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PubMed1989

Studies on poxvirus infection in cats.

The development of clinical disease and the pathogenesis of cowpox were studied in domestic cats inoculated by a variety of routes. Intradermal titration in two cats demonstrated that as little as five pfu of cowpox virus caused a primary skin lesion. Intradermal inoculation of greater than or equal to 10(5) pfu cowpox virus resulted in severe systemic disease. Large amounts of virus (greater than or equal to 10(3) pfu/g) were isolated from skin lesions and the turbinates of cats killed at eight and 11 days post-inoculation (dpi). Lesser amounts of virus (congruent to 10(2) pfu/g) were isolated from lymphoid tissues and the lung, and small amounts of virus were isolated from various other tissues. A white cell-associated viraemia was detected from 5 dpi onwards. Skin scarification with 10(3) or 50 pfu cowpox virus enabled reproduction of the naturally-acquired disease. Cat-to-cat transmission was demonstrated from cats inoculated by skin scarification, but caused only subclinical infection in sentinel cats. Oronasal inoculation resulted in transient coryza and milder generalized disease than skin inoculation, and no transmission to sentinel cats. Preliminary investigations showed vaccinia virus (Lister strain) to be of low infectivity in cats while inoculation of ectromelia virus (Mill Hill strain) did not cause any clinical signs.

Animals↗
PubMed1991

Enhanced recombination associated with the presence of insertion and deletion mutations in poxvirus-infected cells.

Genetic crosses were performed in cells infected by Shope fibroma virus in order to determine whether poxviral recombination is influenced by the types of mutations participating in a cross. Infected cells were cotransfected with marked bacteriophage lambda DNAs and, after DNA recovery, the substrates were packaged into infectious particles using in vitro packaging extracts. This made it possible to analyze the products of poxviral recombination systems using lambda mutants plated on Escherichia coli. It was observed that, regardless of the kind of substitution, all point mutations recombined in virus-infected cells with frequency dependent only on distance. In contrast, when crosses were performed when one of the mutations was an insertion or a deletion, recombination was stimulated by amounts ranging from 20 to 100%. This phenomenon was not dependent on the size of the nonhomology, was observed across a range of marker separations, and was not due to packaging, plating, or reversion artifacts. The best explanation for this marker effect is that regions of nonhomology act to block the migration of strand-exchange intermediates thereby forcing exchange in the immediate vicinity of a nonhomology. This hypothesis is compatible with the failure to detect loop-heteroduplex intermediates and the specific effects of altered marker configurations in four-factor crosses. It is also compatible with the observation that when two nonhomologies were crossed, they appeared to inhibit recombination in the region located between the two elements. These observations suggest a possible way in which poxviral recombination might be targetted into, or away from, regions of particular interest. The similarities between these observations and data derived from phage and fungal experiments also provide fundamental insights into the mechanism of poxviral recombination.

Animals↗
PubMed1991

Cutaneous tumour-like lesions due to poxvirus infection in Chilean flamingos.

Cutaneous tumour-like growths were observed on the face and other areas of the body surface of young Chilean flamingos. In the cells of these lesions, avian pox-specific cytoplasmic inclusion bodies were observed by light microscopy and virus particles were detected under an electron-microscope. It was diagnosed as avian pox.

Animals↗
PubMed2000

Modulation of chemokines by poxvirus infections.

Viruses that successfully replicate within the host have devised strategies to subvert or evade the challenges posed by the innate and adaptive immune responses. Many investigators are now beginning to dissect the diverse and complex interactions involving chemokines, chemokine receptors and viral infection. In recent years, much attention has been focused on the role of chemokines in antiviral defense.

Animals↗
PubMed2000

Interferon-inducible chemokines and immunity to poxvirus infections.

The biological roles of two interferon-inducible chemokines, monokine induced by gamma interferon (Mig) and cytokine responsive gene (Crg-2), in the immune response against vaccinia virus (VV) and ectromelia virus (EV) infections are discussed. To investigate their antiviral effects in vivo, the expression profiles of these chemokines during the course of VV or EV infections were first established. Mig and Crg-2 were induced in multiple organs at high levels early after infection with VV. Both chemokines were rapidly induced in popliteal lymph nodes of C57BL/6 mice but not in BALB/c mice following infection with EV. Secondly, recombinant vaccinia viruses (rVV) encoding Mig or Crg-2 were constructed to investigate the immunobiology of infection in athymic, nude and euthymic, normal mice. Finally, the EV model in combination with recombinant Mig and Crg-2 proteins was used to test their effects on viral replication and immune responses in vivo. The results of these investigations demonstrate that the mechanisms of Mig- and Crg-2-induced viral clearance involve natural killer cells and interferons.

Animals↗
PubMed2003

Shared modes of protection against poxvirus infection by attenuated and conventional smallpox vaccine viruses.

The concern about bioterrorism with smallpox has raised the possibility of widespread vaccination, but the greater prevalence of immunocompromised individuals today requires a safer vaccine, and the mechanisms of protection are not well understood. Here we show that, at sufficient doses, the protection provided by both modified vaccinia Ankara and NYVAC replication-deficient vaccinia viruses, safe in immunocompromised animals, was equivalent to that of the licensed Wyeth vaccine strain against a pathogenic vaccinia virus intranasal challenge of mice. A similar variety and pattern of immune responses were involved in protection induced by modified vaccinia Ankara and Wyeth viruses. For both, antibody was essential to protect against disease, whereas neither effector CD4+ nor CD8+ T cells were necessary or sufficient. However, in the absence of antibody, T cells were necessary and sufficient for survival and recovery. Also, T cells played a greater role in control of sublethal infection in unimmunized animals. These properties, shared with the existing smallpox vaccine, provide a basis for further evaluation of these replication-deficient vaccinia viruses as safer vaccines against smallpox or against complications from vaccinia virus.

Animals↗
PubMed1976

A single genetic element in H-2K affects mouse T-cell antiviral function in poxvirus infection.

Cell transfer experiments using mice with recombinant H-2 haplotypes were used to map the H-2 regions which must be shared by ectromelia-immune T-cell donors and virus-infected recipients for transfer of virus clearance mechanisms in the spleen. K- or D-region genes were necessary and sufficient; I-region genes were not involved. The remainder of the mouse genome could be varied widely without impairing the efficacy of T-cell antiviral function, provided either a K or a D region was shared in the donor-receipient combination. A mutation in a single genetic element of the K region of the H-2 complex abolished the antiviral effect of immune T-cell transfer in a donor-recipient combination which shared the K end.

Animals↗
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↗
PubMed1974

Treatment of poxvirus infections in rabbits with 9-beta-D-arabinofuranosyladenine.

The antiviral efficacy of 9-beta-d-arabinofuranosyladenine (ara-A) was evaluated in localized lesions produced by the intradermal inoculation of rabbits with vaccinia virus (VV) and rabbit Shope fibroma virus (SFV). Ara-A administered intraperitoneally suppressed or significantly reduced the cutaneous pustular lesions produced by VV as well as the benign skin tumors caused by the SFV. With a daily dose of 300 mg/kg given for 5 days starting at the time of infection, or with 600 mg/kg daily starting 3 days after inoculation, we were able to suppress completely the formation of tumors induced by the SFV. The appearance of pustular lesions induced by VV was completely suppressed by a dose of 600 mg of ara-A per kg given for 3 days when the treatment was initiated at the time of infection, but a significant reduction in the number of pustular lesions was obtained with a single dose of 600 mg/kg, or with five doses of 300 mg/kg starting 24 h after inoculation. No toxic effect of ara-A was noted in the treated rabbits.

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