{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T13:56:17Z","timestamp":1789480577685,"version":"build-2803163510"},"reference-count":0,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[1995,1,1]],"date-time":"1995-01-01T00:00:00Z","timestamp":788918400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[1995,1]]},"abstract":"<jats:p>Seven diverse primary isolates of human immunodeficiency virus type 1 (HIV-1) were examined and found to be refractory to neutralization by antisera to recombinant gp120 (rgp120) protein from HIV-1 MN. This stands in marked contrast to the sensitivity exhibited by certain laboratory-adapted viruses. To understand the difference between primary and laboratory-adapted viruses, we adapted the primary virus ACH 168.10 to growth in the FDA\/H9 cell line. ACH 168.10 was chosen because the V3 region of gp120 closely matches that of MN. After 4 weeks, infection became evident. The virus (168A) replicated in FDA\/H9 cells with extensive cytopathic effect but was unchanged in sensitivity to antibody-mediated neutralization. Thus, growth in cell lines is not sufficient to render primary virus sensitive to neutralization. The 168A virus was, however, partially sensitive to CD4 immunoadhesin (CD4-Ig). Adaptation was continued to produce a persistently infected FDA\/H9 culture that displayed minimal cytopathic effect. The virus (168C) was now sensitive to neutralization by MN rgp120 vaccine sera and by MN-specific monoclonal antibodies and showed increased sensitivity to HIVIG and CD4-Ig. 168C encoded three amino acid changes in gp120, including one within the V3 loop (I-166--&gt;R, I-282--&gt;N, G-318--&gt;R). MN-specific monoclonal antibodies bound equally to the surface of cells infected with either neutralization-resistant or -sensitive virus. The coincidence of changes in neutralization sensitivity with changes in cell tropism and cytopathic effect suggests a common underlying mechanism(s) acting through the whole of the envelope protein complex.<\/jats:p>","DOI":"10.1128\/jvi.69.1.39-48.1995","type":"journal-article","created":{"date-parts":[[2020,1,6]],"date-time":"2020-01-06T21:20:07Z","timestamp":1578345607000},"page":"39-48","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":126,"title":["Adaptation to persistent growth in the H9 cell line renders a primary isolate of human immunodeficiency virus type 1 sensitive to neutralization by vaccine sera"],"prefix":"10.1128","volume":"69","author":[{"given":"T","family":"Wrin","sequence":"first","affiliation":[{"name":"Department of Immunology, Research Virology Laboratory, Genentech Inc., South San Francisco, California 94080."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T P","family":"Loh","sequence":"additional","affiliation":[{"name":"Department of Immunology, Research Virology Laboratory, Genentech Inc., South San Francisco, California 94080."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J C","family":"Vennari","sequence":"additional","affiliation":[{"name":"Department of Immunology, Research Virology Laboratory, Genentech Inc., South San Francisco, California 94080."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H","family":"Schuitemaker","sequence":"additional","affiliation":[{"name":"Department of Immunology, Research Virology Laboratory, Genentech Inc., South San Francisco, California 94080."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J H","family":"Nunberg","sequence":"additional","affiliation":[{"name":"Department of Immunology, Research Virology Laboratory, Genentech Inc., South San Francisco, California 94080."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","container-title":["Journal of Virology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.asm.org\/doi\/pdf\/10.1128\/jvi.69.1.39-48.1995","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.asm.org\/doi\/pdf\/10.1128\/jvi.69.1.39-48.1995","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,5]],"date-time":"2022-03-05T13:09:55Z","timestamp":1646485795000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.asm.org\/doi\/10.1128\/jvi.69.1.39-48.1995"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1995,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1995,1]]}},"alternative-id":["10.1128\/jvi.69.1.39-48.1995"],"URL":"https:\/\/doi.org\/10.1128\/jvi.69.1.39-48.1995","relation":{},"ISSN":["0022-538X","1098-5514"],"issn-type":[{"value":"0022-538X","type":"print"},{"value":"1098-5514","type":"electronic"}],"subject":[],"published":{"date-parts":[[1995,1]]},"assertion":[{"value":"1995-01-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}