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#21765641   2011/07/18 Save this To Up

Mucosal immunization induces a higher level of lasting neutralizing antibody response in mice by a replication-competent smallpox vaccine: vaccinia Tiantan strain.

The possible bioterrorism threat using the variola virus, the causative agent of smallpox, has promoted us to further investigate the immunogenicity profiles of existing vaccines. Here, we study for the first time the immunogenicity profile of a replication-competent smallpox vaccine (vaccinia Tiantan, VTT strain) for inducing neutralizing antibodies (Nabs) through mucosal vaccination, which is noninvasive and has a critical implication for massive vaccination programs. Four different routes of vaccination were tested in parallel including intramuscular (i.m.), intranasal (i.n.), oral (i.o.), and subcutaneous (s.c.) inoculations in mice. We found that one time vaccination with an optimal dose of VTT was able to induce anti-VTT Nabs via each of the four routes. Higher levels of antiviral Nabs, however, were induced via the i.n. and i.o. inoculations when compared with the i.m. and s.c. routes. Moreover, the i.n. and i.o. vaccinations also induced higher sustained levels of Nabs overtime, which conferred better protections against homologous or alternating mucosal routes of viral challenges six months post vaccination. The VTT-induced immunity via all four routes, however, was partially effective against the intramuscular viral challenge. Our data have implications for understanding the potential application of mucosal smallpox vaccination and for developing VTT-based vaccines to overcome preexisting antivaccinia immunity.

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#19471247   2009/07/31 Save this To Up

Treatment with cyclooxygenase-2 inhibitors enables repeated administration of vaccinia virus for control of ovarian cancer.

Metastatic ovarian cancer is the leading cause of death among women with gynecologic malignancies in the United States. The lack of effective treatment for patients with advanced ovarian cancer warrants development of innovative therapies. Cancer therapy using oncolytic viruses represents a promising new approach for controlling tumors. Vaccinia virus has been shown to preferentially infect tumor cells but not normal tissue. However, oncolytic therapy using recombinant viruses faces the limitation of viral clearance due to generation of neutralizing antibodies. In the current study, we found that cyclooxygenase-2 (Cox-2) inhibitors circumvented this limitation, enabling repeated administration of vaccinia virus without losing infectivity. We quantified the antivaccinia antibody response using enzyme-linked immunosorbent assay (ELISA) and neutralization assays to show that treatment of Cox-2 inhibitors inhibited the generation of neutralizing antibodies. Furthermore, we showed that combination treatment of Cox-2 inhibitors with vaccinia virus was more effective that either treatment alone in treating MOSEC/luc tumor-bearing mice. Thus, the combination of Cox-2 inhibitors and vaccinia virus represents a potential innovative approach to controlling ovarian tumors.

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#8610439   1996/05/30 Save this To Up

Extracellular enveloped vaccinia virus escapes neutralization.

The vaccinia virus forms two morphologically distinct infectious virus particles: intracellular mature virus (IMV) and extracellular enveloped virus (EEV). The envelope of EEV is a Golgi-derived membrane (wrapping membrane). A mutant (vRB10) lacks the ability to form the EEV. In medium containing a neutralizing antibody (2D5mAb), the vRB10 mutant was diluted out from infected cells, whereas the IHD-J strain of vaccinia virus replicated well. The result indicated that the 2D5mAb specifically neutralized the IMV. The 2D5-resistant EEV appeared at 6-7 hr postinfection, and over 65% of infectious virus in the culture fluid was EEV at 48 hr after infection. The EEV was resistant not only to the 2D5mAb but also against several neutralizing antibodies, including polyclonal antivaccinia serum reactive with proteins of the wrapping membrane. Freeze-thawing and other procedures that may damage the wrapping membrane converted the EEV to a form susceptible to the antibodies. Since specific infectivity was not affected by the damage or by exposure to antibody against the wrapping membrane proteins, the wrapping membrane did not directly participate in penetration. The infection process of vaccinia virus was analyzed by comparison of responses to acid treatment between normal IMV and trypsin-treated IMV. Proteolytically activated IMV infected rapidly responding to acid. The protected form virus, which was noninfectious under usual conditions, was proteolytically activated on cell membrane then responded to the acid. Proteolysis activated the virus, and an acidic condition accelerated fusion between the activated IMV and plasma membrane. The virus in the EEV wrapping membrane was the activated form that has the capacity to fuse with the cell membrane. However, the infection of intact EEV was more sensitive against lysosomotropic agents (NH4Cl, neutral red) than that of the trypsin-activated IMV. Resistance to the 2D5mAb, sensitivity to lysosomotropic agents, and acceleration of infection by acid suggested that the intact EEV penetrated by virus-endosome membrane fusion. The combined effect of the presence of wrapping membrane and the process of internalization via an endocytic mechanism rendered EEV resistant to neutralizing antibodies.

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#1710246   1991/07/10 Save this To Up

Antiviral protection by CD8+ versus CD4+ T cells. CD8+ T cells correlating with cytotoxic activity in vitro are more efficient in antivaccinia virus protection than CD4-dependent IL.

T cell-mediated protection against a recombinant vaccinia virus was evaluated in mice with respect to the relative contributions of CTL vs that of T cell-dependent IL and of CD4+ cells. H-2b mice primed with the wildtype of vesicular stomatitis virus serotype Indiana (VSV-IND wt) mount an in vitro measurable cytotoxic response against the nucleoprotein (NP) of VSV-IND and are protected against a challenge infection with a vaccinia-VSV recombinant virus expressing the NP of VSV-IND (vacc-IND-NP). Their protective mechanism was highly susceptible to in vivo depletion of CD8+ T cells, but resistant to CD4+ depletion or treatment with anti-IFN-gamma and anti-TNF-alpha. Surprisingly, also VSV-CTL nonresponder H-2k mice were protected against a challenging infection with vacc-IND-NP when primed with VSV-IND wt. In contrast to the CTL responder H-2b mice, this protection was highly susceptible to CD4+ T cell depletion and to anti-IFN-gamma or anti-TNF-alpha treatment, but resistant to CD8+ T cell depletion. Antibodies were not responsible because they failed to transfer protection; in contrast CD4+ T cells conferred significant protection. VSV-CTL responder H-2b and nonresponder H-2k mice were protected almost equally well against a challenge dose of 10(3) pfu vacc-IND-NP inoculated intracerebrally. However, after intracerebral challenge with 5 x 10(6) pfu vacc-IND-NP, the CTL nonresponder mice died, whereas the CTL responder mice eliminated the virus by day 5. These results collectively show that CD4+ T cell-dependent IL may mediate antiviral protection, but their efficiency is relatively weak compared with CD8-mediated protection correlating with cytotoxic activity in vitro.

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#2521235   1989/02/01 Save this To Up

Role of lymphokine-secreting CD8+ T cells in cytotoxic T lymphocyte responses against vaccinia virus.

The present study has examined the relative role of CD4+ and CD8+ Th cells in the generation and reactivation of antivaccinia virus memory CTL responses. We show that mice primed in vivo to vaccinia virus generate in vitro antivaccinia virus memory CTL responses through both CD4+ and CD8+ Th cell pathways, with the CD4+ Th pathway being the more prominent of the two. In addition, we show that vaccinia virus-specific CD8+ Th cell function is mediated through production of lymphokines, including IL-2, and that the CD8+ Th cell component in the CTL response is labile, decreasing progressively with increasing time after in vivo priming. Thus, this study demonstrates the existence of two phenotypically distinct Th cell pathways in the generation of antivirus CTL responses.

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#66909   1977/05/12 Save this To Up

Antiviral activities of acyl derivatives of 2,2'-anhydro-1-beta-D-arabinofuranosylcytosine and 1-beta-D-arabinofuranosylcytosine in cell culture.

Antiviral activities of acyl derivatives (3'-O-octanoyl and 3'-O-decanoyl) of 2,2'-anhydro-1-beta-d-arabinofuranosylcytosine (cyclo-C) and 1-beta-d-arabinofuranosylcytosine (Ara-C) were compared with other antiviral nucleosides, and some biological characteristics of the antiviral activity were investigated. Among those synthesized acyl derivatives, 3'-O-decanoyl ara-C was the most active against deoxyribonucleic acid viruses, with an activity comparable to that of Ara-C. Acyl derivatives of cyclo-C were somewhat less active than their Ara-C counterparts. In the value of therapeutic index, 1-beta-d-arabinofuranosyladenine was superior to the others, followed by 5-iodo-2'-deoxyuridine. In comparing the sensitivity of two serotypes of herpes simplex virus it was found that Ara-C and its ester, as well as its cyclo-C counterpart, were more active against the type 2 than the type 1 strain. The activity of 3'-O-decanoyl Ara-C, like that of its parent, was diminished by treatment with cytidine deaminase from mouse kidney, but 3'-O-decanoyl cyclo-C was resistant to this treatment. In comparative studies of 3'- and 5'-O-acyl Ara-C's, antivaccinia virus activity of 3'-O-palmitoyl Ara-C was significantly superior to its 5'-counterpart. The inhibitory activity of 5'-O-decanoyl Ara-C was markedly reduced by the presence of a threefold molar excess of eserine sulfate, a choline esterase inhibitor, whereas the 3'-acyl Ara-C was not affected by the inhibitor in any combination. This result indicates that enzymatic hydrolysis of the 3'-ester to Ara-C, which is inhibited by eserine sulfate, did not occur in this cell culture.

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#1257248   1976/06/02 Save this To Up

Effect of cytosine, arabinoside, iododeoxyuridine, ethyldeoxyuridine, thiocyanatodeoxyuridine, and ribavirin on tail lesion formation in mice infected with vaccinia virus.

Mice infected intravenously with vaccinia virus develop characteristic lesions over the entire tail surface. This experimental virus infection presents a highly sensitive and reliable model for evaluating the antivaccinia activity of antiviral compounds. Ara-C (1-beta-D-arabinofuranosylcytosine), ribavirin (1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide), IUdR (5-iodo-2'-deoxyuridine) as well as two novel analogs of IUdR, EtUdR (5-ethyl-2'-deoxyuridine), and NCSUdR (5-thiocyanato-2'-deoxyuridine), were found to inhibit the formation of vaccinia tail lesions, when administered intraperitoneally once daily for 7 days starting immediately after virus infection. The order of (decreasing) activity was: ara-C greater than IUdR greater than NCSUdR greater than ribavirin greater than EtUdR. Various drug combinations, involving IUdR + ara-C, NCSUdR + ara-C, NCSUdR + IUdR, NSCUdR + ribavirin, etc., were evaluated but none proved more efficacious than either compound administered alone.

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#5694419   1968/06/03 Save this To Up

In vivo antiviral properties of biologically active compounds. II. Studies with influenza and vaccinia viruses.

The in vivo anti-influenza virus and antivaccinia virus activity of 156 biologically active compounds was determined. One of two criteria was used for evaluating activity against the influenza virus. The criteria were increase in survivor number and mean survival time, and reduction in virus-induced lung consolidation in treated, infected Swiss mice. Increase in survivor number and mean survival time were the criteria for evaluation of antivaccinia virus activity. Several drug doses were tested against two virus concentrations to demonstrate antiviral activity more clearly. Two compounds were considered significantly active against the influenza virus: DL-noformicin (NSC 72942) and amantadine hydrochloride (NSC 83653). Eleven compounds had reproducible activity against vaccinia virus: isatin-beta-thiosemicarbazone (NSC 721), 6-azauracil (NSC 3425), 9-alpha-fluoro-2alpha-methylhydrocortisone 21-acetate (NSC 12601), 5-[bis(2-chloroethyl)amino]uracil (NSC 34462), 5-iodo-2'-deoxyuridine (NSC 39661), streptonigrin (NSC 45383), N-methylisatin beta-thiosemicarbazone (NSC 69811), cytovirin (NSC 91770), 9-beta-D-arabinofuranosyladenine (NSC 404241), and 5-(mercaptomethyl)uracil (NSC 529351).

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