Abstract:
:Macaques immunized with uninfected human cells have been shown to be protected from challenge with simian immunodeficiency virus (SIV) propagated in human cells. To identify the potential antigens involved in this protection, macaques were immunized with uninfected human cells, sucrose density gradient-purified culture fluid from uninfected human cells (mock virus), beta-2 microglobulin (beta 2M), immunoaffinity-purified HLA class I and class II proteins from these human cells, and adjuvant. Although all macaques immunized with beta 2M and HLA class I developed high antibody titers to beta 2M, these animals were not protected from a subsequent challenge with infectious SIV grown in human cells. In contrast, the macaques immunized with class II protein (HLA-DR) and mock virus developed antibodies to class II protein and were protected from the intravenous infectious virus challenge. The class II protein- and mock virus-immunized animals which were protected from challenge were given boosters of the appropriate antigen and challenged with the same SIV propagated in macaque cells. All animals became infected, indicating that the protection seen with human class II protein did not extend to protection from infection with SIV containing macaque class II proteins. Since the virus released from SIV-infected macaque cells would contain macaque class II proteins, our results suggest that the initial SIV infected was completely prevented. In addition, the lack of protection from challenge with SIV propagated in macaque cells provided strong evidence that the protection was due to an immune response to the cellular proteins and not to epitopes cross-reactive between class II proteins and the viral proteins, since the identical virus proteins were present in both challenge stocks. These results are the first demonstration that immunization with a purified cellular protein can protect from virus infection.
journal_name
J Viroljournal_title
Journal of virologyauthors
Arthur LO,Bess JW Jr,Urban RG,Strominger JL,Morton WR,Mann DL,Henderson LE,Benveniste REdoi
10.1128/JVI.69.5.3117-3124.1995subject
Has Abstractpub_date
1995-05-01 00:00:00pages
3117-24issue
5eissn
0022-538Xissn
1098-5514journal_volume
69pub_type
杂志文章abstract::The core promoter mutants of hepatitis B virus (HBV) emerge as the dominant viral population at the late HBeAg and the anti-HBe stages of HBV infection, with the A1762T/G1764A substitutions as the hotspot mutations. The double core promoter mutations were found by many investigators to moderately enhance viral genome ...
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doi:10.1128/JVI.18.2.738-744.1976
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pub_type: 杂志文章
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journal_title:Journal of virology
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journal_title:Journal of virology
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journal_title:Journal of virology
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.18.2.481-490.1976
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/jvi.74.19.9134-9143.2000
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:1988-01-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/JVI.38.1.20-26.1981
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journal_title:Journal of virology
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journal_title:Journal of virology
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更新日期:2007-03-01 00:00:00