Author Contributions
Copyright © 2018 Patricia F. Favaro. et al.
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Competing interests
The authors have declared that no competing interests exist.
Citation:
Introduction
In the pre-virological era equine flu outbreaks were described based on clinical signs and on disease spreading pattern. Human flu cases were also described concomitant with those animal outbreaks. By that time there was none/or little knowledge about the agent that was causing those clinical signs in humans and animals. The equine influenza (EI) would cause serious impact in cities where horses were the major type of transportation1.
With science evolution, the agent that was causing flu was first identified from pigs2, from humans in 19333 and from equines in 1956 (H7N7 subtype) and in 1963 (H3N8 subtype)4. The H7N7 EIV subtype is considered to be extinct since 19805 and H3N8 subtype continues to cause outbreaks worldwide.
The techniques HA - hemagglutination assay, HI - inhibition of hemagglutination assay and virus isolation in embryonated chicken eggs, are deeply used to study EIV outbreaks6.With the advance of molecular techniques, globalization and the high visibility of journals/articles/communications, the epidemiology of EIV started to be more deeply studied.
Initially, the EIVs H3N8 subtypes were defined in a single phylogenetic group7 that evolved into two lineages, American and Eurasian, according to the geographic region8. The American lineage diverged into South America, Kentucky and Florida sub-lineages9. The strains from the Florida sub-lineage suffered two mutations in the hemagglutinin and diverged into Florida Clade 1 (FC1) and Clade 2 (FC2)9,10 represented by the strains A/equine/South Africa/4/03 and A/equine/Newmarket/5/03, respectively11. The FC1 and FC2 strains are responsible for the EIV outbreaks that occurred worldwide in the last years and are the predominant EIVs12,13,14,15,16,17,18,19,20,21.
In South America, EIV outbreaks caused by the H3N8 subtype were described in Brazil in 1963, 1969, 1985, 1988, 2001, 2012 and 201516,21,22,23,24,25,26,27,28, in Chile in 1963, 1985, 1992, 2006 and 201229,30,31, in Argentina in 2001 and 2012 30,32 and Uruguay in 2012 30. The H3N8 EIVs that were sequenced were more identical to the North American strains than to the European EIVs16, 21, 28, 30, 33.
In 2012, outbreaks occurred in the United States, Argentina, Brazil, Uruguay and Dubai. The strains had high nucleotide identity and belonged to FC116, 19, 21, 30. According to Perglione et al (2016), the outbreak might have initiated in South America and went to Dubai. Brazil has reported 129 confirmed EIV outbreaks to the OIE in 2012 (World Animal Health Information Database (WAHID) Interface: http://www.oie.int/wahis_2/public/wahid.php/Countryinformation/Reporting].
An outbreak occurred in Brazil in 2015 in a veterinary hospital in the city of São Paulo (State of São Paulo) and different variants were found suggesting the evolution the virus suffered during the same outbreak28.
Before 2012, only a few studies about the circulating EIVs in South America were described. The surveillance studies of EIV in South America provide information about which strains are causing the outbreaks and control/prevention actions that might be applied such as the use of epidemiologically relevant strains in EIV vaccination11.