Influenza virus is the cause of one of the most common infections worldwide. Its effect on the global population carries important economic, healthcare system, and human suffering consequences [1
]. Influenza virus type A is highly contagious and is the most pathogenic of all human influenza viruses [1
Human antibodies recognize two antigens (glycoprotein) expressed on the viral surface called hemagglutinin (HA) and neuraminidase (NA). Changes in these glycoprotein represent antigenic variation (antigen drift) that is responsible for the constant changes within the common strains of seasonal influenza. Influenza is classified into 16 HA subtypes and 9 NA subtypes [1
], and as pointed out, influenza comprises “the oldest emerging virus that is still emerging” [2
Influenza pandemics occur when an influenza virus, that presents an hemagglutinin (HA) molecule for which there is limited or no existing immunity, emerges and efficiently transmits from human to human [3
]. The emergence of a new virus subtype with a new HA is called antigen shift and will condition the lack of immune response to infection by the new virus.
Despite of pandemics during the last century, this disease generally does not represent an actual concern for the overall population. Several publications [1
], as well as the World Health Organization (WHO) and the American Center of Disease Control (CDC), had repeatedly pointed out that in a manner of time, the world would face a new influenza pandemic that would cause significant figures of global morbidity and mortality.
Influenza has a fast person-to-person transmission and a high mortality risk when not treated. Among all the major pandemics, influenza A is the only one that may potentially infect a considerable fraction of the world's population in a few months [2
The genomes of the last three pandemic influenza viruses, 1918 (H1N1), 1957 (H2N2), and 1968 (H3N2), originated from nonhuman reservoirs and all HA genes originated from avian influenza viruses [3
There are two mechanisms intervening in the introduction of a virus with new hemagglutinin (HA) subtypes in the human population: recombination and interspecies transmission. The first mechanism of the current Influenza A (H1N1) pandemic comprises recombined viruses of two swine flu types: one of those has a triple recombination strain containing segments originated from the last human seasonal flu H3N2 and the other one originated by avian and swine flu [4
In early April 2009, cases similar to pneumonia and influenza were notified and reported to the Pan-American Health Organization (PAHO). As research progressed, it was observed that reported Mexican and Californian cases were caused by a similar virus, which triggered the alert of the World Health Organization (WHO) on April 24. On July 11, 2009, the WHO raised its pandemic alert level to 6.
At the beginning of the outbreak there were a significant number of cases reported as possible new H1N1 influenza that, after the PCR test became widely available in May 2009, were labeled as seasonal influenza A (non-H1N1). The National Commission for Medical Arbitration (CONAMED), as the designated authority to monitor all mortality cases due to influenza, compiled a series of clinical files of all suspicious cases. Since the clinical profile of the new H1N1 virus is not significantly different to that of seasonal influenza A (non-H1N1)—described clinical profiles include cough, rhinorrhea, headache, myalgia, arthralgia, fever, dyspnea, and diarrhea [8
]—many of the initial cases filed by CONAMED were later confirmed by rt-PCR testing as seasonal influenza A (non-H1N1).
This study describes the main differences between the new influenza H1N1 and seasonal influenza A virus mortality cases in terms of clinical profile and sociodemographic characteristics which may orient clinicians and authorities in decision-making processes.