So you don’t know it started in Italy then.
seriously, if you have time, read the following article.
It may be boring but it explains quite well the background to how come China managed to control the virus through experience and we don't.
Also, American and European labs, especially in Germany, have been studying for a long time Avian Influenza. Accidents at poultry farms in the past may indicate a pathway for the virus escaping from one of the labs.
Low pathogenic avian influenza (LPAI) H7N9 viruses have recently evolved to gain a polybasic cleavage site in the hemagglutinin (HA) protein, resulting in variants with increased lethality in poultry that meet the criteria for highly pathogenic avian ...
www.ncbi.nlm.nih.gov
QUOTE:
The pandemic potential of avian influenza A (H7N9) viruses has risen substantially since its first emergence as a low pathogenic avian influenza (LPAI) virus in 2013. Risk assessment by the US Centers for Disease Control and Prevention characterizes these viruses to pose a moderate to high pandemic threat to humans [
1,
2]. As of June 2019, avian influenza A (H7N9) viruses had caused six epidemic waves of human disease in China, totalling 1568 laboratory confirmed cases and 616 deaths (~40% case fatality rate) [
3]. For the first four epidemic waves, only LPAI H7N9 viruses circulated and caused asymptomatic or mild disease in poultry [
4]. The lack of observable disease in poultry populations posed a considerable challenge in prevention and control of the disease, and highlighted the need for active surveillance for these viruses.
During the fifth epidemic wave in 2016–2017, several concerning changes were discovered about the LPAI H7N9 viruses. Approximately 21% of epidemic H7N9 virus samples obtained from humans and the environment contained a four amino acid insertion (K-R-T-A) in the hemagglutinin (HA) protease cleavage site, a mutation that is characteristic of high pathogenic avian influenza (HPAI) viruses [
2,
5,
6]. These HPAI H7N9 viruses demonstrated greater morbidity and mortality in poultry [
6]. Although this epidemic wave resulted in the greatest number of confirmed cases of human H7N9 infections (> 700 cases) with 28 of the cases caused by HPAI H7N9 infections [
7,
8], the overall disease severity was similar to previous patients infected with LPAI H7N9 [
4,
9,
10]. However, the geographical spread of these viruses in China extended the furthest during this epidemic, with new areas reporting cases of H7N9 infections for the first time [
4,
6,
11]. Since 2013, the HA genes of LPAI H7N9 viruses have evolved into two main lineages, the Yangtze River Delta and Pearl River Delta lineages [
12], and studies have shown that H7N9 vaccines generated using A/Anhui/1/2013 (LPAI H7N9) induced antibodies that provided moderate recognition of recent HPAI H7N9 viruses [
5].
To control the spread of H7N9 viruses, the Government of China launched a mandatory vaccination program for avian influenza in July of 2017. By November 2017, a newly developed bivalent H5/H7 inactivated vaccine was used to vaccinate over 282 million domestic poultry in China [
13]. A series of strategies including the closure or management of live poultry markets (LPMs) [
14] and vaccination resulted in significant reduction in the number of H7N9 cases or outbreaks detected at LPMs or poultry farms and a corresponding decrease in H7N9 infections in humans, specifically in the Guangdong Province [
13]. It is important to note though that vaccination does not result in sterilizing immunity in vaccinated birds, therefore, continued replication and antigenic drift of these viruses in bird populations continues to pose a threat of a future re-emergence of H7N9 viruses.
The recent evolution of LPAI H7N9 to HPAI H7N9 viruses emphasizes the need to better understand the potential of these viruses to cause severe disease in humans, and what contributes to their pathogenicity. While the main difference between these two viruses is the presence of a polybasic cleavage site (PBC) in HA, whether this alone is required for increased pathogenicity in mice or if other factors are needed was the focus of our study. We investigated the pathogenesis of HPAI H7N9 viruses in the mouse model and identified the determinants of pathogenicity by reverse genetics. We show that introduction of a PBC HA into LPAI H7N9 virus (A/Anhui/1/2013, H7N9-PBC) alone did not elicit a high pathogenic phenotype in mice upon initial exposure to the virus. However, a single passage of the reverse genetics generated H7N9-PBC virus in mice was necessary and sufficient for it to become highly pathogenic and lethal, pointing to a need for host adaptation in the H7N9-PBC virus to achieve its high pathogenic potential in this host. Sequencing of the passaged virus revealed critical mutations in addition to the PBC cleavage site that contributed to high pathogenicity of these viruses.