Giuseppe
Emeritus
J Virol. 2009 Feb 18. [Epub ahead of print]
Experimental infection of pigs with the human 1918 pandemic influenza virus.
Weingartl HM, Albrecht RA, Lager K, Babiuk S, Marszal P, Neufeld J, Embury-Hyatt C, Lekcharoensuk P, Tumpey TM, Garc?a-Sastre A, Richt JA. - National Centre for Foreign Animal Disease (NCFAD), Canadian Food Inspection Agency (CFIA), Winnipeg, Manitoba, Canada; Department of Medical Microbiology, Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Microbiology, Department of Medicine, Division of Infectious Diseases, and Emerging Pathogens Institute, Mount Sinai School of Medicine New York, USA; National Centre for Animal Disease, ARS-USDA, Ames, Iowa, USA; Centers for Disease Control and Prevention, Influenza Division, Atlanta, Georgia, USA; Kansas State University, College of Veterinary Medicine, Manhattan, Kansas, USA; Department of Microbiology ans Immunology, Faculty of Veterinary Medicine, Kasetsart University, Bangkok, Thailand.
Swine influenza was first recognized as a disease entity during the 1918 "Spanish flu" pandemic.
The aim of this work was to determine the virulence of a plasmid-derived human 1918 pandemic H1N1 (1918/rec) influenza virus in swine using a plasmid-derived A/swine/Iowa/15/1930 H1N1 virus (1930/rec), representing the first isolated influenza virus, as a reference.
Four week old piglets were inoculated intratracheally with either the 1930/rec or the 1918/rec virus, or intranasally with the 1918/rec virus.
A transient increase in temperature and mild respiratory signs developed post inoculation in all virus inoculated groups.
In contrast to other mammalian hosts (mice, ferrets and macaques) where infection with the 1918/rec virus was lethal, the pigs did not develop severe respiratory distress or become moribund. Virus titers in the lower respiratory tract as well as macro- and microscopic lesions at 3 and 5 days post infection (dpi) were comparable between the 1930/rec and 1918/rec virus inoculated animals.
In contrast to the 1930/rec infected animals, at 7 dpi, prominent lung lesions were present only in the 1918/rec infected animals, and all the piglets developed antibodies at 7 dpi.
Presented data support the hypothesis that the 1918 pandemic influenza was able to infect and replicate in swine causing a respiratory disease, and that the virus was likely introduced into the pig population during the 1918 pandemic resulting in the current lineage of the classical H1N1 swine influenza viruses.
PMID: 19224986 [PubMed - as supplied by publisher]
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Experimental infection of pigs with the human 1918 pandemic influenza virus.
Weingartl HM, Albrecht RA, Lager K, Babiuk S, Marszal P, Neufeld J, Embury-Hyatt C, Lekcharoensuk P, Tumpey TM, Garc?a-Sastre A, Richt JA. - National Centre for Foreign Animal Disease (NCFAD), Canadian Food Inspection Agency (CFIA), Winnipeg, Manitoba, Canada; Department of Medical Microbiology, Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Microbiology, Department of Medicine, Division of Infectious Diseases, and Emerging Pathogens Institute, Mount Sinai School of Medicine New York, USA; National Centre for Animal Disease, ARS-USDA, Ames, Iowa, USA; Centers for Disease Control and Prevention, Influenza Division, Atlanta, Georgia, USA; Kansas State University, College of Veterinary Medicine, Manhattan, Kansas, USA; Department of Microbiology ans Immunology, Faculty of Veterinary Medicine, Kasetsart University, Bangkok, Thailand.
Swine influenza was first recognized as a disease entity during the 1918 "Spanish flu" pandemic.
The aim of this work was to determine the virulence of a plasmid-derived human 1918 pandemic H1N1 (1918/rec) influenza virus in swine using a plasmid-derived A/swine/Iowa/15/1930 H1N1 virus (1930/rec), representing the first isolated influenza virus, as a reference.
Four week old piglets were inoculated intratracheally with either the 1930/rec or the 1918/rec virus, or intranasally with the 1918/rec virus.
A transient increase in temperature and mild respiratory signs developed post inoculation in all virus inoculated groups.
In contrast to other mammalian hosts (mice, ferrets and macaques) where infection with the 1918/rec virus was lethal, the pigs did not develop severe respiratory distress or become moribund. Virus titers in the lower respiratory tract as well as macro- and microscopic lesions at 3 and 5 days post infection (dpi) were comparable between the 1930/rec and 1918/rec virus inoculated animals.
In contrast to the 1930/rec infected animals, at 7 dpi, prominent lung lesions were present only in the 1918/rec infected animals, and all the piglets developed antibodies at 7 dpi.
Presented data support the hypothesis that the 1918 pandemic influenza was able to infect and replicate in swine causing a respiratory disease, and that the virus was likely introduced into the pig population during the 1918 pandemic resulting in the current lineage of the classical H1N1 swine influenza viruses.
PMID: 19224986 [PubMed - as supplied by publisher]
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