Christopher W. Olsen
University of Wisconsin-Madison
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Virus Research | 2002
Christopher W. Olsen
Since 1997, novel viruses of three different subtypes and five different genotypes have emerged as agents of influenza among pigs in North America. The appearance of these viruses is remarkable because there were no substantial changes in the overall epidemiology of swine influenza in the United States and Canada for over 60 years prior to this time. Viruses of the classical H1N1 lineage were virtually the exclusive cause of swine influenza from the time of their initial isolation in 1930 through 1998. Antigenic drift variants of these H1N1 viruses were isolated in 1991-1998, but a much more dramatic antigenic shift occurred with the emergence of H3N2 viruses in 1997-1998. In particular, H3N2 viruses with genes derived from human, swine and avian viruses have become a major cause of swine influenza in North America. In addition, H1N2 viruses that resulted from reassortment between the triple reassortant H3N2 viruses and classical H1N1 swine viruses have been isolated subsequently from pigs in at least six states. Finally, avian H4N6 viruses crossed the species barrier to infect pigs in Canada in 1999. Fortunately, these H4N6 viruses have not been isolated beyond their initial farm of origin. If these viruses spread more widely, they will represent another antigenic shift for our swine population, and could pose a threat to the worlds human population. Research on these novel viruses may offer important clues to the genetic basis for interspecies transmission of influenza viruses.
Virus Research | 2000
Alexander I. Karasin; Melissa M. Schutten; Lynn A. Cooper; Catherine B. Smith; Kanta Subbarao; Gary A. Anderson; Suzanne Carman; Christopher W. Olsen
Since 1998, H3N2 viruses have caused epizootics of respiratory disease in pigs throughout the major swine production regions of the U.S. These outbreaks are remarkable because swine influenza in North America had previously been caused almost exclusively by H1N1 viruses. We sequenced the full-length protein coding regions of all eight RNA segments from four H3N2 viruses that we isolated from pigs in the Midwestern U.S. between March 1998 and March 1999, as well as from H3N2 viruses recovered from a piglet in Canada in January 1997 and from a pig in Colorado in 1977. Phylogenetic analyses demonstrated that the 1977 Colorado and 1997 Ontario isolates are wholly human influenza viruses. However, the viruses isolated since 1998 from pigs in the Midwestern U.S. are reassortant viruses containing hemagglutinin, neuraminidase and PB1 polymerase genes from human influenza viruses, matrix, non-structural and nucleoprotein genes from classical swine viruses, and PA and PB2 polymerase genes from avian viruses. The HA proteins of the Midwestern reassortant swine viruses can be differentiated from those of the 1995 lineage of human H3 viruses by 12 amino acid mutations in HA1. In contrast, the Sw/ONT/97 virus, which did not spread from pig-to-pig, lacks 11 of these changes.
Journal of Virology | 2000
Alexander I. Karasin; Ian H. Brown; Suzanne Carman; Christopher W. Olsen
ABSTRACT In October 1999, H4N6 influenza A viruses were isolated from pigs with pneumonia on a commercial swine farm in Canada. Phylogenetic analyses of the sequences of all eight viral RNA segments demonstrated that these are wholly avian influenza viruses of the North American lineage. To our knowledge, this is the first report of interspecies transmission of an avian H4 influenza virus to domestic pigs under natural conditions.
Emerging Infectious Diseases | 2007
Gregory C. Gray; Troy McCarthy; Ana W. Capuano; Sharon F. Setterquist; Christopher W. Olsen; Michael C. R. Alavanja; Charles F. Lynch
Swine workers and their spouses are at markedly increased risk of acquiring swine influenza virus infections.
Emerging Infectious Diseases | 2006
Christopher W. Olsen; Alexander I. Karasin; Suzanne Carman; Yan Li; Nathalie Bastien; Davor Ojkic; David Alves; George Charbonneau; Beth M. Henning; Donald E. Low; Laura Burton; George Broukhanski
Since January 2005, H3N2 influenza viruses have been isolated from pigs and turkeys throughout Canada and from a swine farmer and pigs on the same farm in Ontario. These are human/classical swine/avian reassortants similar to viruses that emerged in US pigs in 1998 but with a distinct human-lineage neuraminidase gene.
Emerging Infectious Diseases | 2002
Christopher W. Olsen; Lynnette Brammer; Bernard C. Easterday; Nancy H. Arden; Ermias D. Belay; Inger Baker; Nancy J. Cox
We evaluated seropositivity to swine and human H1 influenza viruses in 74 swine farm owners, employees, their family members, and veterinarians in rural south-central Wisconsin, compared with 114 urban Milwaukee, Wisconsin, residents. The number of swine farm participants with positive serum hemagglutination-inhibition (HI) antibody titers >40 to swine influenza viruses (17/74) was significantly higher (p<0.001) than the number of seropositive urban control samples (1/114). The geometric mean serum HI antibody titers to swine influenza viruses were also significantly higher (p<0.001) among the farm participants. Swine virus seropositivity was significantly (p<0.05) associated with being a farm owner or a farm family member, living on a farm, or entering the swine barn >4 days/week. Because pigs can play a role in generating genetically novel influenza viruses, swine farmers may represent an important sentinel population to evaluate the emergence of new pandemic influenza viruses.
Journal of Clinical Microbiology | 2006
Alexander I. Karasin; Suzanne Carman; Christopher W. Olsen
ABSTRACT Since 2003, three novel genotypes of H1 influenza viruses have been recovered from Canadian pigs, including a wholly human H1N2 virus and human-swine reassortants. These isolates demonstrate that human-lineage H1N2 viruses are infectious for pigs and that viruses with a human PB1/swine PA/swine PB2 polymerase complex can replicate in pigs.
Journal of Clinical Microbiology | 2004
Alexander I. Karasin; Keith West; Suzanne Carman; Christopher W. Olsen
ABSTRACT H3N3 and H1N1 influenza A viruses were isolated from Canadian pigs in 2001 and 2002. These viruses are phylogenetically related to waterfowl viruses and antigenically distinct from reference swine influenza viruses. The isolation of these viruses reemphasizes the potential for interspecies transmission of influenza viruses from waterfowl to pigs in North America.
Journal of Clinical Microbiology | 2002
Alexander I. Karasin; John Landgraf; Sabrina Swenson; Gene Erickson; Sagar Goyal; Mary Woodruff; Gail Scherba; Gary A. Anderson; Christopher W. Olsen
ABSTRACT An H1N2 influenza A virus was isolated from a pig in the United States for the first time in 1999 (A. I. Karasin, G. A. Anderson, and C. W. Olsen, J. Clin. Microbiol. 38:2453-2456, 2000). H1N2 viruses have been isolated subsequently from pigs in many states. Phylogenetic analyses of eight such viruses isolated from pigs in Indiana, Illinois, Minnesota, Ohio, Iowa, and North Carolina during 2000 to 2001 showed that these viruses are all of the same reassortant genotype as that of the initial H1N2 isolate from 1999.
Vaccine | 1998
Kathryn M. Nelson; Brian R. Schram; Martha W. McGregor; Abhineet S. Sheoran; Christopher W. Olsen; D.P. Lunn
Inactivated alum-adjuvanted conventional equine influenza virus vaccines are of poor efficacy and offer limited short-term protection against infection. In sharp contrast, natural infection with equine influenza virus confers long-term protective immunity. In order to identify the protective immune responses to equine influenza virus, the influenza virus-specific IgA, IgGa, IgGb, IgGc and IgG(T) antibody responses in nasal secretions and serum induced by natural infection and a commercial vaccine were studied by ELISA. Two groups of four influenza-naive ponies were established. In the natural infection group, ponies received 10(8.5) EID50 of A/equine/Ky/1/81 by intranasal instillation, were allowed to recover, and then were rechallenged 100 days later. All four ponies exhibited clinical signs of influenza virus infection and viral shedding following primary infection, but were completely protected from challenge infection. Antibody responses to primary infection were characterized by nasal IgA and serum IgGa and IgGb responses. Ponies in the conventional vaccine group received a commercially available vaccine by intramuscular injection followed by a booster injection 3 weeks later. Challenge infection 100 days after vaccination resulted in clinical signs of infection and viral shedding. Antibody responses to vaccination were restricted to serum IgG(T) responses only. These results demonstrate that the protective immunity generated by natural equine influenza virus infection is associated with a mucosal IgA immune response and humoral IgGa and IgGb sub-isotype responses, and that this pattern of response is not generated by conventional vaccines.
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National Center for Immunization and Respiratory Diseases
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