The DNA binding domain of the varicella-zoster virus gene 62 protein interacts with multiple sequences which are similar to the binding site of

The DNA binding domain of the varicella-zoster virus gene 62 protein interacts with multiple sequences which are similar to the binding site of

The DNA binding domain of the varicella-zoster virus gene 62 protein interacts with multiple sequences which are similar to the binding site of
Herpes simplex virus type 1 (HSV-1) can enter cells expressing any one of multiple entry receptors, including the herpesvirus entry mediator (HVEM), nectin-1, and sites in heparan sulfate generated by specific 3-O-sulfotransferases. A wide range of stable aphidicolin sensitivities was represented amongst a collection of virus strains with no prior exposure to this drug, but viruses with polymerase mutations selected for resistance to phosphonoacetic acid (PAA) or to acycloguanosine typically showed increased sensitivity to aphidicolin. Multiple outbreaks of lesions may occur simultaneously, or lesions may form at different times during the same recurrence. We have expressed a fragment of 140k which encompasses region 2 as a non-fusion polypeptide in bacteria. Or if I kiss their toes, etc, it’ll always happen. Of these recombinants containing the transgene in place of the lacZ gene ranged from 19-65%. These results indicate that insertion of foreign genes into the HSV-1 and HSV-2 intergenic regions examined in this study has no or minimal effect on the properties of these parental viruses.

However, by use of a panel of mutagenized probe fragments, we found that the 140k DNA binding domain was less sequence-specific than Vmw175 in its interactions with DNA. A PshAI and BsaAI fragment from pACYC184 (New England Biolabs) was inserted into pBRindi-73linker-intronA+ that had been digested with EcoRV and treated with CIP to yield pBRindi-73linker-intronA+-Cmr-FseI. Get a printable copy (PDF file) of the complete article (2.8M), or click on a page image below to browse page by page. Deletion analysis has mapped the minimal DNA binding domain of the VZV 140k protein, as measured in gel retardation analysis, to lie within residues 472 to 633. Selective pressures on the virus can permit the emergence of variants with enhanced use of one receptor and reduced ability to use another, altering cell tropism and pathogenesis.

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