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Host inhibits replication of European porcine reproductive and respiratory syndrome virus in macrophages by altering differential regulation of type-I interferon transcriptional response
Porcine reproductive and respiratory syndrome (PRRS) is an infectious disease caused by a positive RNA strand arterivirus. PRRS virus (PRRSV) interacts primarily with lung macrophages. Little is known how the virus subverts the innate immune response to initiate its replication in alveolar macrophag...
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| Published in: | Immunogenetics (New York) 2011-07, Vol.63 (7), p.437-448 |
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| container_end_page | 448 |
| container_issue | 7 |
| container_start_page | 437 |
| container_title | Immunogenetics (New York) |
| container_volume | 63 |
| creator | Ait-Ali, Tahar Wilson, Alison D. Carré, Wilfrid Westcott, David G. Frossard, Jean-Pierre Mellencamp, Marnie A. Mouzaki, Daphne Matika, Oswald Waddington, David Drew, Trevor W. Bishop, Stephen C. Archibald, Alan L. |
| description | Porcine reproductive and respiratory syndrome (PRRS) is an infectious disease caused by a positive RNA strand arterivirus. PRRS virus (PRRSV) interacts primarily with lung macrophages. Little is known how the virus subverts the innate immune response to initiate its replication in alveolar macrophages. Large-scale transcriptional responses of macrophages with different levels of susceptibility to PRRSV infection were compared over 30 h of infection. This study demonstrates a rapid and intense host transcriptional remodelling during the early phase of the replication of the virus which correlates with transient repression of type-I interferon transcript as early as 8 h post-infection. These results support the suggestion from previous studies that host innate immune response inhibits replication of European porcine reproductive and respiratory syndrome virus in macrophages by altering differential regulation of type-I interferon transcriptional response. |
| doi_str_mv | 10.1007/s00251-011-0518-8 |
| format | article |
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PRRS virus (PRRSV) interacts primarily with lung macrophages. Little is known how the virus subverts the innate immune response to initiate its replication in alveolar macrophages. Large-scale transcriptional responses of macrophages with different levels of susceptibility to PRRSV infection were compared over 30 h of infection. This study demonstrates a rapid and intense host transcriptional remodelling during the early phase of the replication of the virus which correlates with transient repression of type-I interferon transcript as early as 8 h post-infection. These results support the suggestion from previous studies that host innate immune response inhibits replication of European porcine reproductive and respiratory syndrome virus in macrophages by altering differential regulation of type-I interferon transcriptional response.</description><identifier>ISSN: 0093-7711</identifier><identifier>EISSN: 1432-1211</identifier><identifier>DOI: 10.1007/s00251-011-0518-8</identifier><identifier>PMID: 21380581</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Allergology ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Gene Expression Regulation ; Gene Function ; Hogs ; Host-Pathogen Interactions - genetics ; Human Genetics ; Immune response ; Immunity, Innate - genetics ; Immunology ; Infections ; Infectious diseases ; Interferon ; Interferon Type I - genetics ; Macrophages, Alveolar - immunology ; Macrophages, Alveolar - virology ; Original Paper ; Porcine Reproductive and Respiratory Syndrome - genetics ; Porcine Reproductive and Respiratory Syndrome - immunology ; Porcine respiratory and reproductive syndrome virus ; Porcine respiratory and reproductive syndrome virus - physiology ; Swine ; Transcription, Genetic ; Viral infections ; Virus Replication</subject><ispartof>Immunogenetics (New York), 2011-07, Vol.63 (7), p.437-448</ispartof><rights>Springer-Verlag 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-18d7bb69105db64727266f1ce5ed5bc8786950fb5fd6f5c5d9c284da1b279d133</citedby><cites>FETCH-LOGICAL-c445t-18d7bb69105db64727266f1ce5ed5bc8786950fb5fd6f5c5d9c284da1b279d133</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21380581$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ait-Ali, Tahar</creatorcontrib><creatorcontrib>Wilson, Alison D.</creatorcontrib><creatorcontrib>Carré, Wilfrid</creatorcontrib><creatorcontrib>Westcott, David G.</creatorcontrib><creatorcontrib>Frossard, Jean-Pierre</creatorcontrib><creatorcontrib>Mellencamp, Marnie A.</creatorcontrib><creatorcontrib>Mouzaki, Daphne</creatorcontrib><creatorcontrib>Matika, Oswald</creatorcontrib><creatorcontrib>Waddington, David</creatorcontrib><creatorcontrib>Drew, Trevor W.</creatorcontrib><creatorcontrib>Bishop, Stephen C.</creatorcontrib><creatorcontrib>Archibald, Alan L.</creatorcontrib><title>Host inhibits replication of European porcine reproductive and respiratory syndrome virus in macrophages by altering differential regulation of type-I interferon transcriptional response</title><title>Immunogenetics (New York)</title><addtitle>Immunogenetics</addtitle><addtitle>Immunogenetics</addtitle><description>Porcine reproductive and respiratory syndrome (PRRS) is an infectious disease caused by a positive RNA strand arterivirus. 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These results support the suggestion from previous studies that host innate immune response inhibits replication of European porcine reproductive and respiratory syndrome virus in macrophages by altering differential regulation of type-I interferon transcriptional response.</description><subject>Allergology</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Gene Expression Regulation</subject><subject>Gene Function</subject><subject>Hogs</subject><subject>Host-Pathogen Interactions - genetics</subject><subject>Human Genetics</subject><subject>Immune response</subject><subject>Immunity, Innate - genetics</subject><subject>Immunology</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Interferon</subject><subject>Interferon Type I - genetics</subject><subject>Macrophages, Alveolar - immunology</subject><subject>Macrophages, Alveolar - virology</subject><subject>Original Paper</subject><subject>Porcine Reproductive and Respiratory Syndrome - 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| subjects | Allergology Animals Biomedical and Life Sciences Biomedicine Cell Biology Gene Expression Regulation Gene Function Hogs Host-Pathogen Interactions - genetics Human Genetics Immune response Immunity, Innate - genetics Immunology Infections Infectious diseases Interferon Interferon Type I - genetics Macrophages, Alveolar - immunology Macrophages, Alveolar - virology Original Paper Porcine Reproductive and Respiratory Syndrome - genetics Porcine Reproductive and Respiratory Syndrome - immunology Porcine respiratory and reproductive syndrome virus Porcine respiratory and reproductive syndrome virus - physiology Swine Transcription, Genetic Viral infections Virus Replication |
| title | Host inhibits replication of European porcine reproductive and respiratory syndrome virus in macrophages by altering differential regulation of type-I interferon transcriptional response |
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