cowpox/protease

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Retroviral protease-like gene in the vaccinia virus genome.

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The retroviral protease-encoding region, PR, situated between the gag and pol genes, underwent gene duplication in the lineage now represented by simian retrovirus type 1; the sequence of the duplicated segment has diverged considerably from the present PR sequence [Power, M.D., Marx, P.A., Bryant,

Cleavage of Dicer protein by I7 protease during vaccinia virus infection.

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Dicer is the key component in the miRNA pathway. Degradation of Dicer protein is facilitated during vaccinia virus (VV) infection. A C-terminal cleaved product of Dicer protein was detected in the presence of MG132 during VV infection. Thus, it is possible that Dicer protein is cleaved by a viral

Analysis of cross reactivity of retrovirus proteases using a vaccinia virus-T7 RNA polymerase-based expression system.

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We have used the vaccinia virus-T7 RNA polymerase-based expression system for studies on the activity of proteases from various retroviruses on homologous and heterologous Gag polyproteins in eukaryotic cells. Proteases from human immunodeficiency virus (HIV) types 1 and 2, equine infectious anaemia

Increased antibody responses to human papillomavirus type 16 L1 protein expressed by recombinant vaccinia virus lacking serine protease inhibitor genes.

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The L1 gene of human papillomavirus type 16 (HPV-16) driven by the vaccinia virus major late 4b gene promoter has been inserted into three different sites of the vaccinia virus genome. Insertion into the thymidine kinase (TK) gene was achieved by selection of TK- mutants in BUdR on TK- cells.

Cellular proteases increased in paramyxovirus (Sendai virus) carrier cells possibly responsible for enhanced formation of cowpox virus-specific cell surface antigen.

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Cowpox virus (CPV) growth and its S-ag (cell surface antigen) formation in HVJ (Sendai virus) carrier cells pre-treated with Actinomycin D or Puromycin were not affected as much as those in parent cells. These suggest the different cellular functions of carrier cells. The activity of carrier cell

Intracellular expression and processing of foot-and-mouth disease virus capsid precursors using vaccinia virus vectors: influence of the L protease.

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cDNA cassettes of FMDV have been constructed which encode the capsid precursor (P1-2A) alone or with the proteases L and 3C which are required for processing of this precursor to the products 1AB, 1C, and 1D. These cassettes have been analyzed using in vitro transcription and translation reactions

Hemorrhage in lesions caused by cowpox virus is induced by a viral protein that is related to plasma protein inhibitors of serine proteases.

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Several recombinant cowpox viruses were constructed and used to identify a viral gene that controls the production of hemorrhage in lesions caused by the Brighton Red strain of cowpox virus (CPV-BR). This gene is located in the KpnD fragment of CPV-BR DNA, between 31 and 32 kilobases from the end of

Non-essential genes in the vaccinia virus HindIII K fragment: a gene related to serine protease inhibitors and a gene related to the 37K vaccinia virus major envelope antigen.

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The complete nucleotide sequence of a cloned copy of the HindIII K fragment of the WR strain of vaccinia virus has been determined. Eight open reading frames (ORFs) have been identified, on the basis of size and codon usage. The predicted amino acid sequences of the putative genes have been compared

The vaccinia virus K2L gene encodes a serine protease inhibitor which inhibits cell-cell fusion.

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In certain circumstances, cells infected with vaccinia virus (VV) undergo fusion, but this does not occur in tissue cultures infected with wild-type VV. The VV genome includes three genes (B24R, B13R, and K2L) encoding polypeptides that are structurally related to members of the plasma serine

Interference with vaccinia virus growth caused by insertion of the coding sequence for poliovirus protease 2A.

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Attempts were made to express noninfectious derivatives of full-length type 1 (Mahoney) and type 2 (Lansing) poliovirus cDNAs in live recombinant vaccinia viruses for vaccine purposes. Vaccinia virus (VV) would not tolerate insertions of polio cDNA containing the coding sequence for the polio

A vaccinia serine protease inhibitor which prevents virus-induced cell fusion.

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A deletion mutant lacking the non-essential vaccinia virus gene K2L, a member of the serine protease inhibitor superfamily, was constructed. This virus replicates in vitro in all cell types tested and its virulence and immunogenicity in vivo are comparable to those of the parent virus in

Expression of functional protease and subviral particles by vaccinia virus containing equine infectious anaemia virus gag and 5' pol genes.

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Cells infected with vaccinia viruses expressing the equine infectious anaemia virus (EIAV) gag gene (VGag) or gag plus the 5' pol encoding protease (VGag/PR) were evaluated with monoclonal antibody to a p26 capsid protein linear epitope (QEISKFLTD). Both recombinant viruses expressed Gag precursor

Vaccinia virus encodes two proteins that are structurally related to members of the plasma serine protease inhibitor superfamily.

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Nucleotide sequencing adjacent to the right inverted terminal repetition of the vaccinia virus genome revealed two genes encoding polypeptides that are structurally related to members of the plasma serine protease inhibitor superfamily (SPI). Inclusion in the superfamily is based on extensive amino

Immunogenicity of recombinant Modified Vaccinia Ankara Viruses (rMVA) expressing HIV-1 Indian subtype C gag-protease and env-gp120 genes in mice.

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India has currently an estimated 5.1 million HIV-infected individuals, and almost 95%of them are infected with subtype C strain. Therefore, it is imperative that a vaccine from locally circulating Indian HIV-1 subtype C be developed which would induce a robust immune response in the recipients. In

REACTIVATION OF PROTEASE-INACTIVATED VACCINIA VIRUS BY HOMOLOGOUS AND MUTANT VIRUSES.

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