{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T13:40:09Z","timestamp":1776087609623,"version":"3.50.1"},"reference-count":0,"publisher":"S. Karger AG","issue":"2-3","license":[{"start":{"date-parts":[[2018,1,1]],"date-time":"2018-01-01T00:00:00Z","timestamp":1514764800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2018,1,1]],"date-time":"2018-01-01T00:00:00Z","timestamp":1514764800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurodegener Dis"],"published-print":{"date-parts":[[2018]]},"abstract":"<jats:p>HTLV-1-associated myelopathy\/tropical spastic paraparesis (HAM\/TSP) is a chronic neuroinflammatory disease related to human T lymphotropic virus type 1 (HTLV-1) infection. Interferon type III (IFN-\u03bb), which includes IL28, IL29, and IL28R, and affects the outcome of viral infections, might be complicated in the progression of HAM\/TSP. Here, we investigated the host-virus interactions in the manifestation of HAM\/TSP, using IL28B, IL29, IL28R, HTLV-1 Tax, HTLV-1 basic leucine zipper factor (HBZ), and proviral load (PVL). The study groups consisted of 20 patients with HAM\/TSP, 20 asymptomatic HTLV-1 carriers (ACs), and 20 healthy controls (HCs). The means of PVL, Tax, and &lt;i&gt;HBZ&lt;\/i&gt; gene expressions in the HAM\/TSP group (&lt;i&gt;p&lt;\/i&gt; = 0.004, 0.006, and &amp;#x3c; 0.0001, respectively) were significantly higher than in the AC group. The comparison of IL28B, IL29, and IL28R expression in the HAM\/TSP, AC, and HC groups revealed no significant difference between the first 2, but lower concentrations in the HCs (IL28B: &lt;i&gt;p&lt;\/i&gt; = 0.03, 0.01; IL29: &lt;i&gt;p&lt;\/i&gt; = 0.07, 0.01; and IL28R: &lt;i&gt;p &amp;#x3c;&lt;\/i&gt; 0.0001, respectively). In the HAM\/TSP group, correlations were seen between Tax and HBZ (&lt;i&gt;R&lt;\/i&gt; = 0.61, &lt;i&gt;p&lt;\/i&gt; = 0.004) and between Tax and IL29 (&lt;i&gt;R&lt;\/i&gt; = 0.45, &lt;i&gt;p&lt;\/i&gt; = 0.04). Negative correlations were observed between Tax and IL28B (&lt;i&gt;R&lt;\/i&gt; = \u20130.49, &lt;i&gt;p&lt;\/i&gt; = 0.02) and between HBZ and IL28R (&lt;i&gt;R&lt;\/i&gt; = \u20130.43, &lt;i&gt;p&lt;\/i&gt; = 0.06). In the ACs, an inverse correlation was found between Tax and IL28B (&lt;i&gt;R&lt;\/i&gt; = \u20130.42, &lt;i&gt;p&lt;\/i&gt; = 0.06). These findings suggest that IL29, IL28B, and IL28R interfere in the infection of HAM\/TSP, mainly via Tax activation.<\/jats:p>","DOI":"10.1159\/000490058","type":"journal-article","created":{"date-parts":[[2018,7,10]],"date-time":"2018-07-10T21:02:23Z","timestamp":1531256543000},"page":"150-155","source":"Crossref","is-referenced-by-count":25,"title":["Interferon Lambda Family along with HTLV-1 Proviral Load, Tax, and HBZ Implicated in the Pathogenesis of Myelopathy\/Tropical Spastic Paraparesis"],"prefix":"10.1159","volume":"18","author":[{"given":"Sayed-Hamidreza","family":"Mozhgani","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hamid\u00a0Reza","family":"Jahantigh","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Houshang","family":"Rafatpanah","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Narges","family":"Valizadeh","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Asadollah","family":"Mohammadi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Samira","family":"Basharkhah","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seyed\u00a0Abdolrahim","family":"Rezaee","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"127","published-online":{"date-parts":[[2018,7,10]]},"container-title":["Neurodegenerative Diseases"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/490058","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/490058","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T16:35:34Z","timestamp":1745426134000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000490058"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2018]]},"references-count":0,"journal-issue":{"issue":"2-3","published-online":{"date-parts":[[2018,8,17]]},"published-print":{"date-parts":[[2018,8,28]]}},"URL":"https:\/\/doi.org\/10.1159\/000490058","archive":["Portico"],"relation":{},"ISSN":["1660-2854","1660-2862"],"issn-type":[{"value":"1660-2854","type":"print"},{"value":"1660-2862","type":"electronic"}],"subject":[],"published":{"date-parts":[[2018]]}}}