Avian Influenza zoonosis

• Where the virus has been detected in cases of pneumonia in humans in Asia, the genome has an avian origin, but the virus has not evolved to transmit directly from human to human.

Another example of zoonosis has been the H7N9 subtype that was detected in 14 fatal cases of 63 humans in China.

• The genome of this subtype is genetically related to poultry viruses in live bird and pigeon markets.
• Although the H5N1 and H7N9 subtypes have been phylogenetically associated with poultry, close contact is a key factor, as well as other humanspecific health factors.

The World Health Organization also considers H9N2 to a lesser extent, which is of low pathogenicity in chickens, but has been detected in humans.

PATHOGENESIS OF AVIAN INFLUENZA VIRUS H5N2 OF MEXICAN LINEAGE

The pathogenesis of the first Mexican AIVs of low and high pathogenicity were performed in vivo experiments. In these studies, it has been
evidenced that:

• AIV H5N2BP/1994 inoculated into 4-week-old domestic chickens causes low mortality with moderate respiratory signs.
• The virus spreads to the lung, lymphoid organs and visceral organs, causing tissue necrosis and lymphocyte depletion in lymphoid organs;
• AIV H5N2AP also spreads to other organs such as the heart, brain, trachea and cecal tonsils causing necrosis, hemorrhages and loss of cilia in tracheal epithelium.
• The cause of death of chickens experimentally infected with AIV H5N2AP is associated with damage to the capillary endothelium and thrombocytopenia leading to widespread vascular damage.
• Experimentally, it was also shown that the H5N2AP virus is present in the peripheral blood 28 hours after inoculation and up to 72 hours after the end of the experiment.

Pathogeny study

The study of pathogenesis of AIVH5N2 in other avian species such as duck, plover, turkey, pheasant and quail inoculated with the virus by the intravenous route do not become ill and do not infect to chickens free of specific pathogens that coexisted with the infected wild birds.

• In another study, the pathogenesis of AIV H5N2BP/2007 in domestic ducks experimentally infected by intranasal and intratracheal routes, showed that this virus does not cause clinical signs in the duck but can be isolated from turbinates, larynx, trachea and lungs in the first 48 hours after inoculation and cause inflammation with mild to moderate lymphocytic infiltration.

Excretion kinetics studies

Excretion kinetics studies of Mexican lineage AIV H5N2BP/2007 were detected by virus excretion in the oropharynx and cloaca at least 21 days after inoculation in chickens and ducks.

• While other authors have reported that inoculation of the H5N2BP subtype of Mexican lineage in ducks is excreted between two to fourteen days after inoculation by the respiratory route and from zero to seven days after inoculation by the cloaca.

It was also observed that AIV H5N2BP/2007 with mexican lineage inoculated in domestic duck can be excreted initially digestive and subsequently respiratory and vice versa in chicken.

Nucleotide mutations

Most of the nucleotide mutations studied in AIV have been concentrated in the HA gene cleavage region because the difference between the amino acid sequence of the HA of an outbreak virus and the vaccine virus can be determined, which decreases protection.

This characteristic shift in tropism between respiratory and digestive tissue has been observed in chickens and ducks inoculated with H7N3BP, H7N2BP, H7N3BP and H7N9BP from wild ducks, chickens and domestic turkeys. The explanation for the change in tropism can be associated with:

• Nucleotide mutations occurring in the HA gene and in the NA gene during viral replication and transmission in the animal as has been observed in the H11N9 subtype of wild duck.
• Or because it has genes from other virus subtypes with which there has been recombination between chicken and duck viruses; as is the case of subtype H9N2BP in domestic duck from South Korea and subtype H5N2BP in wild geese in Africa.

Accumulation of basic amino acids

The accumulation of basic amino acids in the HA cleavage region that is associated with high virus virulence in chickens is also analyzed, but the presence or lack of this basic amino acid region in some cases corresponds to viruses of low pathogenicity, suggesting the involvement of other genes in virulence, such as PB1-F2, PB2 and NS1 where mutations have been found by puric or pyrimidic base associated with virulence.

Figure 3. Human infections by avian influenza viruses, rare but possible.

SITUATION OF AVIAN INFLUENZA VIRUSES (AIV) IN MEXICO

AIV H5N2

On May 23, 1994, the first isolation of low pathogenicity AIV H5N2 was reported, and in December of that year the first isolation of AIV H5N2AP in commercial poultry by the Laboratory of the U.S.-Mexico Commission for the Prevention of Foot-and-Mouth Disease and Other Animal Diseases (CPA). The AIV H5N2AP was eradicated in June 1995.

However, to date, AIV H5N2BP is prevalent in commercial farms and backyard hens, but because of its low pathogenicity it can go clinically undetected as birds can recover.

In 24 years of presence of the H5N2BP subtype, there are no reports showing that the virus has mutated to the highly pathogenic presentation, and its genome is of avian origin.

AIV H7N3

In June 2012, AIV subtype H7N3 with highly pathogenic molecular and biological characteristics appeared for the first time in poultry production units producing eggs for consumption in the State of Jalisco. After being controlled, it was epidemiologically absent for 17 weeks, appearing in January 2013, and present to date in some regions where there is technified poultry or backyard poultry farming.

• The complete genome of AIV subtype H7N3 has phylogenetic origin with AIV from wild ducks of the United States and not with humans or pigs.

The highly pathogenic AIV subtype H7N3 present in hens from the State of Jalisco was identified antigenically and molecularly in the conjunctivae of two poultry workers from this region who presented conjunctivitis without fever or respiratory disease.

• Experimentally, this unadapted viral isolate causes fatal disease in mice and is easily transmitted directly between ferrets, as well as easily replicating in human bronchial cells.

At present, subtypes H5 and H7 are avian influenza viruses that must be reported to SENASICA and OMSA. With respect to AIVs isolated or detected in wild birds in Mexico, low pathogenic type A influenza viruses H7N3, H6N2, H4N2 and H5NX subtypes have been reported in migratory wild ducks.

Figure 4. Avian influenza virus H5N1, impact on human health.

Currently, the H5N1 and H7N9 avian influenza viruses of asian lineage are the subtypes with the greatest impact on people’s health and their origin is due to the close contact between different species of production birds, wild ducks and the people who raise and trade them.

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