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At least 91 records · Page 5Linked to original sources
PubMed2005

Antiviral chemotherapy facilitates control of poxvirus infections through inhibition of cellular signal transduction.

The EGF-like domain of smallpox growth factor (SPGF) targets human ErbB-1, inducing tyrosine phosphorylation of certain host cellular substrates via activation of the receptor's kinase domain and thereby facilitating viral replication. Given these findings, low molecular weight organic inhibitors of ErbB-1 kinases might function as antiviral agents against smallpox. Here we show that CI-1033 and related 4-anilinoquinazolines inhibit SPGF-induced human cellular DNA synthesis, protein tyrosine kinase activation, and c-Cbl association with ErbB-1 and resultant internalization. Infection of monkey kidney BSC-40 and VERO-E6 cells in vitro by variola strain Solaimen is blocked by CI-1033, primarily at the level of secondary viral spreading. In an in vivo lethal vaccinia virus pneumonia model, CI-1033 alone promotes survival of animals, augments systemic T cell immunity and, in conjunction with a single dose of anti-L1R intracellular mature virus particle-specific mAb, fosters virtually complete viral clearance of the lungs of infected mice by the eighth day after infection. Collectively, these findings show that chemical inhibitors of host-signaling pathways exploited by viral pathogens may represent potent antiviral therapies.

Animals↗
PubMed2006

Enhancement of CD8+ T cell immunity in the lung by CpG oligodeoxynucleotides increases protective efficacy of a modified vaccinia Ankara vaccine against lethal poxvirus infection even in a CD4-deficient host.

Immunostimulatory CpG oligodeoxynucleotides (ODN) have proven effective as adjuvants for protein-based vaccines, but their impact on immune responses induced by live viral vectors is not known. We found that addition of CpG ODN to modified vaccinia Ankara (MVA) markedly improved the induction of longer-lasting adaptive protective immunity in BALB/c mice against intranasal pathogenic vaccinia virus (Western Reserve; WR). Protection was mediated primarily by CD8(+) T cells in the lung, as determined by CD8-depletion studies, protection in B cell-deficient mice, and greater protection correlating with CD8(+) IFN-gamma-producing cells in the lung but not with those in the spleen. Intranasal immunization was more effective at inducing CD8(+) T cell immunity in the lung, and protection, than i.m. immunization. Addition of CpG ODN increased the CD8(+) response but not the Ab response. Depletion of CD4 T cells before vaccination with MVA significantly diminished protection against pathogenic WR virus. However, CpG ODN delivered with MVA was able to substitute for CD4 help and protected CD4-depleted mice against WR vaccinia challenge. This study demonstrates for the first time a protective adjuvant effect of CpG ODN for a live viral vector vaccine that may overcome CD4 deficiency in the induction of protective CD8(+) T cell-mediated immunity.

Adjuvants, Immunologic↗
PubMed1990

Chlamydial and poxvirus infections of circulating monocytes of a flap-necked chameleon (Chamaeleo dilepis).

Of blood films examined from 170 specimens of 15 Chamaeleo spp. in Tanzania, three C. dilepis had an intracytoplasmic inclusion within monocytes. One of the lizards was maintained in captivity and was sequentially bled over a 55 day period. At 46 days, a second type of inclusion was occasionally seen within monocytes. The lizard became ill and was euthanatized on day 55. All circulating monocytes were found to have either one or both types of inclusions. Histologic examination of multiple tissues demonstrated similar inclusions within macrophages in the spleen and liver. Transmission electron microscopic examination of monocytes revealed the presence of a chlamydia-like organism and pox-like virus. These pathogens have not been reported previously in chameleons, nor has a combined infection of circulating monocytes with these two pathogens been reported for any animal.

Animals↗
PubMed1992

Inhibition of agonist-induced activation of phospholipase C following poxvirus infection.

Recent studies indicate that viruses may influence polyphosphoinositide levels. This study has examined the effects of vaccinia virus infection on phospholipase C activity. Infection of BS-C-1 cells, an African Green Monkey kidney cell line, or A431 cells, a human carcinoma cell line, with vaccinia virus inhibits receptor-mediated phospholipase C activation. As a consequence, agonist-mediated Ca2+ mobilization in BS-C-1 cells also was inhibited by vaccinia virus infection. Alleviation of the inhibition of phospholipase C activation was observed in vaccinia virus-infected cells treated with cycloheximide without influencing uninfected cells. Treatment of infected cells with alpha-amanitin, an inhibitor of host mRNA synthesis but not virus mRNA synthesis, failed to alleviate the inhibition of phospholipase C activation. Together these results suggest that a virus-encoded gene product mediates the inhibition of phospholipase C activation without the need of a virus-induced host factor. Analysis of the processes involved in the formation of inositol (1,4,5)-trisphosphate and mobilization of intracellular Ca2+ indicate that the vaccinia virus gene product exerts its inhibitory effects at the level of phospholipase C activity. This may occur by either directly reducing the amount of phospholipase C, reducing the specific activity of phospholipase C, or by inhibiting the association of phospholipase C with its substrate, phosphatidylinositol 4,5-bisphosphate.

Adenosine Triphosphate↗
PubMed1976

Poxvirus infection of the baboon (Papio cynocephalus).

Ten serial passages of monkeypox (MPV), vaccinia, variola, and chimpanzeepox (chimp-9) viruses were performed in baboons (Papio cynocephalus) via skin scarification. Comparisons of clinical and virological results indicate that MPV and vaccinia are very closely related and that variola and chimp-9 viruses are identical. These findings suggest that infections of simians with chimp-9 virus resulted from contact with variola virus, the source of which is still unknown. On the other hand, MPV in monkeys may have resulted from contact with recently vaccinated humans, serial passage through simian hosts resulting in the biological alterations that produced MPV.

Animals↗
PubMed1977

Factors concerning the immunity to poxvirus infection.

Two kinds of early antigens were shown in vaccinia-infected cells, one heat (56 degrees, 30 min)-stable (ES antigen) and the other heat-labile (EL antigen). Both antigens do not induce circulating neutralizing antibody in rabbits, but resistance to intradermal inoculation of active virus was observed when animals were immunized with either antigen in combination with Freund's complete adjuvant. Vaccinia-specific haemagglutinin (VHA) associated with infected cell membrane was purified and its antigenicity was also studied. Rabbits showed a good antibody response to VHA and some animals also showed neutralizing antibody, though in a small amount, to either intracellular (ICV) or extracellular (EVC) virus. Rabbits immunized with membrane antigens obtained from either VHA-positive or negative virus in combination with Freund's adjuvant showed skin restance to challenge with active virus. It was suggested that antibody against ECV might be responsible for the resistance.

Animals↗
PubMedDate not supplied

Poxvirus infection in a spectacled Amazon parrot (Amazona albifrons).

Avian pox was determined to be the cause of death of a spectacled Amazon parrot (Amazona albifrons). Intracytoplasmic inclusion bodies were visualized by light microscopy in esophageal and bronchial epithelial lesions. Electron microscopy revealed pox-virus virions in the inclusions.

Animals↗