PARIS -- The strain of flu virus that has brewed in Mexico and unleashed a global health alert is beginning to shed some mystery but nagging questions remain unanswered, experts say.

Harnessing the power of genomics, the US Centers for Disease Control (CDC) has already sequenced the tiny pathogen and placed the data online for flu specialists around the world.

This has unveiled a new member of a well-known family of H1N1 influenza viruses -- a microbe built from bits of strains that have circulated among humans, birds and pigs and whose origins span three continents.

"We have some gene segments that are North American swine influenza viruses," Nancy Cox, director of the CDC's influenza division, said last week.

"Some gene segments are North American avian influenza viruses, one gene segment from a human influenza virus and two gene segments that are normally found from swine influenza viruses in Asia and in Europe."

The other big piece of news is this: the virus' genetic profile means it is apparently resistant to a cheap, commonly-used flu drug called amantadine, but responds to two newer antiviral treatments, Tamiflu and Relenza.

Many experts are deeply relieved by this.

They have long feared that the world's next flu pandemic could involve not just a strain that is potentially lethal, but one that is resistant to anti-viral weapons.

Yet beyond these two important bits of information, the virus is a puzzle that will only be unravelled by belts-and-braces epidemiology.

"You cannot move from (identifying) a structure to (understanding its) function," Angus Nicoll, head of the influenza program at the European Centre for Disease Prevention and Control (ECDC) in Stockholm, said on Tuesday.

"It's like, I look at a car and I say, 'well that looks rather pretty' but I don't know how well it's going to handle until I turn the engine on. Just by looking at the structure of it, you cannot tell everything."

The biggest questions are these: how contagious is the virus? And how virulent is it?

"We don't have information on how it acts, how it transmits," said Gregory Hartl of the World Health Organization (WHO).

Such questions can only be answered by reliable data: who falls sick from the virus and when and where; how many of them die or recover; whether they respond to treatment or do not need it; their age and health profile, and so on.

John Oxford, a top virologist at St. Bartholomew’s and the Royal London Hospital, said there was a strange discrepancy about figures at this early stage of the epidemic.

The only deaths have occurred in Mexico, nowhere else, he noted.

As of Tuesday, the country had 20 confirmed mortalities in a probable national death toll of 152, while the number of cases under observation in Mexico has reached 1,614. The next most affected country, the United States, has had 64 confirmed cases, none fatal.

"I would say it looks like a mild virus at the moment, certainly for people who have got it outside Mexico," said Oxford, who added that this striking difference in apparent lethality "is a bit of a black box."

One explanation for the difference could -- hypothetically -- be that patients in Mexico were treated too late or with insufficient antiviral drugs, he said.

Another -- again in the realms of theory -- is that as the weeks passed after the initial outbreak, the viral strain mutated into a less virulent form, said Oxford.

As a result, patients with only the milder versions of the virus were now showing up outside Mexico, according to this scenario.

Also unclear is where the virus and how the virus emerged.

The finger of suspicion points to a hog farm, given the well-known ability of pigs to harbor several strains of virus simultaneously, which allows the microbes to swap genes as they sloppily reproduce.

But only verification will determine if this is true, or whether more farms in other locations, and human intervention too, also played a role.