ICP4, ICP27, ICP22, and ICP0

ICP4, ICP27, ICP22, and ICP0

ICP4, ICP27, ICP22, and ICP0
Purchase with confidence, knowing that we stand behind the performance of our antibodies with the InvitrogenTM antibody performance guarantee. The purpose of the current study was to compare the production of chemokines induced by viral infection at sites known to harbor virus after ocular inoculation in order to determine the relationship between viral load and chemokine expression. This was expressed in mammalian cells together with gL and the resulting gHFc-gL heterodimer was purified using Protein A Sepharose. Virol., 71, 3534, 1997) that a replication defective mutant of HSV-1, which expresses a substantial level of viral genes without producing virus particles, is as efficient as wild-type HSV-1 in eliciting an HSV-specific cytotoxic T-lymphocyte (CTL) response. In this report, we have further evaluated the immunogenic potential of HSV-1-derived replication defective mutants by examining the generation of HSV-specific CTL following immunization with viruses that are severely restricted in viral gene expression due to mutations in one or more HSV α genes (ICP4, ICP27, ICP22, and ICP0). We interpret these results as suggesting chemokine expression within the cornea in response to herpes simplex virus type 1 infection is driven by factors other than antigenic stimulation. The HSV mutants used in this study are impaired in their ability to express gB while a majority of them still express RR1.

Our findings demonstrate that a single immunization with these mutants is able to generate a strong CTL response not only to RR1 822–829, but also to gB498–505 despite their inability to express wild-type levels of gB. Furthermore, a single immunization with any individual mutant can also provide immune protection against HSV challenge. These results suggest that mutants which are restricted in gene expression may be used as effective immunogens in vivo.

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