The initial outbreak was called the "H1N1 influenza", or "Swine Flu" by American media. It is called pandemic H1N1/09 virus by the World Health Organization, while the U.S. Centers for Disease Control refer to it as "novel influenza A (H1N1)" or "2009 H1N1 flu". In the Netherlands, it was originally called "Pig Flu", but is now called "New Influenza A (H1N1)" by the national health institute, although the media and general population use the name "Mexican Flu". South Korea and Israel briefly considered calling it the "Mexican virus". Later, the South Korean press used "SI", short for "swine influenza". Taiwan suggested the names "H1N1 flu" or "new flu", which most local media adopted. The World Organization for Animal Health proposed the name "North American influenza". The European Commission adopted the term "novel flu virus".
The virus is a novel strain of influenza. Existing vaccines against seasonal flu provide no protection. A study at the U.S. Centers for Disease Control and Prevention (CDC) published in May 2009 found that children had no preexisting immunity to the new strain but that adults, particularly those over 60, had some degree of immunity. Children showed no cross-reactive antibody reaction to the new strain, adults aged 18 to 64 had 6-9%, and older adults 33%. Much reporting of early analysis repeated that the strain contained genes from five different flu viruses: North American swine influenza, North American avian influenza, human influenza, and two swine influenza viruses typically found in Asia and Europe.
Further analysis showed that several of the proteins of the virus are most similar to strains that cause mild symptoms in humans, leading virologist Wendy Barclay to suggest on May 1, 2009 that the initial indications are that the virus was unlikely to cause severe symptoms for most people. Other leading researchers indicated that all segments of the virus were in fact swine in origin, despite it being a multiple reassortment. The first complete genome sequence of the pandemic strain was deposited in public databases on April 27, 2009, by scientists from the U.S. Centers for Disease Control and Prevention in Atlanta. Scientists in Winnipeg later completed the full genetic sequencing of viruses from Mexico and Canada on May 6, 2009.
The Pandemic (H1N1) 2009 virus is contagious and is believed to spread from human to human in much the same way as seasonal flu. The most common mechanisms by which it spreads are by droplets from coughs and sneezes of infected people, and also potentially touching a surface or the hand of a person contaminated with the virus and then touching one's eyes, nose or mouth, although there is no direct evidence for this. The Pandemic (H1N1) 2009 virus is more contagious than seasonal flu, and infected people are contagious for longer than had been thought. The US CDC had recommended that people should wait at least a day after their fever subsides (usually 3–4 days after the onset of symptoms) before resuming normal activities, but it has been found that they can continue to shed virus for several days after that. The contagiousness of the virus may change as it mutates.
The virulence of swine flu virus is mild and the mortality rates are very low. In mid-2009 the US Centers for Disease Control and Prevention (CDC) noted that most infections were mild, similar to seasonal flu, and that recovery tended to be fairly quick. The number of deaths as of September 2009 is sometimes misleadingly said to be a tiny fraction of the annual number of deaths from seasonal flu, but comparisons of human fatality figures with seasonal influenza are prone to underestimate impact of the pandemic and the pandemic H1N1/09 virus was in fact the dominant strain of influenza causing illness in the 2009/10 flu season.
Research carried out at Imperial College London has shown that, unlike seasonal flu, the Pandemic (H1N1) 2009 virus can infect cells deep in the lungs. Seasonal flu can only infect cells with receptor type a2-6 which are typically located in the nose and throat but H1N1/09 can also infect cells with receptor type a2-3. This may explain why some patients experience severe respiratory symptoms. (The H5N1 virus is also able to infect cells deep in the lungs with receptor type a2-3 but cannot infect cells with receptor type a2-6 making it less contagious than H1N1/09.)
From April 2009 to November 2009, in the US, 3,900 people have died of the H1N1 pandemic virus, sometimes compared to 36,000 people per year die from the "common flu", mostly in winter, although the former figure is for confirmed cases, whereas the latter is an estimate. The death rate of H1N1 in the US could be calculated as less than 0.02% from November 2009 figures from the CDC, and has been explicitly calculated as 0.026% in England.