to time I am trying to reflect only on the possible. It is possible that a miraculous drug will allow us to safely return to normal. It is also possible that everyone around us keeps their distance long enough and no one spreads infection. But for now we are being asked to remain in place for at least a month. There is little surety of when it will be safe to resume normal life as we know little about this new strain of virus.

I thought it would be helpful to know as much as we can comprehend. I found this article that is really well written about this very clever virus. It will inform and make us cautious enough to defeat this threat.

Stay safe,

John Osler


This is the most-read story in Washington Post history. “It tries to explain how an outbreak like coronavirus spreads and what it takes to “flatten the curve.” (The Washington Post)


The Washington Post is providing this story for free so that all readers have access to this important information about the coronavirus.

The article is by Sarah Kaplan, William Wan and Joel Achenbach

Viruses have spent billions of years perfecting the art of surviving without living — a frighteningly effective strategy that makes them a potent threat in today’s world.

That’s especially true of the deadly new coronavirus that has brought global society to a screeching halt. It’s little more than a packet of genetic material surrounded by a spiky protein shell one-thousandth the width of an eyelash, and it leads such a zombielike existence that it’s barely considered a living organism.

But as soon as it gets into a human airway, the virus hijacks our cells to create millions more versions of itself.

There is a certain evil genius to how this coronavirus pathogen works: It finds easy purchase in humans without them knowing. Before its first host even develops symptoms, it is already spreading its replicas everywhere, moving onto its next victim. It is powerfully deadly in some but mild enough in others to escape containment. And for now, we have no way of stopping it.

As researchers race to develop drugs and vaccines for the disease that has already sickened 350,000 and killed more than 15,000 people, and counting, this is a scientific portrait of what they are up against.

‘Between chemistry and biology’

Respiratory viruses tend to infect and replicate in two places: In the nose and throat, where they are highly contagious, or lower in the lungs, where they spread less easily but are much more deadly.

This new coronavirus, SARS-CoV-2, adeptly cuts the difference. It dwells in the upper respiratory tract, where it is easily sneezed or coughed onto its next victim. But in some patients, it can lodge itself deep within the lungs, where the disease can kill. That combination gives it the contagiousness of some colds, along with some of the lethality of its close molecular cousin SARS, which caused a 2002-2003 outbreak in Asia.

Another insidious characteristic of this virus: By giving up that bit of lethality, its symptoms emerge less readily than those of SARS, which means people often pass it to others before they even know they have it.

It is, in other words, just sneaky enough to wreak worldwide havoc.

Viruses much like this one have been responsible for many of the most destructive outbreaks of the past 100 years: the flus of 1918, 1957 and 1968; and SARS, MERS and Ebola. Like the coronavirus, all these diseases are zoonotic — they jumped from an animal population into humans. And all are caused by viruses that encode their genetic material in RNA. That’s no coincidence, scientists say. The zombielike existence of RNA viruses makes them easy to catch and hard to kill.

Outside a host, viruses are dormant. They have none of the traditional trappings of life: metabolism, motion, the ability to reproduce. And they can last this way for quite a long time. Recent laboratory research showed that, although SARS-CoV-2 typically degrades in minutes or a few hours outside a host, some particles can remain viable — potentially infectious — on cardboard for up to 24 hours and on plastic and stainless steel for up to three days. In 2014, a virus frozen in permafrost for 30,000 years that scientists retrieved was able to infect an amoeba after being revived in the lab.

When viruses encounter a host, they use proteins on their surfaces to unlock and invade its unsuspecting cells. Then they take control of those cells’ molecular machinery to produce and assemble the materials needed for more viruses.

“It’s switching between alive and not alive,” said Gary Whittaker, a Cornell University professor of virology. He described a virus as being somewhere “between chemistry and biology.”

Among RNA viruses, coronaviruses — named for the protein spikes that adorn them like points of a crown — are unique for their size and relative sophistication. They are three times bigger than the pathogens that cause dengue, West Nile and Zika, and are capable of producing extra proteins that bolster their success.

“Let’s say dengue has a tool belt with only one hammer,” said Vineet Menachery, a virologist at the University of Texas Medical Branch. This coronavirus has three different hammers, each for a different situation.

Among those tools is a proofreading protein, which allows coronaviruses to fix some errors that happen during the replication process. They can still mutate faster than bacteria but are less likely to produce offspring so riddled with detrimental mutations that they can’t survive.

Meanwhile, the ability to change helps the germ adapt to new environments, whether it’s a camel’s gut or the airway of a human unknowingly granting it entry with an inadvertent scratch of her nose.

Scientists believe that the SARS virus originated as a bat virus that reached humans via civet cats sold in animal markets. This current virus, which can also be traced to bats, is thought to have had an intermediate host, possibly an endangered scaly anteater called a pangolin.

“I think nature has been telling us over the course of 20 years that, ‘Hey, coronaviruses that start out in bats can cause pandemics in humans, and we have to think of them as being like influenza, as long-term threats,’” said Jeffery Taubenberger, virologist with the National Institute of Allergy and Infectious Diseases.

Funding for research on coronaviruses increased after the SARS outbreak, but in recent years that funding has dried up, Taubenberger said. Such viruses usually simply cause colds and were not considered as important as other viral pathogens, he said.

Once inside a cell, a virus can make 10,000 copies of itself in a matter of hours. Within a few days, the infected person will carry hundreds of millions of viral particles in every teaspoon of his blood.

The onslaught triggers an intense response from the host’s immune system: Defensive chemicals are released. The body’s temperature rises, causing fever. Armies of germ-eating white blood cells swarm the infected region. Often, this response is what makes a person feel sick.

Andrew Pekosz, a virologist at Johns Hopkins University, compared viruses to particularly destructive burglars: They break into your home, eat your food, use your furniture and have 10,000 babies. “And then they leave the place trashed,” he said.

Unfortunately, humans have few defenses against these burglars.

Most antimicrobials work by interfering with the functions of the germs they target. For example, penicillin blocks a molecule used by bacteria to build their cell walls. The drug works against thousands of kinds of bacteria, but because human cells don’t use that protein, we can ingest it without being harmed.

But viruses function through us. With no cellular machinery of their own, they become intertwined with ours. Their proteins are our proteins. Their weaknesses are our weaknesses. Most drugs that might hurt them would hurt us, too.

For this reason, antiviral drugs must be extremely targeted and specific, said Stanford virologist Karla Kirkegaard. They tend to target proteins produced by the virus (using our cellular machinery) as part of its replication process. These proteins are unique to their viruses. This means the drugs that fight one disease generally don’t work across multiple ones.

And because viruses evolve so quickly, the few treatments scientists do manage to develop don’t always work for long. This is why scientists must constantly develop new drugs to treat HIV, and why patients take a “cocktail” of antivirals that viruses must mutate multiple times to resist.

“Modern medicine is constantly needing to catch up to new emerging viruses,” Kirkegaard said.

Understanding these proteins could be critical to developing a vaccine, said Alessandro Sette, head of the center for infectious disease at the La Jolla Institute for Immunology. Previous research has shown that the spike proteins on SARS are what trigger the immune system’s protective response. In a paper published this month, Sette found the same is true of SARS-CoV-2.

This gives scientists reason for optimism, according to Sette. It affirms researchers’ hunch that the spike protein is a good target for vaccines. If people are inoculated with a version of that protein, it could teach their immune system to recognize the virus and allow them to respond to the invader more quickly.

“It also says the novel coronavirus is not that novel,” Sette said.

And if SARS-CoV-2 is not so different from its older cousin SARS, then the virus is probably not evolving very fast, giving scientists developing vaccines time to catch up.

In the meantime, Kirkegaard said, the best weapons we have against the coronavirus are public health measures, such as testing and social distancing, and our own immune systems.

For all its evil genius and efficient, lethal design, Kirkegaard said, “the virus doesn’t really want to kill us. It’s good for them, good for their population, if you’re walking around being perfectly healthy.”

Evolutionarily speaking, experts believe, the ultimate goal of viruses is to be contagious while also gentle on their hosts — less a destructive burglar and more a considerate house guest.

That’s because highly lethal viruses like SARS and Ebola tend to burn themselves out, leaving no one alive to spread them.

But a germ that’s merely annoying can perpetuate itself indefinitely. One 2014 study found that the virus causing oral herpes has been with the human lineage for 6 million years.

Seen through this lens, the novel coronavirus that is killing thousands across the world is still early in its life. It replicates destructively, unaware that there’s a better way to survive.

But bit by bit, over time, its RNA will change. Until one day, not so far in the future, it will be just another one of the handful of common cold coronaviruses that circulate every year, giving us a cough or sniffle and nothing more.

That would be nice.

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