3 results on '"Pulit-Penaloza, Joanna A."'
Search Results
2. Mammalian pathogenicity and transmissibility of low pathogenic avian influenza H7N1 and H7N3 viruses isolated from North America in 2018.
- Author
-
Belser JA, Sun X, Brock N, Pulit-Penaloza JA, Jones J, Zanders N, Davis CT, Tumpey TM, and Maines TR
- Subjects
- Animals, Bronchi cytology, Bronchi virology, Cell Line, Chickens virology, Disease Outbreaks, Epithelial Cells virology, Female, Ferrets virology, Humans, Influenza in Birds virology, Influenza, Human virology, Male, Mice, Mice, Inbred BALB C, North America, Orthomyxoviridae Infections virology, Poultry virology, Poultry Diseases virology, Turkeys virology, Virulence, Influenza A Virus, H7N1 Subtype pathogenicity, Influenza A Virus, H7N3 Subtype pathogenicity, Influenza in Birds transmission, Poultry Diseases transmission
- Abstract
ABSTRACT Low pathogenic avian influenza (LPAI) H7 subtype viruses are infrequently, but persistently, associated with outbreaks in poultry in North America. These LPAI outbreaks provide opportunities for the virus to develop enhanced virulence and transmissibility in mammals and have previously resulted in both occasional acquisition of a highly pathogenic avian influenza (HPAI) phenotype in birds and sporadic cases of human infection. Two notable LPAI H7 subtype viruses caused outbreaks in 2018 in North America: LPAI H7N1 virus in chickens and turkeys, representing the first confirmed H7N1 infection in poultry farms in the United States, and LPAI H7N3 virus in turkeys, a virus subtype often associated with LPAI-to-HPAI phenotypes. Here, we investigated the replication capacity of representative viruses from these outbreaks in human respiratory tract cells and mammalian pathogenicity and transmissibility in the mouse and ferret models. We found that the LPAI H7 viruses replicated to high titre in human cells, reaching mean peak titres generally comparable to HPAI H7 viruses. Replication was efficient in both mammalian species, causing mild infection, with virus primarily limited to respiratory tract tissues. The H7 viruses demonstrated a capacity to transmit to naïve ferrets in a direct contact setting. These data support the need to perform routine risk assessments of LPAI H7 subtype viruses, even in the absence of confirmed human infection.
- Published
- 2020
- Full Text
- View/download PDF
3. Pathogenesis and Transmission of Novel Highly Pathogenic Avian Influenza H5N2 and H5N8 Viruses in Ferrets and Mice.
- Author
-
Pulit-Penaloza JA, Sun X, Creager HM, Zeng H, Belser JA, Maines TR, and Tumpey TM
- Subjects
- Animals, Birds virology, Cell Line, Epidemiological Monitoring, Epithelial Cells pathology, Epithelial Cells virology, Europe epidemiology, Female, Ferrets virology, Humans, Influenza A Virus, H5N1 Subtype genetics, Influenza A Virus, H5N2 Subtype genetics, Male, Mice, Mice, Inbred BALB C, North America epidemiology, Orthomyxoviridae Infections epidemiology, Orthomyxoviridae Infections mortality, Poultry virology, Public Health, Reassortant Viruses genetics, Republic of Korea epidemiology, Respiratory Mucosa pathology, Respiratory Mucosa virology, Survival Analysis, Virulence, Influenza A Virus, H5N1 Subtype pathogenicity, Influenza A Virus, H5N2 Subtype pathogenicity, Orthomyxoviridae Infections pathology, Orthomyxoviridae Infections transmission, Reassortant Viruses pathogenicity
- Abstract
Unlabelled: A novel highly pathogenic avian influenza (HPAI) H5N8 virus, first detected in January 2014 in poultry and wild birds in South Korea, has spread throughout Asia and Europe and caused outbreaks in Canada and the United States by the end of the year. The spread of H5N8 and the novel reassortant viruses, H5N2 and H5N1 (H5Nx), in domestic poultry across multiple states in the United States pose a potential public health risk. To evaluate the potential of cross-species infection, we determined the pathogenicity and transmissibility of two Asian-origin H5Nx viruses in mammalian animal models. The newly isolated H5N2 and H5N8 viruses were able to cause severe disease in mice only at high doses. Both viruses replicated efficiently in the upper and lower respiratory tracts of ferrets; however, the clinical symptoms were generally mild, and there was no evidence of systemic dissemination of virus to multiple organs. Moreover, these influenza H5Nx viruses lacked the ability to transmit between ferrets in a direct contact setting. We further assessed viral replication kinetics of the novel H5Nx viruses in a human bronchial epithelium cell line, Calu-3. Both H5Nx viruses replicated to a level comparable to a human seasonal H1N1 virus, but significantly lower than a virulent Asian-lineage H5N1 HPAI virus. Although the recently isolated H5N2 and H5N8 viruses displayed moderate pathogenicity in mammalian models, their ability to rapidly spread among avian species, reassort, and generate novel strains underscores the need for continued risk assessment in mammals., Importance: In 2015, highly pathogenic avian influenza (HPAI) H5 viruses have caused outbreaks in domestic poultry in multiple U.S. states. The economic losses incurred with H5N8 and H5N2 subtype virus infection have raised serious concerns for the poultry industry and the general public due to the potential risk of human infection. This recent outbreak underscores the need to better understand the pathogenesis and transmission of these viruses in mammals, which is an essential component of pandemic risk assessment. This study demonstrates that the newly isolated H5N2 and H5N8 viruses lacked the ability to transmit between ferrets and exhibited low to moderate virulence in mammals. In human bronchial epithelial (Calu-3) cells, both H5N8 and H5N2 viruses replicated to a level comparable to a human seasonal virus, but significantly lower than a virulent Asian-lineage H5N1 (A/Thailand/16/2004) virus. The results of this study are important for the evaluation of public health risk., (Copyright © 2015, American Society for Microbiology. All Rights Reserved.)
- Published
- 2015
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.