Last data update: May 13, 2024. (Total: 46773 publications since 2009)
Records 1-2 (of 2 Records) |
Query Trace: Pekosz A[original query] |
---|
Defining the risk of SARS-CoV-2 variants on immune protection.
DeGrace MM , Ghedin E , Frieman MB , Krammer F , Grifoni A , Alisoltani A , Alter G , Amara RR , Baric RS , Barouch DH , Bloom JD , Bloyet LM , Bonenfant G , Boon ACM , Boritz EA , Bratt DL , Bricker TL , Brown L , Buchser WJ , Carreo JM , Cohen-Lavi L , Darling TL , Davis-Gardner ME , Dearlove BL , Di H , Dittmann M , Doria-Rose NA , Douek DC , Drosten C , Edara VV , Ellebedy A , Fabrizio TP , Ferrari G , Florence WC , Fouchier RAM , Franks J , Garca-Sastre A , Godzik A , Gonzalez-Reiche AS , Gordon A , Haagmans BL , Halfmann PJ , Ho DD , Holbrook MR , Huang Y , James SL , Jaroszewski L , Jeevan T , Johnson RM , Jones TC , Joshi A , Kawaoka Y , Kercher L , Koopmans MPG , Korber B , Koren E , Koup RA , LeGresley EB , Lemieux JE , Liebeskind MJ , Liu Z , Livingston B , Logue JP , Luo Y , McDermott AB , McElrath MJ , Meliopoulos VA , Menachery VD , Montefiori DC , Mhlemann B , Munster VJ , Munt JE , Nair MS , Netzl A , Niewiadomska AM , O'Dell S , Pekosz A , Perlman S , Pontelli MC , Rockx B , Rolland M , Rothlauf PW , Sacharen S , Scheuermann RH , Schmidt SD , Schotsaert M , Schultz-Cherry S , Seder RA , Sedova M , Sette A , Shabman RS , Shen X , Shi PY , Shukla M , Simon V , Stumpf S , Sullivan NJ , Thackray LB , Theiler J , Thomas PG , Trifkovic S , Treli S , Turner SA , Vakaki MA , vanBakel H , VanBlargan LA , Vincent LR , Wallace ZS , Wang L , Wang M , Wang P , Wang W , Weaver SC , Webby RJ , Weiss CD , Wentworth DE , Weston SM , Whelan SPJ , Whitener BM , Wilks SH , Xie X , Ying B , Yoon H , Zhou B , Hertz T , Smith DJ , Diamond MS , Post DJ , Suthar MS . Nature 2022 605 (7911) 640-652 The global emergence of many severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants jeopardizes the protective antiviral immunity induced following infection or vaccination. To address the public health threat caused by the increasing SARS-CoV-2 genomic diversity, the National Institute of Allergy and Infectious Diseases (NIAID) within the National Institutes of Health (NIH) established the SARS-CoV-2 Assessment of Viral Evolution (SAVE) program. This effort was designed to provide a real-time risk assessment of SARS-CoV-2 variants potentially impacting transmission, virulence, and resistance to convalescent and vaccine-induced immunity. The SAVE program serves as a critical data-generating component of the United States Government SARS-CoV-2 Interagency Group to assess implications of SARS-CoV-2 variants on diagnostics, vaccines, and therapeutics and for communicating public health risk. Here we describe the coordinated approach used to identify and curate data about emerging variants, their impact on immunity, and effects on vaccine protection using animal models. We report the development of reagents, methodologies, models, and pivotal findings facilitated by this collaborative approach and identify future challenges. This program serves as a template for the response against rapidly evolving pandemic pathogens by monitoring viral evolution in the human population to identify variants that could erode the effectiveness of countermeasures. |
Tropism and infectivity of influenza virus, including highly pathogenic avian H5N1 virus, in ferret tracheal differentiated primary epithelial cell cultures
Zeng H , Goldsmith CS , Maines TR , Belser JA , Gustin KM , Pekosz A , Zaki SR , Katz JM , Tumpey TM . J Virol 2013 87 (5) 2597-607 Tropism and adaptation of influenza viruses to new hosts is partly dependent on the distribution of the sialic acid (SA) receptors to which the viral hemagglutinin (HA) binds. Ferrets have been established as a valuable in vivo model of influenza virus pathogenesis and transmission because of similarities to humans in the distribution of HA receptors and in clinical signs of infection. In this study, we developed a ferret tracheal differentiated primary epithelial cell culture model that consisted of a layered epithelium structure with ciliated and nonciliated cells on its apical surface. We found that human-like (alpha2,6-linked) receptors predominated on ciliated cells, whereas avian-like (alpha2,3-linked) receptors, which were less abundant, were presented on nonciliated cells. When we compared the tropism and infectivity of three human (H1 and H3) and two avian (H1 and H5) influenza viruses, we observed that the human influenza viruses primarily infected ciliated cells and replicated efficiently, whereas a highly pathogenic avian H5N1 virus (A/Vietnam/1203/2004) replicated efficiently within nonciliated cells despite a low initial infection rate. Furthermore, compared to other influenza viruses tested, VN/1203 virus replicated more efficiently in cells isolated from the lower trachea and at a higher temperature (37 degrees C) compared to a lower temperature (33 degrees C). VN/1203 virus infection also induced higher levels of immune mediator genes and cell death, and virus was recovered from the basolateral side of the cell monolayer. This ferret tracheal differentiated primary epithelial cell culture system provides a valuable in vitro model for studying cellular tropism, infectivity, and the pathogenesis of influenza viruses. |
- Page last reviewed:Feb 1, 2024
- Page last updated:May 13, 2024
- Content source:
- Powered by CDC PHGKB Infrastructure