Back in school we memorized the parts of a cell: the cell wall, nucleus, Golgi bodies, lots of stuff.
But a virus is different. It's on the border of a living and nonliving collection of molecules, mostly proteins and a string of RNA or DNA. It doesn't eat or sleep; it's sole function is to parasitize its host cell and make copies of itself.
He says the spiky crown of the coronavirus is what makes it a hazard to humans.
"This particular virus has a piece of RNA, ribonucleic acid, that contains the genes for how it functions in the world," DeLucia said. "That string of RNA is encased in a fatty liquid membrane, like a fat droplet, and sticking out of that membrane are the viral proteins we've seen in various pictures. Those proteins direct how the virus engages and interacts with the cells of our body."
It's called the coronavirus because those spikes reminded its discoverers of a crown, or corona in Latin.
DeLucia says those spiky proteins on the surface of the virus allow it to infect our cells.
"It just so happens that this virus takes advantage of a receptor protein on the surface of human epithelial cells called ACE 2, or Angiotensin-Converting Enzyme 2 receptor."
The coronavirus is then pulled into the cell and begins replicating itself.
He says the developers of a coronavirus vaccine are targeting those spiky proteins.
"So if our bodies will make antibodies against that spike protein, it will prevent that spike protein from interacting with the ACE 2 receptor on our cells," he says.
The viral one-two punch
DeLucia says what makes the novel coronavirus so dangerous is how perfectly those spiky proteins match our cell receptors, and where in our body the virus attacks us.
"The virus filters down into our lower respiratory tract and binds with high affinity to cells there," he said. "And when those infected cells start dying, the airways get filled up with cellular debris."
He adds that not only does the virus kill respiratory tract cells, it triggers a cascade of inflammatory and immune responses.
"Our bodies are trying to fight off the virus, and that inflammatory response differs depending on the conditions of the infection and the person's particular immune system," DeLucia said.
He said the virus and the overactive immune response, lung inflammation in particular, together cause the large number of deaths.
From bats to humans
A recent study shows that the novel coronavirus shares 96% of genetic material with one found in bats, strong evidence that it jumped from them to humans.
DeLucia says it's just chance that mutations in the bat virus made it a perfect match for human epithelial cells. "That allows it to infect us with greater affinity than the typical virus jumping out of an animal to human," he said.
The novel coronavirus is actually called SARS-CoV-2, a new version of the SARS-CoV-1 virus we saw in 2002. But DeLucia says this SARS (Severe Acute Respiratory Syndrome) virus is more contagious than the SARS 'classic'.
"People who have no symptoms are able to easily transmit the new virus, which wasn't the case with SARS 1," he said.
If you remember, SARS 1 was contained because of aggressive isolation protocols, and it hasn't been seen since. That may not be the case with SARS 2.
The coronavirus family
According to DeLucia, the coronavirus group was not well studied before SARS 1.
"Some members of the coronavirus family are known to cause the common cold, but there are very few researchers who study these viruses," he said. "So, our understanding of their biology and how they affect our immune systems is poorly understood."
It also isn't known whether those who are infected develop immunity to the virus.
"The thinking is that people infected with the coronavirus won't suffer re-infections immediately," he said, pointing to data from China.
"It also indicates that the people working on vaccines will have a fighting chance of developing a vaccine that is meaningful," he added.
DeLucia says that viruses with RNA-based genetic material are prone to rapid mutations, but the novel coronavirus is different. It has a slower mutation rate because its RNA chain is longer than usual, and therefore more stable.
"That's the good news about these viruses," he said. "They don't change nearly as rapidly or quickly as, say, HIV or the influenza virus."
The virus' stability is good news for doctors treating patients and researchers working on a vaccine.
Will warm weather stop it?
The big question facing health officials and policy makers is when will the outbreak peak.
"That's a huge question," DeLucia said. "We are still in the logarithmic phase of virus infectivity," the steep slope of the upward curve. "And that means for every case we see, five to 10 cases will potentially appear several days to a week later."
"Without adequate testing to show what our underlying population infectious rate is, it's difficult to analyze what that curve looks like," he said.
He's not optimistic that warm weather will bring an end to its spread.
"Think about Australia," he said. "It's summer down there, and they have ongoing infections. So you know, all bets are off in terms of whether the heat will destroy the virus."
Even if the virus does take a summer break, it may return in the fall and start the infection cycle all over again.
But DeLucia said by then a vaccine might exist, along with antiviral therapies.
"So we'll be much better prepared, even if it does come back," he said. "Although we can't predict one way or the other at this time."
He said one lesson from the current outbreak is that knowledge is the best weapon against panic and fear. "Preparation is absolutely critical, and part of why we're not prepared today is because we haven't spent the money that we needed to study these things," he said.