AG index page FAO homepage
Print this page | Close

H7N9 Background

On 31 March 2013, the authorities of the People's Republic of China reported the first human cases of infection with the novel avian influenza A(H7N9) to the World Health Organization in line with the International Health Regulations of 2007.


The disease situation in humans continues to evolve, with new cases reported regularly by the Chinese authorities (see H7N9 Situation Updates ). Cases have been confined to China with the exception of tourists testing positive in other countries but nevertheless linked to China as the place of exposure. Human H7N9 infections follow a seasonal pattern peaking in the winter months with most cases observed between October and March and sporadic cases during the summer.


Around 38 percent of reported human infections have had a fatal outcome. Reports to the World Health Organization (WHO) suggest that 80 percent of human cases have had direct or indirect contact with live poultry prior to the onset of disease, including LBM visits, transportation, slaughtering and handling of poultry.


This is the first time that a low pathogenic (LPAI) influenza A virus of the H7N9 subtype has been identified in humans, and only subsequently in domestic poultry (chickens, domestic pigeons and a few ducks) through follow-up virological surveillance in live bird markets (LBMs) linked to human cases. Extensive poultry surveillance in neighbouring countries or those with poultry trade links to China has not detected the virus so far.


Origin of H7N9


Influenza A(H7N9) evolved through several reassortment events putatively from early 2012 onwards.


The four parental viruses have been previously detected in wild birds (H7 virus and N9 viruses) and chickens (two different H9N2 viruses) in Asia.


The H7N9 virus was first detected in March 2013 in two human cases in China. Since then, the virus continues to antigenetically evolve and to undergo reassortment with locally circulating H9N2 viruses.


Avian infection with H7N9


The virus does not cause disease in domestic poultry. This implies: i) poultry flocks can be infected without showing clinical signs of disease; and ii) laboratory testing represents the only way to confirm infection in poultry.

The People’s Republic of China continues to report virus detections in poultry and the environment.
Laboratory studies show that:

  1. Inoculated chickens and quail shed high amounts of virus without showing signs of disease. Transmission to naïve direct contact chickens and quails occurs readily.
  2. Inoculated geese and pigeons shed little virus, as did mallard and Pekin ducks. Muscovy ducks showed an intermediate amount of virus shedding. None of the animals showed any clinical sign.
  3. Oropharyngeal shedding has been much higher than cloacal shedding. Oropharyngeal swabs are therefore recommended for sampling.
  4. Inoculated passerines/songbirds (finches, sparrows) and a parakeet species (budgerigar) shed intermediate amounts of H7N9 and transmitted the virus inefficiently, possibly via shared water. Disease signs or death were observed in a few animals.

Wild birds including song birds kept in captivity are not believed to play a role in the transmission and persistence of this virus. Nevertheless, one infected tree sparrow was detected through active surveillance in Shanghai, and experimental infection of sparrows and other birds kept in captivity demonstrated that some birds shed virus for up to 8 days with limited transmission to other birds in contact.


Human infection


The strain of influenza A(H7N9) virus that emerged in 2013 is able to infect humans and cause severe disease .There had been no previous reports of infection of humans with viruses of the H7N9 subtype prior to this time. Information on human infection with influenza A(H7N9) is available from WHO.

Reports suggest most human cases had direct or indirect contact with poultry prior to the onset of disease. Case control studies suggest contact with poultry or a visit to a live poultry market in the two weeks prior to disease inset was a significant risk factor. In a number of cases where testing of poultry or environmental samples from markets associated with human cases was performed, H7N9 virus has been detected.   

More specifically, cases have been reported in humans who:

  • visited live bird market;
  • slaughtered poultry or pigeons;
  • transported poultry;
  • brought live poultry into their home.

WHO reports that there is no evidence suggesting sustained human-to-human transmission.
Influenza A(H7N9) virus appears to infect humans more easily than H5N1 highly pathogenic avian influenza based on its genetic properties for adaptation to mammalian cells.


General facts on avian influenza

  • Aquatic wild birds especially Anseriformes and Charadriformes are the reservoir for influenza viruses, generally without showing any signs of disease.
  • Spill over of influenza virus from wild birds to domestic poultry occurs  regularly through direct and indirect contact
  • Some influenza virus subtypes from wild birds have adapted to poultry and some cause disease.
  • Avian influenza viruses in poultry can be low pathogenic (i.e. causing little or no signs of disease), or highly pathogenic (i.e. resulting in severe disease and high mortality).
  • Low pathogenic viruses of the H5 and H7 subtype can mutate into highly pathogenic viruses.


Other zoonotic influenza viruses


A range of influenza viruses from domestic animals have caused zoonotic infections. Two of the most significant examples are H5N1 highly pathogenic avian influenza (HPAI) and pandemic influenza A(H1N1) 2009.


  • Outbreak in Southeast Asia started in 2003, although the virus was already documented in China in 1996 with the first reported zoonotic cases in 1997 in Hong Kong SAR.
  • Infects numerous avian species, both domestic and wild.
  • Rarely infects humans, and has also been detected in a range of mammals including cats, tigers, leopards, pigs, lions, civets.
  • Transmitted from birds to birds and birds to humans (or other mammals).
  • Range of the virus extended to Central Asia, Europe, parts of Middle East and some countries in Africa in 2005–2006 and to south Asia in 2006 and 2007.
  • In late 2014 and 2015 H5N1 HPAI was re-introduced into poultry populations in West Africa, the Middle East and South Asia, while Eastern Europe reported findings in wild birds and sporadic poultry outbreaks.


A(H1N1) 2009:

  • Infects humans and swine species pigs and causes a low mortality illness comparable to seasonal influenza viruses in humans.
  • Was first detected in North America in early 2009 and spread worldwide among humans due to the lack of immunity to this novel virus in the human population.
  • WHO declared the beginning of the post-pandemic period in August 2010. It is now considered a seasonal human virus and included in the trivalent seasonal influenza vaccines.
  • H1N1 has been isolated from swine herds in various countries with the pigs likely infected from human workers. The origin of A(H1N1) 2009 has not been established but the virus is a reassortant of swine influenza viruses.


Global response to H5N1 HPAI and H1N1 resulted in improved:

  • sensitization and vigilance of the international community;
  • pandemic preparedness at national, regional and international levels; and
  • collaboration across disciplines (e.g. human health, animal health and wildlife).