{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T01:01:28Z","timestamp":1785546088549,"version":"3.56.0"},"reference-count":50,"publisher":"Microbiology Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2006,1,1]]},"abstract":"<jats:p><jats:italic>Vaccinia virus<\/jats:italic>(VACV) is the vaccine that was used to eradicate smallpox and is being developed as a recombinant vaccine for other pathogens. Removal of genes encoding immunomodulatory proteins expressed by VACV may enhance virus immunogenicity and improve its potential as a vaccine. Protein A41 is a candidate for removal, having sequence similarity to the VACV chemokine-binding protein, vCKBP, and an association with reduced inflammation during dermal infection. Here, it is shown that, at low doses, VACV strain Western Reserve (WR) lacking<jats:italic>A41L<\/jats:italic>(v\u0394A41L) was slightly more virulent than wild-type and revertant controls after intranasal infection of BALB\/c mice. The primary immune response to v\u0394A41L was marked by an increase in the percentage of VACV-specific gamma interferon-producing CD8<jats:sup>+<\/jats:sup>T cells and enhancement of cytotoxic T-cell responses in the spleen. However, this augmentation of cellular response was not seen in lung infiltrates. Splenic CD8<jats:sup>+<\/jats:sup>T-cell responses were also enhanced when VACV strain modified vaccinia virus Ankara (MVA) lacking<jats:italic>A41L<\/jats:italic>was used to immunize mice. Lastly, immunization with VACV MVA lacking<jats:italic>A41L<\/jats:italic>provided better protection than control viruses to subsequent challenge with a 300 LD<jats:sub>50<\/jats:sub>dose of VACV WR. This study provides insight into the immunomodulatory role of A41 and suggests that MVA lacking A41 may represent a more efficacious vaccine.<\/jats:p>","DOI":"10.1099\/vir.0.81417-0","type":"journal-article","created":{"date-parts":[[2005,12,16]],"date-time":"2005-12-16T18:12:49Z","timestamp":1134756769000},"page":"29-38","source":"Crossref","is-referenced-by-count":81,"title":["Deletion of gene A41L enhances vaccinia virus immunogenicity and vaccine efficacy"],"prefix":"10.1099","volume":"87","author":[{"given":"Richard H.","family":"Clark","sequence":"first","affiliation":[{"name":"Department of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia C.","family":"Kenyon","sequence":"additional","affiliation":[{"name":"Department of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathan W.","family":"Bartlett","sequence":"additional","affiliation":[{"name":"Department of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David C.","family":"Tscharke","sequence":"additional","affiliation":[{"name":"EBV Biology Laboratory, Division of Immunology and Infectious Diseases, Queensland Institute of Medical Research, Herston, QLD 4006, Australia"},{"name":"Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-0440, USA"},{"name":"Department of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Geoffrey L.","family":"Smith","sequence":"additional","affiliation":[{"name":"Department of Virology, Faculty of Medicine, 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