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RESULTS

Coexistence of H7/H9, N9/N2, and H5/N1 in poultry markets determined by real-time RT-PCR.Poultry and environment specimens were collected from 12 poultry markets epidemiologically linked to 10 human H7N9 infection cases that occurred between 4 and 20 April 2013 in Hangzhou. Specimens positive for the H7 and N9 segments were found in all 12 of the poultry markets (Table 1; see also Table S1 in the supplemental material). Coexistence of H7N9 and H9N2, even with H5N1, was detected in chickens and ducks. Among 15 pharyngeal and rectal swabs from chickens in two live poultry markets, 6 were found positive for H7, N9, H9, N2, H5, and H1 and 4 positive for H7, N9, H9, and N2. In eight pharyngeal and rectal swabs from ducks in one live poultry market, two were positive for H7, N9, H9, and N2 and two positive for H7 and N9. In one pharyngeal swab from a quail, only H9N2 was detected. The environments of these poultry markets linked to H7N9 cases were heavily contaminated by influenza A H7N9 and H9N2 viruses, with or without H5N1 virus. A total of 46 of 86 specimens (53.5%) from the environment in all 12 markets were positive for H7, N9, H9, and N2. Thus, the novel H7N9 virus likely coexisted generally with at least an H9N2 virus in live poultry markets.

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The recent increase in zoonotic avian influenza A(H7N9) disease in China is a cause of public health concern. Most of the A(H7N9) viruses previously reported have been of low pathogenicity. We report the fatal case of a patient in China who was infected with an A(H7N9) virus having a polybasic amino acid sequence at its hemagglutinin cleavage site (PEVPKRKRTAR/GL), a sequence suggestive of high pathogenicity in birds. Its neuraminidase also had R292K, an amino acid change known to be associated with neuraminidase inhibitor resistance. Both of these molecular features might have contributed to the patient’s adverse clinical outcome. The patient had a history of exposure to sick and dying poultry, and his close contacts had no evidence of A(H7N9) disease, suggesting human-to-human transmission did not occur. Enhanced surveillance is needed to determine whether this highly pathogenic avian influenza A(H7N9) virus will continue to spread.

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http://jvi.asm.org/content/early/2017/10/20/JVI.00921-17.abstract

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https://www.researchgate.net/publication/286291036_Zoonosis_Update_on_H9N2_Avian_Influenza_Virus

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JOURNAL 2: Transmissibility of H7N9 and H9N2 AIV

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JOURNAL 2: Transmissibility of H7N9 and H9N2 AIV

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This journal shows that H7N9 does not infect chicken well as H9N2 but it has higher affinity towards the human receptors. The transmission of H7N9 from chicken to human is also not very effective.

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JOURNAL 1: Assortment of Internal Genes of H7N9 Virus Contributing to High Pathogenicity in Mice

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JOURNAL 1: Assortment of Internal Genes of H7N9 Virus Contributing to High Pathogenicity in Mice

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I have highlighted the important points which show the genes that contribute to the high pathogenicity of H7N9 and why H7N9 is also more pathogenic than H9N2.

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H9N2

The microneutralization (MN) assay is a modification of the serum virus neutralization assay and is a serological test to detect the presence of functional systemic antibodies that prevent infectivity of virus. When infectious virus is mixed with serum antibody, the virus infectivity can be "neutralized" if the antibodies bind to blocking epitopes on the virus. The neutralization effect can be demonstrated by inoculation of susceptible cells or organisms with the antibody-virus mixture, such as cells in culture, embryonated eggs, or susceptible hosts. The results of the MN assay described here are measured based on cell culture in a microtiter plate format and a color change detected by an automated plate reader. The test is performed with a constant amount of virus and serial dilutions of serum samples to an end point where virus neutralization is no longer detected. The neutralizing antibody titer is thus the reciprocal number of the last dilution of serum with neutralizing activity. The MN assay can be used to detect antibody from pigs with natural exposure or vaccination and can potentially be used to predict cross-protection between strains of influenza A virus.

https://www.ncbi.nlm.nih.gov/pubmed/24899441

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E.coli
Bacteria culture

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In such work, the bienzymatic strategy was proposed by using the first enzyme as tracer tagged on immunomagnetic beads which could be accumulated on the magneto-gold electrode and the second enzyme was immobilized on the gold electrode by layer-by-layer assembly technique. H9N2 avian influenza virus was captured using immunomagnetic beads based on a sandwich-type immunoassay and then detected on the HRP-modified magneto-gold electrode [91]. The linear range of this method was from 0.05 to 2 μg mL− 1 with an LOD of 1 ng mL− 1. According to Zhou et al. [91], the reported immunosensor displayed a rapid detection of H9N2 virus (1 h) with high sensitivity and good reproducibility (RSD of 4.8%) and could be used in complex samples such as serum samples, and thus expanded to other multienzymatic amplification systems in order to construct more sensitive immunosensors for on-site medical diagnostic application. Recently, Singh et al. [90] proposed a label-free immunosensor based on dielectrophoretically deposited SWCNT for detection of influenza virus H1N1. The resistance of the SWCNT-based electrode channels increased with the binding of the influenza virus to the antibodies, and the immunosensors showed a linear behavior when the virus concentration varied from 1 to 10⁴ PFU mL− 1 along with a detection time of 30 min [90]. According to the authors, the SWCNT-based immunosensor has potential applications in a point-of-care test kit for rapid and simple clinical diagnosis or a component of a portable lab-on-a-chip system [90].

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Determination of avian influenza A (H9N2) virions by inductively coupled plasma mass spectrometry based magnetic immunoassay withgold nanoparticles labeling

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Determination of avian influenza A (H9N2) virions by inductively coupled plasma mass spectrometry based magnetic immunoassay withgold nanoparticles labeling

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H9N2
Hi test (procedures)

a. A constant amount of hemagglutinating (HA) antigen is added to each well in a microtiter plate.

b. The test serum is then placed in the first well and serially diluted.

c.  The plates are incubated for one hour and then chicken RBCs are added to each well. If antibody is present in the test serum the RBCs will not agglutinate with the HA antigen.

d.  HI NEGATIVE wells will have a diffuse sheet of agglutinated RBCs covering       the bottom.

e.  HI POSITIVE wells will have a well circumscribed button of unagglutinated       RBCs

http://cal.vet.upenn.edu/projects/poultry/Syllabus/page20.htm

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A novel method for detection of H9N2 influenza viruses by an aptamer-real time-PCR

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A novel method for detection of H9N2 influenza viruses by an aptamer-real time-PCR

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sorry ameer, a bug transfer the case picture here

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H9N2 infection severity, corresponds with different time-line of E.coli infection.

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H9N2 infection severity, corresponds with different time-line of E.coli infection.

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I think this is useful.

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Summary of H9N2 virus as potential pandemic influenza virus

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Summary of H9N2 virus as potential pandemic influenza virus

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The avian H9N2 virus, RGWF10, and the H9N2 avian-human reassortant virus, which transmitted efficiently to the direct contact ferrets, failed to transmit to the aerosol contacts. Particularly, the ferrets infected with the reassortant virus displayed clinical signs, including sneezing, and shed virus titers similar to those observed for the parental H3N2 virus. Therefore the inability to transmit by aerosol cannot be attributed to lack of sufficient viral shedding or sneezing. It appears that avian H9N2 viruses, including those that have acquired SAα2-6 receptor specificity, still lack a key component necessary for efficient aerosol transmission among mammals and, perhaps, humans. It would be reasonable to speculate that the molecular restriction lies within the surface glycoproteins, particularly the HA. Despite this restriction in aerosol transmission, three key factors in avian H9N2 viruses should be noted. First, a number of studies have demonstrated that H9N2 viruses are undergoing extensive evolution and reassortment fueling their pandemic potential. Second, there have been several lines of evidence that H9N2 viruses have transmitted to pigs, the proposed intermediate host that is permissive to both avian and human influenza viruses. The pig could therefore serve as an ideal environment for avian H9N2 viruses to acquire alterations favoring human infection and possibily human-to-human transmission. Third, serological data from separate studies suggest that there may be more human cases of H9N2 infection than previously anticipated , and that the possibility of a limited level of human-to-human transmission cannot be absolutely excluded . Therefore, avian H9N2 viruses are in an ideal position to undergo further adaptation for more efficient transmission among mammals and humans.

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In March 1999, a new pandemic threat appeared when influenza A H9N2 viruses infected two children in Hong Kong. These two virus isolates are similar to an H9N2 virus isolated from a quail in Hong Kong in late 1997. Although differing in their surface hemagglutinin and neuraminidase components, a notable feature of these H9N2 viruses is that the six genes encoding the internal components of the virus are similar to those of the 1997 H5N1 human and avian isolates. This common feature emphasizes the apparent propensity of avian viruses with this genetic complement to infect humans and highlights the potential for the emergence of a novel human pathogen.

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Importance of H9N2 virus as a potential pandemic influenza virus

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Importance of H9N2 virus as a potential pandemic influenza virus

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H9N2 avian influenza A viruses are endemic in poultry of many Eurasian countries and have caused repeated human infections in Asia since 1998. To evaluate the potential threat of H9N2 viruses to humans, we investigated the replication and transmission efficiency of H9N2 viruses in the ferret model. Five wild-type (WT) H9N2 viruses, isolated from different avian species from 1988 through 2003, were tested in vivo and found to replicate in ferrets. However these viruses achieved mild peak viral titers in nasal washes when compared to those observed with a human H3N2 virus. Two of these H9N2 viruses transmitted to direct contact ferrets, however no aerosol transmission was detected in the virus displaying the most efficient direct contact transmission. A leucine (Leu) residue at amino acid position 226 in the hemagglutinin (HA) receptor-binding site (RBS), responsible for human virus-like receptor specificity, was found to be important for the transmission of the H9N2 viruses in ferrets. In addition, an H9N2 avian-human reassortant virus, which contains the surface glycoprotein genes from an H9N2 virus and the six internal genes of a human H3N2 virus, showed enhanced replication and efficient transmission to direct contacts. Although no aerosol transmission was observed, the virus replicated in multiple respiratory tissues and induced clinical signs similar to those observed with the parental human H3N2 virus. Our results suggest that the establishment and prevalence of H9N2 viruses in poultry pose a significant threat for humans.

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Low pathogenic (LP) and high pathogenic (HP) AI from merck

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Low pathogenic (LP) and high pathogenic (HP) AI from merck

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Clinical Findings and Lesions:

Clinical signs, severity of disease, and mortality rates vary depending on AI virus strain and host species.

Low Pathogenicity Avian Influenza Viruses:LP AI viruses typically produce respiratory signs such as sneezing, coughing, ocular and nasal discharge, and swollen infraorbital sinuses in poultry. Sinusitis is common in domestic ducks, quail, and turkeys. Lesions in the respiratory tract typically include congestion and inflammation of the trachea and lungs. In layers and breeders, there may be decreased egg production or fertility, ova rupture (evident as yolk in the abdominal cavity) or involution, or mucosal edema and inflammatory exudates in the lumen of the oviduct. A few layer and breeder chickens may have acute renal failure and visceral urate deposition (visceral gout). The morbidity and mortality is usually low unless accompanied by secondary bacterial or viral infections or aggravated by environmental stressors. Sporadic infections by any subtype of LP AI viruses can occur, but H9N2 LP AI is common in poultry in Asia, the Middle East, and North Africa.

High Pathogenicity Avian Influenza Viruses:Even in the absence of secondary pathogens, HP AI viruses cause severe, systemic disease with high mortality in chickens, turkeys, and other gallinaceous poultry; mortality can be as high as 100% in a few days. In peracute cases, clinical signs or gross lesions may be lacking before death. However, in acute cases, lesions may include cyanosis and edema of the head, comb, wattle, and snood (turkey); edema and red discoloration of the shanks and feet due to subcutaneous ecchymotic hemorrhages; petechial hemorrhages on visceral organs and in muscles; and blood-tinged oral and nasal discharges. In severely affected birds, greenish diarrhea is common. Birds that survive the peracute infection may develop CNS involvement evident as torticollis, opisthotonos, incoordination, paralysis, and drooping wings. The location and severity of microscopic lesions are highly variable and may consist of edema, hemorrhage, and necrosis in parenchymal cells of multiple visceral organs, skin, and CNS.