The coronavirus’s late-winter attack on the national capital region came from multiple, separate introductions, and the pathogen quickly spread among people who had not traveled outside the region recently or had known contact with infected people, according to a genetic analysis of virus samples from more than 100 patients.

The study, from Johns Hopkins University scientists, highlights the challenge in preventing the arrival and spread of the highly contagious virus within a region that anchors the Northeast Corridor and boasts three international airports and a highly mobile population.

The researchers report high levels of genetic diversity in the 114 genomes they completed, based on samples from patients treated in Johns Hopkins-affiliated hospitals in Maryland and the District from March 11 to March 31. The research has not yet been published in a peer-reviewed journal but has been posted online at the preprint server medRxiv.

There are five major genetic groupings, known as clades, of the novel coronavirus, and all five were represented in the viral samples from patients. That suggested a single introduction could not have triggered all of those March infections. Instead, the virus must have been arriving at many different times.

Another important finding: The different genetic profiles of the virus infecting people in the Washington region did not correspond to any clear difference in disease severity among patients.

Where the virus came from is not covered by the report, and the researchers could not tell if the introductions came directly from places overseas or from points within the United States. A study by scientists at New York University showed that much of the early coronavirus spread in New York City was due to introductions from Europe.

“There were probably five or more introductions sometime before the end of March,” said study co-author Shirlee Wohl, a genomics expert at the Johns Hopkins Bloomberg School of Public Health. “Even as early as March, the first three weeks of the outbreak, we were already seeing diversity rivaling the global diversity of this virus.”

This latest study and others preceding it provide clear evidence that the United States, and certainly big cities on the East Coast, were dealing with community spread of the virus well in advance of major shutdown efforts, including the Trump administration’s decision to ban travel from most European countries starting March 13.

“The number of introductions that occurred would make it difficult to enact a travel ban, would make it difficult to do anything except screen everybody with a diagnostic test,” said study co-author Peter Thielen, a molecular biologist at Johns Hopkins Applied Physics Laboratory.

The diversity of virus in the national capital region “highlights the connectedness of the region to both the national and global epidemic, and the challenges that would likely confront any control strategy predicated on low rates of introduction,” the report states.

The NYU study found that the virus may have been spreading in New York as early as late January. A scientific conference attended by international travelers in Boston in late February has been dubbed a “superspreader” event that seeded the virus in many places in the United States.

According to the new Hopkins report, Maryland reported its first case of covid-19, the disease caused by the virus, on March 5. Two days later, the District and Virginia reported their first cases. Those patients were probably infected many days before, Thielen said.

Only 22 percent of the patients studied by the Hopkins researchers had traveled to places with known outbreaks of the virus, the report said.

All viruses mutate, and by the time the coronavirus reached the national capital region, it had mutated slightly. The Hopkins scientists counted a total of 153 genetic mutations in their virus samples, compared with the reference sample from Wuhan, China, where the outbreak is believed to have ignited.

But most mutations actually impair the fitness of the virus or have no effect at all. The Hopkins research did not find evidence that the variants of the virus led to any difference in patient outcomes, regardless of sex, race, symptoms or underlying conditions.

“The diversity of virus genetics, clinical symptoms, and patient outcomes suggests that viral mutations are not the main driver of clinical presentation,” the new study states.

Several recent studies have suggested that one mutation, known as D614G, has altered the structure of the spike protein of the virus in a way that could potentially facilitate transmission. That mutation is now seen across the planet, including in many of the virus samples in the national capital region, but the scientific community has not endorsed the conjecture that the virus has become more contagious.

Thielen pointed out that, without a vaccine, and with relatively few people having been exposed and having antibodies to the virus, the coronavirus is sailing along with no natural or artificial obstacles.

“Right now, with no immunity in the population, there’s not much pressure on the virus to evade immunity, which is what would drive transmissibility,” Thielen said.