<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Oh, Dayoung</style></author><author><style face="normal" font="default" size="100%">Shaojie Han</style></author><author><style face="normal" font="default" size="100%">Marylène Tignon</style></author><author><style face="normal" font="default" size="100%">Nadège Balmelle</style></author><author><style face="normal" font="default" size="100%">Ann Brigitte Cay</style></author><author><style face="normal" font="default" size="100%">Friso Griffioen</style></author><author><style face="normal" font="default" size="100%">Brecht Droesbeke</style></author><author><style face="normal" font="default" size="100%">Nauwynck, Hans J</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Differential infection behavior of African swine fever virus (ASFV) genotype I and II in the upper respiratory tract.</style></title><secondary-title><style face="normal" font="default" size="100%">Vet Res</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">African Swine Fever</style></keyword><keyword><style  face="normal" font="default" size="100%">African Swine Fever Virus</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Endothelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Sus scrofa</style></keyword><keyword><style  face="normal" font="default" size="100%">Swine</style></keyword><keyword><style  face="normal" font="default" size="100%">Swine Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Trachea</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2023</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2023 Dec 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">54</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;African swine fever virus (ASFV) is a substantial threat to pig populations worldwide, contributing to economic disruption and food security challenges. Its spread is attributed to the oronasal transmission route, particularly in animals with acute ASF. Our study addresses the understudied role of nasal mucosa in ASFV infection, using a nasal explant model. The explants remained viable and revealed a discernible ASFV infection in nasal septum and turbinates post-inoculation. Interestingly, more infected cells were found in the turbinates despite its thinner structure. Further analyses showed (i) a higher replication of genotype II strain BEL18 than genotype I strain E70 in the epithelial cell layer, (ii) a preference of ASFV infection for the lamina propria and a tropism of ASFV for various susceptible cell types in different areas in the nasal mucosa, including epithelial cells, macrophages, and endothelial cells. Using porcine respiratory epithelial cells (PoRECs), isolated from nasal tissue, we found a difference in infection mechanism between the two genotypes, with genotype I favoring the basolateral surface and genotype II preferring the apical surface. Moreover, disruption of intercellular junctions enhanced infection for genotype I. This study demonstrated that ASFV may use the respiratory mucosa for entry using different cell types for replication with a genotype difference in their infection of respiratory epithelial cells.&lt;/p&gt;
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