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Treatment of CEF culture, prepared from 11-day-old embryos, with recombinant chicken gamma interferon (rChIFN-\u03b3) and lipopolysaccharide (LPS) resulted in production of NO which was suppressed by the addition of<jats:italic>N<\/jats:italic><jats:sup>G<\/jats:sup>-monomethyl<jats:sc>l<\/jats:sc>-arginine (NMMA), an inhibitor of inducible NO synthase (iNOS). Incubation of CEF cultures for 72 h prior to treatment with rChIFN-\u03b3 plus LPS was required for optimal NO production. Significant differences in NO production were observed in CEF derived from MDV-resistant N2a (major histocompatibility complex [MHC],<jats:italic>B<\/jats:italic><jats:sup>21<\/jats:sup><jats:italic>B<\/jats:italic><jats:sup>21<\/jats:sup>) and MDV-susceptible S<jats:sub>13<\/jats:sub>(MHC,<jats:italic>B<\/jats:italic><jats:sup>13<\/jats:sup><jats:italic>B<\/jats:italic><jats:sup>13<\/jats:sup>) and P2a (MHC,<jats:italic>B<\/jats:italic><jats:sup>19<\/jats:sup><jats:italic>B<\/jats:italic><jats:sup>19<\/jats:sup>) chickens. N2a-derived CEF produced NO earlier and at higher levels than CEF from the other two lines. The lowest production of NO was detected in P2a-derived CEF. NO production in chicken splenocyte cultures followed a similar pattern, with the highest levels of NO produced in cultures from N2a chickens and the lowest levels produced in cultures from P2a chickens. Replication of MDV and HVT was significantly inhibited in CEF cultures treated with rChIFN-\u03b3 plus LPS and producing NO. The addition of NMMA to CEF treated with rChIFN-\u03b3 plus LPS reduced the inhibition. MDV infection of chickens treated with<jats:italic>S<\/jats:italic>-methylisothiourea, an inhibitor of iNOS, resulted in increased virus load compared to nontreated chickens. These results suggest that NO may play an important role in control of MDV replication in vivo.<\/jats:p>","DOI":"10.1128\/jvi.74.8.3605-3612.2000","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T10:06:37Z","timestamp":1027764397000},"page":"3605-3612","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":109,"title":["Inhibitory Effects of Nitric Oxide and Gamma Interferon on In Vitro and In Vivo Replication of Marek's Disease Virus"],"prefix":"10.1128","volume":"74","author":[{"given":"Zheng","family":"Xing","sequence":"first","affiliation":[{"name":"<!--label omitted: 1-->Unit of Avian Health, Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karel A.","family":"Schat","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Unit of Avian Health, Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"144","DOI":"10.4049\/jimmunol.147.1.144","article-title":"Nitric oxide production is required for murine resident peritoneal macrophages to suppress mitogen-stimulated T cell proliferation: role of IFN-\u03b3 in the induction of the nitric oxide synthesizing pathway","volume":"147","author":"Albina J. 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