Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cowpox”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1982

Sequence of terminal regions of cowpox virus DNA: arrangement of repeated and unique sequence elements.

One terminal EcoRI fragment of the genome of cowpox virus (CPV) strain Brighton red has been cloned in plasmid pBR325, and the nucleotide sequence of the 2,725-base-pair Sal I fragment corresponding to that at the end of the viral genome has been determined. The fragment consists of three unique sequence regions flanking two sets of repeated sequence. The repeated sequence sets are composed of four types of subunits, the majority of which are arranged in higher-order repeat units. The subunits are themselves closely related; two are subsets of a third, whereas the fourth is a recombinant of the first two. The fragment possesses no long open reading frames (maximal coding potential, 65 amino acids). The sequence of this CPV DNA Sal I fragment is compared with that of the corresponding fragment of vaccinia virus WR DNA [Baroudy, B. M., Venkatesan, S. & Moss, B. (1982) Cell 28, 315-324; Venkatesan, S., Baroudy, B. M. & Moss, B. (1981) Cell 25, 805-813]. Two of the unique sequence regions of the two viruses are related to the extent of 96%, and the third contains at least one sequence of 112 residues that is 98% homologous. As for the repeated sequence sets, those of vaccinia virus are composed of only two, rather than four, types of subunit, one of which is identical to one of the CPV subunits, whereas the other differs from another CPV subunit by only three mismatches and one deletion. However, the arrangement of subunits in the two viruses is different, that in vaccinia virus DNA being simpler. Both subunits as well as repeat units probably arose as a result of unequal crossover.

Base Sequence↗
PubMed1984

Spontaneous deletions and duplications of sequences in the genome of cowpox virus.

Examination of the genomes of 10 white-pock variants of cowpox virus strain Brighton red (CPV-BR) revealed that 9 of them had lost 32 to 38 kilobase pairs (kbp) from their right-hand ends and that the deleted sequences had been replaced by inverted copies of regions from 21 to 50 kbp long from the left-hand end of the genome. These variants thus possess inverted terminal repeats (ITRs) from 21 to 50 kbp long; all are longer than the ITRs of CPV-BR (10 kbp). The 10th variant is a simple deletion mutant that has lost the sequences between 32 and 12 kbp from the right-hand end of the genome. The limits of the inner ends of the observed deletions (between 32 and 38 kbp from the right-hand end of the CPV-BR genome) appear to be defined by the location of the nearest essential gene on the one hand and the location of the gene that encodes "pock redness" on the other. The genomes of the deletion/duplication white-pock variants appear to have been generated either by single crossover recombinational events between two CPV-BR genomes aligned in opposite directions or by the nonreciprocal transfer of genetic information. The sites where such recombination/transfer occurred were sequenced in four variants. In all of them, the sequences adjacent to such sites show no sequence homology or any other unusual structural feature. The analogous sites at the internal ends of the two ITRs of CPV-BR also were sequenced and also show no unusual features. It is likely that the ITRs of CPV-BR and of its white-pock variants, and probably those of other orthopox-virus genomes, arise as a result of nonhomologous recombination or by random nonreciprocal transfer of genetic information.

Base Sequence↗
PubMed1976

Factors involved in the expression of cowpox virus-specific antigen in Sendai virus carrier cells.

Formation of cowpox virus-specific cell surface antigen (CPVS-ag) HVJ (Sendai virus) carrier cells compared to that in parent cells. Temperature shifts from 32 to 35 to 37 degrees C for these carrier cultures reduced this enhancing activity, making them equivalent to parent cells. The eclips phase and one-step growth of CPV in the carrier cells were shorter than in normal cells. Extracts of carrier cells exhibited a stimulating activity causing the temporary rise and subsequent lowering of CPV infectivity in their reactions with CPV in vitro, suggesting a cellular acceleration of CPV uncoating. The S-ag forming ability of these carrier cells did not decrease as much as that of parent cellsin the presence of actinomycin D or puromycin. The results indicate that persistent infection with HVJ, especially the temperature-sensitive variant, promotes the first step of intracellular growth of CPV, resulting in enhanced formation of S-ag.

Animals↗
PubMed1987

Monoclonal antibodies to cowpox virus: polypeptide analysis of several major antigens.

Monoclonal antibodies directed against major antigens induced by cowpox virus (CPV) were produced. The specificities of these antibodies were established by immunoprecipitation, immunoblotting and several serological analyses, and from the cross-reactivities of these antibodies with cells infected with various other poxviruses, ectromelia virus (EV), vaccinia virus and Shope fibroma virus. The antibodies defined included ones reacting with each of the known major antigens of poxviruses, i.e. the common antigen of all poxviruses (probably NP antigen), the Orthopoxvirus-specific antigen (probably LS antigen), the haemagglutinin, the cell surface antigen, the common A-type inclusions in CPV and EV, and the antigen involved in neutralization.

Animals↗
PubMed1988

Cloning and characterization of the gene encoding the major protein of the A-type inclusion body of cowpox virus.

We have mapped and determined the nucleotide sequence of the cowpox virus (CPV) gene coding for the protein of A-type inclusion bodies (ATI). The ATI gene was mapped to the central part of the largest HindIII restriction fragment of the CPV genome. Vaccinia virus (VV) also contained a similar sequence at the equivalent position in its genome, which even under stringent conditions hybridized with the CPV ATI gene. Nucleotide sequence analysis revealed that the upstream region of the coding frame contained a sequence closely resembling the VV late promoter consensus sequence and that the gene encoded a protein of Mr 150,000.

Amino Acid Sequence↗
PubMed2004

Cowpox virus CrmA, Myxoma virus SERP2 and baculovirus P35 are not functionally interchangeable caspase inhibitors in poxvirus infections.

Cowpox virus (CPV) expresses the serpin (serine proteinase inhibitor) CrmA, an anti-inflammatory, anti-apoptotic protein required for production of red pocks on chicken chorioallantoic membranes (CAMs). In vitro, CrmA inhibits several caspases and granzyme B. Altering the critical P1-aspartate in the CrmA reactive centre loop to alanine resulted in a virus (CPV-CrmA-D303A) that resembled CPV deleted for CrmA (CPVDeltaCrmA : : lacZ); on CAMs it produced white, inflammatory pocks with activated caspase-3 and reduced virus yields, suggesting that CrmA activities are mediated via proteinase inhibition. CrmA in CPV was replaced with SERP2 from Myxoma virus (MYX) or baculovirus P35, which inhibit similar proteinases in vitro. SERP2 and P35 each blocked caspase-3-mediated apoptosis but were unable to control inflammation of CAMs. However, SERP2 and P35 restored virus yields, indicating that the decreased virus titres seen with CPVDeltaCrmA : : lacZ resulted from apoptosis rather than inflammation. To compare the activities of CrmA and SERP2 further, rabbits were infected with MYX recombinant viruses. Intradermal infection of rabbits with MYX was uniformly lethal, generating raised primary lesions and many secondary lesions. In contrast, deletion of SERP2 from MYX (MYXDeltaSERP2 : : lacZ) caused little mortality and produced flat primary lesions with few secondary lesions. Replacement of SERP2 with CrmA (MYXDeltaSERP2 : : CrmA) resulted in partial complementation with flat primary lesions, many secondary lesions and death in 70 % of the rabbits. Therefore, CrmA and SERP2 were not functionally interchangeable during infection of CAMs or rabbits, implying that these serpins have activities that are not evident from biochemical studies with human caspases.

Animals↗
PubMed1967

Effect of interferon on deoxyribonuclease induction in chick fibroblast cultures infected with cowpox virus.

An exonuclease which degrades native deoxyribonucleic acid at pH 9.2 was induced in chick embryo fibroblast cultures and in human amnion cells by infection with cowpox virus. Highly purified chick embryo interferon suppressed the induction of the enzyme in the homologous cell system but not in the human amnion cell cultures. "Mock" interferon prepared from uninfected chicken eggs and purified in the same manner as biologically active interferon preparations had no effect on the induction of the enzyme.

Amnion↗
PubMed1987

Messenger RNAs of a strongly-expressed late gene of cowpox virus contain 5'-terminal poly(A) sequences.

We have identified and characterized one of the most strongly-expressed genes of cowpox virus (CPV). This is the gene encoding the major protein component of the A-type inclusion bodies produced by this virus. This gene (designated the 160K gene) is transcribed late during the infection. Analyses of its mRNAs showed that these late RNAs, unlike all other characterized late mRNAs of poxviruses, are uniform in length. However, the most remarkable feature of the mRNAs of the 160K gene is the structure of their 5'-termini. Most of these mRNAs have 5'-terminal poly(A) sequences containing 5-21 residues. Furthermore, these 5'-terminal poly(A) sequences are not complementary to the corresponding region of the template strand of the viral DNA. Instead, the nucleotide sequences of the mRNA and the viral DNA diverge at the site of the three As in the sequence 5'-TAAATG-3' containing the gene's initiation codon. Consequently, the poly(A) provides the leader sequences of these mRNAs. These unusual 5'-terminal structures suggest that the late mRNAs of pox-virus genes are generated by a novel process.

Amino Acid Sequence↗
PubMed1987

[Cowpox virus infection in a young girl].

An genuine cowpox virus was isolated in a 6-year-old girl with a circumscribed skin lesion between the thumb and forefinger. In the beginning, the lesion was a proliferating skin change, which later became ulcerative with central hemorrhagic necrosis (umbilicated pock). Electron microscopy as well as histological, biological (cell and host range) and serological methods were used to characterize the virus. Cats and rodents are discussed as potential virus carriers. Voluntary vaccination against orthopox should be provided for persons at risk of infection.

Child↗