From the very article you've linked:
Making a vaccine for a new flu strain is very different from making a vaccine for something completely new like COVID-19, the novel coronavirus that emerged in 2019. Doctors and scientists first developed viable flu vaccines in the 1940s, so they were not starting from scratch when they went to work on the 1957 flu vaccine. Still, Hilleman bypassed regulatory agencies in his efforts to push the vaccine forward because he worried those agencies would slow the process down.
And an apt analogy from The Atlantic on testing:
Like other drugs, vaccines require a long testing process to see whether they indeed protect people from disease, and do so safely. What this company—and others—has done is copy a bit of the virus’s RNA that one day could prove to work as a vaccine. It’s a promising first step, but to call it a discovery is like announcing a new surgery after sharpening a scalpel.
Though genetic sequencing is now extremely fast, making vaccines is as much art as science. It involves finding a viral sequence that will reliably cause a protective immune-system memory but not trigger an acute inflammatory response that would itself cause symptoms. (While the influenza vaccine cannot cause the flu, the CDC warns that it can cause “flu-like symptoms.”) Hitting this sweet spot requires testing, first in lab models and animals, and eventually in people. One does not simply ship a billion viral gene fragments around the world to be injected into everyone at the moment of discovery.
And since SARS is the closest relevant relative of Covid-19 (same source):
During the SARS outbreak in 2003, researchers moved from obtaining the genomic sequence of the virus and into a phase 1 clinical trial of a vaccine in 20 months. Fauci wrote that his team has since compressed that timeline to just over three months for other viruses, and for the new coronavirus, “they hope to move even faster.”
[...] Overall, if all pieces fell into place, Hatchett guesses it would be 12 to 18 months before an initial product could be deemed safe and effective. That timeline represents “a vast acceleration compared with the history of vaccine development,” he told me. But it’s also unprecedentedly ambitious. “Even to propose such a timeline at this point must be regarded as hugely aspirational,” he added.
Fauci’s initial optimism seemed to wane, too. Last week he said that the process of vaccine development was proving “very difficult and very frustrating.” For all the advances in basic science, the process cannot proceed to an actual vaccine without extensive clinical testing, which requires manufacturing many vaccines and meticulously monitoring outcomes in people. [...]
“If we’re putting all our hopes in a vaccine as being the answer, we’re in trouble,” Jason Schwartz, an assistant professor at Yale School of Public Health who studies vaccine policy, told me. The best-case scenario, as Schwartz sees it, is the one in which this vaccine development happens far too late to make a difference for the current outbreak. The real problem is that preparedness for this outbreak should have been happening for the past decade, ever since SARS. “Had we not set the SARS-vaccine-research program aside, we would have had a lot more of this foundational work that we could apply to this new, closely related virus,” he said. But, as with Ebola, government funding and pharmaceutical-industry development evaporated once the sense of emergency lifted. “Some very early research ended up sitting on a shelf because that outbreak ended before a vaccine needed to be aggressively developed.”
Some experts have expressed skepticism that current single-focus on the spike protein of SARS-CoV-2 would suffice:
The Moderna vaccine consists of an RNA molecule. Like many of the other SARS-CoV-2 vaccines in development, it is designed to train the immune system to make antibodies that recognize and block the spike protein that the virus uses to enter human cells.
“I think it’s reasonable as a first pass, but we will learn that, perhaps, antibody responses to the spike exclusively may not be the whole story,” says [Michael] Diamond [--a viral immunologist at Washington University in St. Louis, Missouri]. A successful SARS-CoV-2 vaccine might need to prompt the body to generate antibodies that block other viral proteins, for instance, or make T cells that can recognize and kill infected cells.
Also (same source):
If humans do develop immunity, how long does it last?
That’s another big unknown. Immunity is short-lived for the coronaviruses that cause common colds; even people who have high levels of antibodies against these viruses can still become infected, says Stanley Perlman, a coronavirologist at the University of Iowa in Iowa City.
The evidence is more equivocal for the two other coronaviruses that have triggered epidemics: those that cause severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). Perlman says his team has found that after people recover from MERS, their antibodies against the virus drop precipitously. He also says that his team has gathered data — not yet published — showing that SARS antibodies are still present in the body 15 years after infection. But it’s not clear whether this immune response is enough to prevent reinfection. “We don’t have good evidence of long-lasting immunity, but we also don’t have really good data from both SARS and MERS,” Perlman adds.
The same source discusses the risks of "disease enhancement" which are thought to be fairly low for SARS-CoV-2, but not inexistent. Actually Wikipedia has a somewhat deeper/different perspective on this:
Non-human primates vaccinated with modified vaccinia Ankara (MVA) virus encoding full-length SARS-COV spike glycoprotein and challenged with the SARS-CoV virus had lower viral loads but suffered from acute lung injury due to antibody enhancement. [...] Antibody-dependent enhancement as been observed in both severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) animal models allowing the respective viruses to enter cells expressing Fc𝛾R including myeloid lineage cells.
Moreover, antibody-dependent enhancement of acute lung injury has been documented in both SARS and MERS. Rabbits intranasally infected with MERS-COV developed a pulmonary infection characterized by viremia and perivascular inflammation of the lung. Interestingly, when challenged with MERS-COV a second time, rabbits were not protected from disease, despite having measurable antibody responses. Moreover, the rabbits developed more severe lung disease on re-exposure to MERS-COV. Similarly in SARS, mice vaccinated against SARS-COV had measurable antibody responses. However, all mice within two days of challenge developed lung pathology. The lack of protection from antibodies, and exacerbation of lung pathology has been a major challenge for coronavirus vaccine development and may similarly impact SARS-COV-2 vaccine research.