Journal articles: 'Virus challenge'

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Ryan Cross. "Virus variants challenge vaccines." C&EN Global Enterprise 99, no. 4 (February 1, 2021): 4. http://dx.doi.org/10.1021/cen-09904-leadcon.

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Shi, Yi. "New Virus, New Challenge." Innovation 1, no. 1 (May 2020): 100005. http://dx.doi.org/10.1016/j.xinn.2020.04.005.

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Khatissian, Emmanuel, Valérie Monceaux, Marie-Christine Cumont, Marie-Paule Kieny, Anne-Marie Aubertin, and Bruno Hurtrel. "Persistence of Pathogenic Challenge Virus in Macaques Protected by Simian Immunodeficiency Virus SIVmacΔnef." Journal of Virology 75, no. 3 (February 1, 2001): 1507–15. http://dx.doi.org/10.1128/jvi.75.3.1507-1515.2001.

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ABSTRACT Live attenuated simian immunodeficiency virus (SIV) is the most efficient vaccine yet developed in monkey models of human immunodeficiency virus infection. In all successful vaccine trials, attenuation was achieved by inactivating at least the nefgene. We investigated some virological and immunological characteristics of five rhesus macaques immunized with anef-inactivated SIVmac251 molecular clone (SIVmac251Δnef) and challenged 15 months later with the pathogenic SIVmac251 isolate. Three animals were killed 2 weeks postchallenge (p.c.) to search for the challenge virus and to assess immunological changes in various organs. The other two animals have been monitored up for 7 years p.c., with clinical and nefgene changes being noted. The animals killed showed no increase in viral load and no sign of a secondary immune response, although the challenged virus was occasionally detected by PCR. In one of the monkeys being monitored, the vaccine virus persisted and an additional deletion occured in nef. In the other monkey that was monitored, the challenge and the vaccine (Δnef) viruses were both detected by PCR until a virus with a hybrid nefallele was isolated 48 months p.c. This nef hybrid encodes a 245-amino-acid protein. Thus, our results show (i) that monkeys were not totally protected against homologous virus challenge but controlled the challenge very efficiently in the absence of a secondary immune response, and (ii) that the challenge and vaccine viruses may persist in a replication-competent form for long periods after the challenge, possibly resulting in recombination between the two viruses.

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Song, Yufeng, Xiang Wang, Hongbo Zhang, Xinying Tang, Min Li, Jufang Yao, Xia Jin, Hildegund C. J. Ertl, and Dongming Zhou. "Repeated Low-Dose Influenza Virus Infection Causes Severe Disease in Mice: a Model for Vaccine Evaluation." Journal of Virology 89, no. 15 (May 20, 2015): 7841–51. http://dx.doi.org/10.1128/jvi.00976-15.

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ABSTRACTInfluenza infection causes severe disease and death in humans. In traditional vaccine research and development, a single high-dose virus challenge of animals is used to evaluate vaccine efficacy. This type of challenge model may have limitations. In the present study, we developed a novel challenge model by infecting mice repeatedly in short intervals with low doses of influenza A virus. Our results show that compared to a single high-dose infection, mice that received repeated low-dose challenges showed earlier morbidity and mortality and more severe disease. They developed higher vial loads, more severe lung pathology, and greater inflammatory responses and generated only limited influenza A virus-specific B and T cell responses. A commercial trivalent influenza vaccine protected mice against a single high and lethal dose of influenza A virus but was ineffective against repeated low-dose virus challenges. Overall, our data show that the repeated low-dose influenza A virus infection mouse model is more stringent and may thus be more suitable to select for highly efficacious influenza vaccines.IMPORTANCEInfluenza epidemics and pandemics pose serious threats to public health. Animal models are crucial for evaluating the efficacy of influenza vaccines. Traditional models based on a single high-dose virus challenge may have limitations. Here, we describe a new mouse model based on repeated low-dose influenza A virus challenges given within a short period. Repeated low-dose challenges caused more severe disease in mice, associated with higher viral loads and increased lung inflammation and reduced influenza A virus-specific B and T cell responses. A commercial influenza vaccine that was shown to protect mice from high-dose challenge was ineffective against repeated low-dose challenges. Overall, our results show that the low-dose repeated-challenge model is more stringent and may therefore be better suited for preclinical vaccine efficacy studies.

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Mumford, J. A., J. M. Wood, C. Folkers, and G. C. Schild. "Protection against experimental infection with influenza virus A/equine/Miami/63 (H3N8) provided by inactivated whole virus vaccines containing homologous virus." Epidemiology and Infection 100, no. 3 (June 1988): 501–10. http://dx.doi.org/10.1017/s0950268800067236.

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SummaryThirty-one ponies immunized with inactivated virus vaccine containing A/equine/Miami/63 (H3N8) virus and six seronegative ponies were experimentally challenged with the homologous virus strain. All G unvaccinated ponies and 11 out of 31 vaccinated ponies became infected. A clear relationship between pre-challenge antibody, measured by single radial haemolysis (SRH), and protection was demonstrated as judged by virus excretion, febrile responses and antibody responses. Those ponies with SRH antibody levels > 74 mm2 were completely protected against challenge infection by the intranasal route.

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Rahman, Md Rezwanur. "Zika Virus An Upcoming Challenge?" Delta Medical College Journal 5, no. 1 (February 4, 2017): 1–3. http://dx.doi.org/10.3329/dmcj.v5i1.31416.

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Anderson, Larry J., and Edward E. Walsh. "The Challenge of Respiratory Syncytial Virus Human Challenge Studies." New England Journal of Medicine 386, no. 7 (February 17, 2022): 696–97. http://dx.doi.org/10.1056/nejme2118465.

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McDermott, Adrian B., Jacque Mitchen, Shari Piaskowski, Ivna De Souza, Levi J. Yant, Jason Stephany, Jessica Furlott, and David I. Watkins. "Repeated Low-Dose Mucosal Simian Immunodeficiency Virus SIVmac239 Challenge Results in the Same Viral and Immunological Kinetics as High-Dose Challenge: a Model for the Evaluation of Vaccine Efficacy in Nonhuman Primates." Journal of Virology 78, no. 6 (March 15, 2004): 3140–44. http://dx.doi.org/10.1128/jvi.78.6.3140-3144.2004.

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ABSTRACT Simian immunodeficiency virus (SIV) challenge of rhesus macaques provides a relevant model for the assessment of human immunodeficiency virus (HIV) vaccine strategies. To ensure that all macaques become infected, the vaccinees and controls are exposed to large doses of pathogenic SIV. These nonphysiological high-dose challenges may adversely affect vaccine evaluation by overwhelming potentially efficacious vaccine responses. To determine whether a more physiologically relevant low-dose challenge can initiate infection and cause disease in Indian rhesus macaques, we used a repeated low-dose challenge strategy designed to reduce the viral inoculum to more physiologically relevant doses. In an attempt to more closely mimic challenge with HIV, we administered repeated mucosal challenges with 30, 300, and 3,000 50% tissue culture infective doses (TCID50) of pathogenic SIVmac239 to six animals in three groups. Infection was assessed by sensitive quantitative reverse transcription-PCR and was achieved following a mean of 8, 5.5, and 1 challenge(s) in the 30, 300, and 3,000 TCID50 groups, respectively. Mortality, humoral immune responses, and peak plasma viral kinetics were similar in five of six animals, regardless of challenge dose. Interestingly, macaques challenged with lower doses of SIVmac239 developed broad T-cell immune responses as assessed by ELISPOT assay. This low-dose repeated challenge may be a valuable tool in the evaluation of potential vaccine regimes and offers a more physiologically relevant regimen for pathogenic SIVmac239 challenge experiments.

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Brasel, Trevor, Jason E. Comer, Shane Massey, Jeanon Smith, Jennifer Smith, Matthew Hyde, Andrew Kocsis, et al. "Mucosal Challenge Ferret Models of Ebola Virus Disease." Pathogens 10, no. 3 (March 4, 2021): 292. http://dx.doi.org/10.3390/pathogens10030292.

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Recent studies have shown the domestic ferret (Mustela putorius furo) to be a promising small animal model for the study of Ebola virus (EBOV) disease and medical countermeasure evaluation. To date, most studies have focused on traditional challenge routes, predominantly intramuscular and intranasal administration. Here, we present results from a non-clinical pathogenicity study examining oronasal, oral, and ocular mucosal challenge routes in ferrets. Animals were challenged with 1, 10, or 100 plaque forming units EBOV followed by monitoring of disease progression and biosampling. Ferrets administered virus via oronasal and oral routes met euthanasia criteria due to advanced disease 5–10 days post-challenge. Conversely, all ferrets dosed via the ocular route survived until the scheduled study termination 28-day post-challenge. In animals that succumbed to disease, a dose/route response was not observed; increases in disease severity, febrile responses, serum and tissue viral load, alterations in clinical pathology, and gross/histopathology findings were similar between subjects. Disease progression in ferrets challenged via ocular administration was unremarkable throughout the study period. Results from this study further support the ferret as a model for EBOV disease following oral and nasal mucosa exposure.

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Moser, Charlotte A., Sarah Cookinham, Susan E. Coffin, H. Fred Clark, and Paul A. Offit. "Relative Importance of Rotavirus-Specific Effector and Memory B Cells in Protection against Challenge." Journal of Virology 72, no. 2 (February 1, 1998): 1108–14. http://dx.doi.org/10.1128/jvi.72.2.1108-1114.1998.

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ABSTRACT Adult BALB/c mice were orally inoculated with murine (strain EDIM), simian (strain RRV), or bovine (strain WC3) rotavirus. Six or 16 weeks after inoculation, mice were challenged with EDIM. At the time of challenge and in the days immediately following challenge, production of rotavirus-specific immunoglobulin A (IgA), IgG, and IgM by small intestinal lamina propria lymphocytes (LPL) was determined by fragment culture, and quantities of virus-specific antibodies at the intestinal mucosal surface were determined by intestinal lavage. Mice immunized with EDIM were completely protected against EDIM challenge both 6 and 16 weeks after immunization. Protection was associated with production of high levels of IgA by LPL and detection of virus-specific IgA at the intestinal mucosal surface. In addition, animals immunized and later challenged with EDIM did not develop a boost in antibody responses, suggesting that they were also not reinfected. We also found that in mice immunized with nonmurine rotaviruses, (i) quantities of virus-specific IgA generated following challenge were greater 16 weeks than 6 weeks after immunization, (ii) immunization enhanced the magnitude but did not hasten the onset of production of high quantities of virus-specific IgA by LPL after challenge, and (iii) immunization induced partial protection against challenge; however, protection was not associated with either production of virus-specific antibodies by LPL or detection of virus-specific antibodies at the intestinal mucosal surface.

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Schmitz, Jörn E., R. Paul Johnson, Harold M. McClure, Kelledy H. Manson, Michael S. Wyand, Marcelo J. Kuroda, Michelle A. Lifton, et al. "Effect of CD8+ Lymphocyte Depletion on Virus Containment after Simian Immunodeficiency Virus SIVmac251 Challenge of Live Attenuated SIVmac239Δ3-Vaccinated Rhesus Macaques." Journal of Virology 79, no. 13 (July 1, 2005): 8131–41. http://dx.doi.org/10.1128/jvi.79.13.8131-8141.2005.

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ABSTRACT Although live attenuated vaccines can provide potent protection against simian immunodeficiency virus (SIV) and simian-human immunodeficiency virus challenges, the specific immune responses that confer this protection have not been determined. To test whether cellular immune responses mediated by CD8+ lymphocytes contribute to this vaccine-induced protection, we depleted rhesus macaques vaccinated with the live attenuated virus SIVmac239Δ3 of CD8+ lymphocytes and then challenged them with SIVmac251 by the intravenous route. While vaccination did not prevent infection with the pathogenic challenge virus, the postchallenge levels of virus in the plasmas of vaccinated control animals were significantly lower than those for unvaccinated animals. The depletion of CD8+ lymphocytes at the time of challenge resulted in virus levels in the plasma that were intermediate between those of the vaccinated and unvaccinated controls, suggesting that CD8+ cell-mediated immune responses contributed to protection. Interestingly, at the time of challenge, animals expressing the Mamu-A*01 major histocompatibility complex class I allele showed significantly higher frequencies of SIV-specific CD8+ T-cell responses and lower neutralizing antibody titers than those in Mamu-A*01 − animals. Consistent with these findings, the depletion of CD8+ lymphocytes abrogated vaccine-induced protection, as judged by the peak postchallenge viremia, to a greater extent in Mamu-A*01 + than in Mamu-A*01 − animals. The partial control of postchallenge viremia after CD8+ lymphocyte depletion suggests that both humoral and cellular immune responses induced by live attenuated SIV vaccines can contribute to protection against a pathogenic challenge and that the relative contribution of each of these responses to protection may be genetically determined.

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Reynolds, Matthew R., Andrea M. Weiler, Shari M. Piaskowski, Holly L. Kolar, Ann J. Hessell, Madelyn Weiker, Kim L. Weisgrau, et al. "Macaques Vaccinated with Simian Immunodeficiency Virus SIVmac239Δnef Delay Acquisition and Control Replication after Repeated Low-Dose Heterologous SIV Challenge." Journal of Virology 84, no. 18 (June 30, 2010): 9190–99. http://dx.doi.org/10.1128/jvi.00041-10.

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ABSTRACT An effective human immunodeficiency virus (HIV) vaccine will likely need to reduce mucosal transmission and, if infection occurs, control virus replication. To determine whether our best simian immunodeficiency virus (SIV) vaccine can achieve these lofty goals, we vaccinated eight Indian rhesus macaques with SIVmac239Δnef and challenged them intrarectally (i.r.) with repeated low doses of the pathogenic heterologous swarm isolate SIVsmE660. We detected a significant reduction in acquisition of SIVsmE660 in comparison to that for naïve controls (log rank test; P = 0.023). After 10 mucosal challenges, we detected replication of the challenge strain in only five of the eight vaccinated animals. In contrast, seven of the eight control animals became infected with SIVsmE660 after these 10 challenges. Additionally, the SIVsmE660-infected vaccinated animals controlled peak acute virus replication significantly better than did the naïve controls (Mann-Whitney U test; P = 0.038). Four of the five SIVsmE660 vaccinees rapidly brought virus replication under control by week 4 postinfection. Unfortunately, two of these four vaccinated animals lost control of virus replication during the chronic phase of infection. Bulk sequence analysis of the circulating viruses in these animals indicated that recombination had occurred between the vaccine and challenge strains and likely contributed to the increased virus replication in these animals. Overall, our results suggest that a well-designed HIV vaccine might both reduce the rate of acquisition and control viral replication.

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Sutton, Matthew S., Charles M. Burns, Andrea M. Weiler, Alexis J. Balgeman, Andrew Braasch, Gabrielle Lehrer-Brey, Thomas C. Friedrich, and Shelby L. O'Connor. "Vaccination with Live Attenuated Simian Immunodeficiency Virus (SIV) Protects from Mucosal, but Not Necessarily Intravenous, Challenge with a Minimally Heterologous SIV." Journal of Virology 90, no. 12 (March 9, 2016): 5541–48. http://dx.doi.org/10.1128/jvi.00192-16.

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ABSTRACTFew studies have evaluated the impact of the viral challenge route on protection against a heterologous simian immunodeficiency virus (SIV) challenge. We vaccinated seven macaques with a live attenuated SIV that differed from SIVmac239Δnef by 24 amino acids, called m3KOΔnef. All animals were protected from an intrarectal SIVmac239 challenge, whereas only four animals were protected from subsequent intravenous SIVmac239 challenge. These data suggest that immune responses elicited by vaccination with live attenuated SIV in an individual animal can confer protection from intrarectal challenge while remaining insufficient for protection from intravenous challenge.IMPORTANCEOur study is important because we show that vaccinated animals can be protected from a mucosal challenge with a heterologous SIV, but the same animals are not necessarily protected from intravenous challenge with the same virus. This is unique because in most studies, either vaccinated animals are challenged multiple times by the same route or only a single challenge is performed. An individually vaccinated animal is rarely challenged multiple times by different routes, so protection from different challenge routes cannot be measured in the same animal. Our data imply that vaccine-elicited responses in an individual animal may be insufficient for protection from intravenous challenge but may be suitable for protection from a mucosal challenge that better approximates human immunodeficiency virus (HIV) exposure.

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Ambrose, Zandrea, Lara Compton, Michael Piatak, Ding Lu, W. Gregory Alvord, Mariusz S. Lubomirski, James E. K. Hildreth, Jeffrey D. Lifson, Christopher J. Miller, and Vineet N. KewalRamani. "Incomplete Protection against Simian Immunodeficiency Virus Vaginal Transmission in Rhesus Macaques by a Topical Antiviral Agent Revealed by Repeat Challenges." Journal of Virology 82, no. 13 (April 23, 2008): 6591–99. http://dx.doi.org/10.1128/jvi.02730-07.

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ABSTRACT The rising prevalence of human immunodeficiency virus type 1 (HIV-1) infection in women, especially in resource-limited settings, accentuates the need for accessible, inexpensive, and female-controlled preexposure prophylaxis strategies to prevent mucosal transmission of the virus. While many compounds can inactivate HIV-1 in vitro, evaluation in animal models for mucosal transmission of virus may help identify which approaches will be effective in vivo. Macaques challenged intravaginally with pathogenic simian immunodeficiency virus (SIVmac251) provide a model to preclinically evaluate candidate microbicides. 2-Hydroxypropyl-β-cyclodextrin (BCD) prevents HIV-1 and SIV infection of target cells at subtoxic doses in vitro. Consistent with these findings, intravaginal challenge of macaques with SIVmac251 preincubated with BCD prevented mucosal transmission, as measured by plasma viremia and antiviral antibodies, through 10 weeks postchallenge. In an initial challenge, BCD applied topically prior to SIVmac251 prevented intravaginal transmission of virus compared to controls (P < 0.0001). However, upon a second virus challenge following BCD pretreatment, the majority of the previously protected animals became infected. The mechanism through which animals become infected at a frequency similar to that of controls after prior exposure to BCD and SIVmac251 in subsequent intravaginal virus challenges (P = 0.63), despite the potent antiviral properties of BCD, remains to be determined. These results highlight the unpredictability of antiviral compounds as topical microbicides and suggest that repeated exposures to candidate treatments should be considered for in vivo evaluation.

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Dobrosavljević, Ivan, Dejan Vidanović, Maja Velhner, Biljana Miljković, and Branislav Lako. "Simultaneous detection of vaccinal and field infectious bursal disease viruses in layer chickens challenged with a very virulent strain after vaccination." Acta Veterinaria Hungarica 62, no. 2 (June 1, 2014): 264–73. http://dx.doi.org/10.1556/avet.2014.003.

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Infectious bursal disease virus is an important poultry pathogen. It is distributed worldwide and causes significant economic losses. In this study, a system was adopted for the simultaneous monitoring of vaccine and virulent strains using reverse transcription polymerase chain reaction (RT-PCR). After the decay of maternal antibodies, chickens were vaccinated at the age of 37 days with a virus of intermediate virulence and challenged at 5, 10 and 14 days post vaccination (dpv). The challenge was done with IBDV strain CH/99. Sequencing of the hypervariable region of VP2 has shown that CH/99 belongs to the very virulent group of viruses. The vaccine virus could be found in the bursa of Fabricius, spleen, thymus and bone marrow until 24 dpv. The CH/99 challenge virus was found in the bursa and lymphoid organs when chickens were challenged at 5 and 10 dpv. When challenge was performed at 14 dpv, the pathogenic virus could not be found in the bursa and other lymphoid organs.

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Powell, T. J., R. Spann, M. Nguyenduc, and E. W. Lamon. "Induction of effective immunity to Moloney murine sarcoma virus using monoclonal anti-idiotypic antibody as immunogen." Journal of Immunology 142, no. 4 (February 15, 1989): 1318–24. http://dx.doi.org/10.4049/jimmunol.142.4.1318.

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Abstract We have isolated an anti-idiotypic mAb (RS1.1.3), which recognizes an idiotope present on several IgM mAb specific for Moloney murine leukemia virus (M-MuLV)-determined cell surface Ag. The binding of RS1.1.3 to idiotypic antibody could be inhibited by specific Ag. Intraperitoneal immunization of mice with purified RS1.1.3 antibody-induced effective immunity against Moloney murine sarcoma virus challenge. A single injection of RS1.1.3 7 days before virus challenge resulted in a 27% reduction in tumor load compared to non-immune control mice challenged with the same dose of virus, whereas multiple injections of RS1.1.3 before virus challenge resulted in a 75% reduction in tumor load. The protective effect of anti-idiotype immunization appeared to be T dependent, because immunization of athymic mice had no effect on their susceptibility to tumor virus challenge. Administration of the anti-idiotypic antibody after virus inoculation caused an increase in tumor load of nearly 50% compared to non-immune controls. BALB/c mice immunized with RS1.1.3 developed anti-anti-idiotypic antibodies, as well as M-MuLV Ag-specific antibodies. Analysis of sera from RS1.1.3-immune mice subsequently challenged with Moloney murine sarcoma virus indicated an inverse relationship between tumor load and M-MuLV-specific serum IgG titers induced by the RS1.1.3 immunization. These results indicate that anti-idiotypic mAb may be used as immunogen to induce Ag-specific antibody responses, and to cause effective immunity to a retro-virus-induced tumor.

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Stipkovits, L., R. Glavits, V. Palfi, A. Beres, L. Egyed, B. Denes, M. Somogyi, and S. Szathmary. "Pathologic Lesions Caused by Coinfection of Mycoplasma gallisepticum and H3N8 Low Pathogenic Avian Influenza Virus in Chickens." Veterinary Pathology 49, no. 2 (August 8, 2011): 273–83. http://dx.doi.org/10.1177/0300985811415702.

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Chickens were infected under experimental conditions with Mycoplasma gallisepticum and low pathogenic avian influenza (LPAI) strain A/mallard/Hungary/19616/07 (H3N8). Two groups of chickens were aerosol challenged with M. gallisepticum strain 1226. Seven days later, one of these groups and one mycoplasma-free group was challenged with LPAI H3N8 virus; one group without challenge remained as negative control. Eight days later, the birds were euthanized and examined for gross pathologic and histologic lesions. The body weight was measured, and the presence of antimycoplasma and antiviral antibodies was tested before the mycoplasma challenge, before the virus challenge, and at the end of the study to confirm both infections. Chickens in the mycoplasma-infected group developed antibodies against M. gallisepticum but not against the influenza virus. Chickens of the group infected with the influenza virus became serologically positive only against the virus, while the birds in the coinfected group developed antibodies against both agents. The LPAI H3N8 virus strain did not cause decrease in body weight and clinical signs, and macroscopic pathological lesions were not present in the chickens. The M. gallisepticum infection caused respiratory signs, airsacculitis, and peritonitis characteristic of mycoplasma infection. However, the clinical signs and pathologic lesions and the reduction in weight gain were much more significant in the group challenged with both M. gallisepticum and LPAI H3N8 virus than in the group challenged with M. gallisepticum alone.

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Parr, Margaret B., and Earl L. Parr. "Mucosal Immunity to Herpes Simplex Virus Type 2 Infection in the Mouse Vagina Is Impaired by In Vivo Depletion of T Lymphocytes." Journal of Virology 72, no. 4 (April 1, 1998): 2677–85. http://dx.doi.org/10.1128/jvi.72.4.2677-2685.1998.

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ABSTRACT Intravaginal (IVAG) inoculation of wild-type herpes simplex virus type 2 (HSV-2) in mice causes epithelial infection followed by lethal neurological illness, while IVAG inoculation of attenuated HSV-2 causes epithelial infection followed by development of protective immunity against subsequent IVAG challenge with wild-type virus. The role of T cells in this immunity was studied by in vivo depletion of these cells with monoclonal antibodies. Three groups of mice were used for each experiment: nonimmune/challenged mice, immune/challenged mice, and immune depleted mice [immune mice depleted of a T-cell subset(s) shortly before challenge with HSV-2]. Mice were assessed for epithelial infection 24 h after challenge, virus protein in the vaginal lumen 3 days after challenge, and neurological illness 8 to 14 days after challenge. Monoclonal antibodies to CD4, CD8, or Thy-1 markedly reduced T cells in blood, spleen, and vagina, but major histocompatibility complex class II antigens were still partially upregulated in the vaginal epithelium after virus challenge, indicating that virus-specific memory T-cell function was not entirely eliminated from the vagina. Nevertheless, immune mice depleted of CD4+and CD8+ T cells, Thy-1+ T cells, or CD8+ T cells alone had greater viral infection in the vaginal epithelium than nondepleted immune mice, indicating that T cells contribute to immunity against vaginal HSV-2 infection. All immune depleted mice retained substantial immunity to epithelial infection and were immune to neurological illness, suggesting that other immune mechanisms such as virus-specific antibody may also contribute to immunity.

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Vargas Rodriguez, Juan Sebastian. "The challenge given by Zika virus." Family Medicine and Community Health 6, no. 4 (December 1, 2018): 208–10. http://dx.doi.org/10.15212/fmch.2018.0117.

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Bender, Kaye, and F. E. Thompson,. "West Nile Virus: A Growing Challenge." AJN, American Journal of Nursing 103, no. 6 (June 2003): 32–39. http://dx.doi.org/10.1097/00000446-200306000-00018.

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Thomson, B. J. "Hepatitis C virus: the growing challenge." British Medical Bulletin 89, no. 1 (November 13, 2008): 153–67. http://dx.doi.org/10.1093/bmb/ldp003.

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Roberts, Helen, Christine Middlemiss, and Nigel Gibbens. "Schmallenberg virus: Responding to the challenge." Veterinary Journal 194, no. 1 (October 2012): 1–2. http://dx.doi.org/10.1016/j.tvjl.2012.08.028.

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Eschbaumer, Michael, Regula Wäckerlin, Giovanni Savini, Stéphan Zientara, Corinne Sailleau, Emmanuel Bréard, Martin Beer, and Bernd Hoffmann. "Contamination in bluetongue virus challenge experiments." Vaccine 29, no. 26 (June 2011): 4299–301. http://dx.doi.org/10.1016/j.vaccine.2011.04.049.

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Askonas, B. A. "Influenza virus, a challenge to immunologists." Research in Immunology 140, no. 5-6 (January 1989): 627–34. http://dx.doi.org/10.1016/0923-2494(89)90125-9.

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Geisbert, Thomas W., Joan B. Geisbert, Anders Leung, Kathleen M. Daddario-DiCaprio, Lisa E. Hensley, Allen Grolla, and Heinz Feldmann. "Single-Injection Vaccine Protects Nonhuman Primates against Infection with Marburg Virus and Three Species of Ebola Virus." Journal of Virology 83, no. 14 (April 22, 2009): 7296–304. http://dx.doi.org/10.1128/jvi.00561-09.

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ABSTRACT The filoviruses Marburg virus and Ebola virus cause severe hemorrhagic fever with high mortality in humans and nonhuman primates. Among the most promising filovirus vaccines under development is a system based on recombinant vesicular stomatitis virus (VSV) that expresses a single filovirus glycoprotein (GP) in place of the VSV glycoprotein (G). Here, we performed a proof-of-concept study in order to determine the potential of having one single-injection vaccine capable of protecting nonhuman primates against Sudan ebolavirus (SEBOV), Zaire ebolavirus (ZEBOV), Cote d'Ivoire ebolavirus (CIEBOV), and Marburgvirus (MARV). In this study, 11 cynomolgus monkeys were vaccinated with a blended vaccine consisting of equal parts of the vaccine vectors VSVΔG/SEBOVGP, VSVΔG/ZEBOVGP, and VSVΔG/MARVGP. Four weeks later, three of these animals were challenged with MARV, three with CIEBOV, three with ZEBOV, and two with SEBOV. Three control animals were vaccinated with VSV vectors encoding a nonfilovirus GP and challenged with SEBOV, ZEBOV, and MARV, respectively, and five unvaccinated control animals were challenged with CIEBOV. Importantly, none of the macaques vaccinated with the blended vaccine succumbed to a filovirus challenge. As expected, an experimental control animal vaccinated with VSVΔG/ZEBOVGP and challenged with SEBOV succumbed, as did the positive controls challenged with SEBOV, ZEBOV, and MARV, respectively. All five control animals challenged with CIEBOV became severely ill, and three of the animals succumbed on days 12, 12, and 14, respectively. The two animals that survived CIEBOV infection were protected from subsequent challenge with either SEBOV or ZEBOV, suggesting that immunity to CIEBOV may be protective against other species of Ebola virus. In conclusion, we developed an immunization scheme based on a single-injection vaccine that protects nonhuman primates against lethal challenge with representative strains of all human pathogenic filovirus species.

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Kiseleva, Irina, Elena Krutikova, Ekaterina Stepanova, Svetlana Donina, Maria Pisareva, Vera Krivitskaya, Andrey Rekstin, Erin Grace Sparrow, Guido Torelli, and Larisa Rudenko. "Cross-Protective Efficacy of Monovalent Live Influenza B Vaccines against Genetically Different Lineages of B/Victoria and B/Yamagata in Ferrets." BioMed Research International 2018 (August 30, 2018): 1–11. http://dx.doi.org/10.1155/2018/9695628.

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Background.Currently, two genetic lineages of influenza B virus, B/Victoria and B/Yamagata, are cocirculating in humans in various countries. This situation has raised a question regarding the possibility of cross-protection between B components of live attenuated influenza vaccine (LAIV) belonging to different lineages. This study aimed to assess in naïve ferrets the potential protective activity of monovalent B-LAIVs against challenge with homologous and heterologous wild-type (WT) influenza B viruses.Methods.Groups of seronegative female ferrets 5-6 months of age were given one dose of monovalent LAIV based on B/Victoria or B/Yamagata lineage virus. Ferrets were challenged 21 days later with B/Victoria or B/Yamagata WT virus. Ferrets were monitored closely for clinical signs and morbidity outcomes including febrile response, body weight loss, nasal symptoms, and level of activity one week prior to vaccination and for three days following vaccination/challenge. Nasal washes were collected three days after vaccination/challenge. Samples of lung tissue were taken three days after challenge. All samples were analyzed for the presence of challenge virus by culturing in embryonated chicken eggs and real-time polymerase chain reaction. Antibody response to vaccination was assessed by routine hemagglutination inhibition assay and microneutralization test.Results.Vaccination led to intensive production of specific neutralizing and antihemagglutinating antibodies to vaccine virus, protected ferrets from homologous challenge infection, and significantly reduced clinical signs and replication of homologous challenge virus. In contrast, cross-lineage serum antibodies were not detected. However, ferrets vaccinated with monovalent B-LAIV had a significantly lower level of heterologous challenge virus in the respiratory tract than those given challenge virus only.Conclusions.Monovalent B-LAIV has the potential to be cross-protective against infection with genetically different influenza lineages. Further studies are required to confirm this effect.

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Harmache, Abdallah, Christian Vitu, François Guiguen, Pierre Russo, Giuseppe Bertoni, Michel Pepin, Robert Vigne, and Marie Suzan. "Priming with tat-Deleted Caprine Arthritis Encephalitis Virus (CAEV) Proviral DNA or Live Virus Protects Goats from Challenge with Pathogenic CAEV." Journal of Virology 72, no. 8 (August 1, 1998): 6796–804. http://dx.doi.org/10.1128/jvi.72.8.6796-6804.1998.

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ABSTRACT We previously reported that infection of goats with caprine arthritis encephalitis virus (CAEV) tat− proviral DNA or virus results in persistent infection, since the animals seroconverted and direct virus isolation from cultures of blood-derived macrophages was positive. In this study we wanted to determine whether goats injected with CAEV tat− proviral DNA or virus were protected against challenge with the pathogenic homologous virus and to investigate whether CAEV tat− was still pathogenic. All animals injected with CAEV tat− became infected as indicated by seroconversion and virus isolation. Challenge at 8 or 9 months postinfection demonstrated protection in four of four animals injected with CAEV tat− but did not in three of three mock-inoculated challenged goats. Challenge virus was undetectable in the blood macrophages of protected animals during a period of 6 or 10 months postchallenge. In two of four protected animals, however, we were able to detect the challenge wild-type virus by reverse transcriptase PCR on RNA directly extracted from synovial membrane cells surrounding the inoculation site. This result suggests that protection was achieved without complete sterilizing immunity. Animals injected with CAEV tat− and mock challenged developed inflammatory lesions in the joints, although these lesions were not as severe as those in CAEV wild-type-injected goats. These results confirm the dispensable role of Tat in CAEV replication in vivo for the establishment of infection and pathogenesis and demonstrate in another lentivirus infection model the efficacy of live attenuated viruses to induce resistance to superinfection.

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McCurdy, Lewis H., John A. Rutigliano, Teresa R. Johnson, Man Chen, and Barney S. Graham. "Modified Vaccinia Virus Ankara Immunization Protects against Lethal Challenge with Recombinant Vaccinia Virus Expressing Murine Interleukin-4." Journal of Virology 78, no. 22 (November 15, 2004): 12471–79. http://dx.doi.org/10.1128/jvi.78.22.12471-12479.2004.

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ABSTRACT Recent events have raised concern over the use of pathogens, including variola virus, as biological weapons. Vaccination with Dryvax is associated with serious side effects and is contraindicated for many people, and the development of a safer effective smallpox vaccine is necessary. We evaluated an attenuated vaccinia virus, modified vaccinia virus Ankara (MVA), by use of a murine model to determine its efficacy against an intradermal (i.d.) or intranasal (i.n.) challenge with vaccinia virus (vSC8) or a recombinant vaccinia virus expressing murine interleukin-4 that exhibits enhanced virulence (vSC8-mIL4). After an i.d. challenge, 15 of 16 mice who were inoculated with phosphate-buffered saline developed lesions, one dose of intramuscularly administered MVA was partially protective (3 of 16 mice developed lesions), and the administration of two or three doses of MVA was completely protective (0 of 16 mice developed lesions). In unimmunized mice, an i.n. challenge with vSC8 caused a significant but self-limited illness, while vSC8-mIL4 resulted in lethal infections. Immunization with one or two doses of MVA prevented illness and reduced virus titers in mice who were challenged with either vSC8 or vSC8-mIL4. MVA induced a dose-related neutralizing antibody and vaccinia virus-specific CD8+-T-cell response. Mice immunized with MVA were fully protected from a low-dose vSC8-mIL4 challenge despite a depletion of CD4+ cells, CD8+ cells, or both T-cell subsets or an antibody deficiency. CD4+- or CD8+-T-cell depletion reduced the protection against a high-dose vSC8-mIL4 challenge, and the depletion of both T-cell subsets was associated with severe illness and higher vaccinia virus titers. Thus, MVA induces broad humoral and cellular immune responses that can independently protect against a molecularly modified lethal poxvirus challenge in mice. These data support the continued development of MVA as an alternative candidate vaccine for smallpox.

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Fan, Xueting, Qiudong Su, Feng Qiu, Yao Yi, Liping Shen, Zhiyuan Jia, Pu Liang, Yening Zou, and Shengli Bi. "Intranasal inoculate of influenza virus vaccine against lethal virus challenge." Vaccine 36, no. 29 (July 2018): 4354–61. http://dx.doi.org/10.1016/j.vaccine.2018.05.075.

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Johnson, R. Paul, Jeffrey D. Lifson, Susan C. Czajak, Kelly Stefano Cole, Kelledy H. Manson, Rhona Glickman, Janet Yang, et al. "Highly Attenuated Vaccine Strains of Simian Immunodeficiency Virus Protect against Vaginal Challenge: Inverse Relationship of Degree of Protection with Level of Attenuation." Journal of Virology 73, no. 6 (June 1, 1999): 4952–61. http://dx.doi.org/10.1128/jvi.73.6.4952-4961.1999.

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ABSTRACT Three different deletion mutants of simian immunodeficiency virus (SIV) that vary in their levels of attenuation were tested for the ability to protect against mucosal challenge with pathogenic SIV. Four female rhesus monkeys were vaccinated by intravenous inoculation with SIVmac239Δ3, four with SIVmac239Δ3X, and four with SIVmac239Δ4. These three vaccine strains exhibit increasing levels of attenuation: Δ3 < Δ3X <Δ4. The vaccinated monkeys were challenged by vaginal exposure to uncloned, pathogenic SIVmac251 at 61 weeks after the time of vaccination. On the basis of viral RNA loads in plasma, cell-associated virus loads in peripheral blood, and CD4 cell counts, strong protective effects were observed in all three groups of vaccinated monkeys. However, the degree of protection correlated inversely with the level of attenuation; the least-attenuated strain, SIVmac239Δ3, gave the greatest protection. One monkey in the Δ3X group and two in the Δ4 group clearly became superinfected by the challenge virus, but these animals had levels of SIV RNA in plasma that were considerably lower than those of naive animals that were challenged in parallel. Protection against vaginal challenge appears easier to achieve than protection against intravenous challenge, since four other SIVmac239Δ4-vaccinated monkeys showed no protection when challenged intravenously with a much lower inoculum of the same challenge virus stock. Protection against vaginal challenge in the Δ4-vaccinated group occurred in the absence of detectable serum neutralizing activities and appeared to be associated with the development of an early SIV-specific cytotoxic-T-lymphocyte response. Our results demonstrate that mucosal protection can be achieved by systemic immunization with the highly attenuated SIVmac239Δ4 more than 1 year prior to the time of challenge.

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Connor, Ruth I., David C. Montefiori, James M. Binley, John P. Moore, Sebastian Bonhoeffer, Agegnehu Gettie, Elizabeth A. Fenamore, et al. "Temporal Analyses of Virus Replication, Immune Responses, and Efficacy in Rhesus Macaques Immunized with a Live, Attenuated Simian Immunodeficiency Virus Vaccine." Journal of Virology 72, no. 9 (September 1, 1998): 7501–9. http://dx.doi.org/10.1128/jvi.72.9.7501-7509.1998.

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ABSTRACT Despite evidence that live, attenuated simian immunodeficiency virus (SIV) vaccines can elicit potent protection against pathogenic SIV infection, detailed information on the replication kinetics of attenuated SIV in vivo is lacking. In this study, we measured SIV RNA in the plasma of 16 adult rhesus macaques immunized with a live, attenuated strain of SIV (SIVmac239Δnef). To evaluate the relationship between replication of the vaccine virus and the onset of protection, four animals per group were challenged with pathogenic SIVmac251 at either 5, 10, 15, or 25 weeks after immunization. SIVmac239Δnef replicated efficiently in the immunized macaques in the first few weeks after inoculation. SIV RNA was detected in the plasma of all animals by day 7 after inoculation, and peak levels of viremia (105 to 107 RNA copies/ml) occurred by 7 to 12 days. Following challenge, SIVmac251 was detected in all of the four animals challenged at 5 weeks, in two of four challenged at 10 weeks, in none of four challenged at 15 weeks, and one of four challenged at 25 weeks. One animal immunized with SIVmac239Δnef and challenged at 10 weeks had evidence of disease progression in the absence of detectable SIVmac251. Although complete protection was not achieved at 5 weeks, a transient reduction in viremia (approximately 100-fold) occurred in the immunized macaques early after challenge compared to the nonimmunized controls. Two weeks after challenge, SIV RNA was also reduced in the lymph nodes of all immunized macaques compared with control animals. Taken together, these results indicate that host responses capable of reducing the viral load in plasma and lymph nodes were induced as early as 5 weeks after immunization with SIVmac239Δnef, while more potent protection developed between 10 and 15 weeks. In further experiments, we found that resistance to SIVmac251 infection did not correlate with the presence of antibodies to SIV gp130 and p27 antigens and was achieved in the absence of significant neutralizing activity against the primary SIVmac251 challenge stock.

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Ko, Sung-Youl, Wataru Akahata, Eun Sung Yang, Wing-Pui Kong, Crystal W. Burke, Shelley P. Honnold, Donald K. Nichols, et al. "A virus-like particle vaccine prevents equine encephalitis virus infection in nonhuman primates." Science Translational Medicine 11, no. 492 (May 15, 2019): eaav3113. http://dx.doi.org/10.1126/scitranslmed.aav3113.

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Western, Eastern, and Venezuelan equine encephalitis viruses (WEEV, EEEV, and VEEV, respectively) are important mosquito-borne agents that pose public health and bioterrorism threats. Despite considerable advances in understanding alphavirus replication, there are currently no available effective vaccines or antiviral treatments against these highly lethal pathogens. To develop a potential countermeasure for viral encephalitis, we generated a trivalent, or three-component, EEV vaccine composed of virus-like particles (VLPs). Monovalent VLPs elicited neutralizing antibody responses and protected mice and nonhuman primates (NHPs) against homologous challenges, but they were not cross-protective. In contrast, NHPs immunized with trivalent VLPs were completely protected against aerosol challenge by each of these three EEVs. Passive transfer of IgG from immunized NHPs protected mice against aerosolized EEV challenge, demonstrating that the mechanism of protection was humoral. Because they are replication incompetent, these trivalent VLPs represent a potentially safe and effective vaccine that can protect against diverse encephalitis viruses.

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Palya, Vilmos, Tímea Tatár-Kis, Edit Walkóné Kovács, István Kiss, Zalán Homonnay, Yannick Gardin, Krisztián Kertész, and Ádám Dán. "Efficacy of a Recombinant Turkey Herpesvirus AI (H5) Vaccine in Preventing Transmission of Heterologous Highly Pathogenic H5N8 Clade 2.3.4.4b Challenge Virus in Commercial Broilers and Layer Pullets." Journal of Immunology Research 2018 (November 21, 2018): 1–14. http://dx.doi.org/10.1155/2018/3143189.

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Outbreaks caused by the highly pathogenic avian influenza virus (HPAIV) H5N8 subtype clade 2.3.4.4 were first reported in 2014 in South Korea then spread very rapidly in Asia, to Europe, and for the first time, to North America. Efficacy of a recombinant HVT-AI (H5) vaccine (rHVT-H5) to provide clinical protection as well as to significantly reduce the shedding of an H5N8 challenge virus has already been demonstrated in SPF chickens. The aim of our studies was to test the efficacy of the same rHVT-H5 vaccine in controlling the transmission of a recent Hungarian HPAIV H5N8 challenge virus in commercial chickens. Broilers and layers were vaccinated at day old according to the manufacturer’s recommendation and then challenged with a 2017 Hungarian HPAIV H5N8 (2.3.4.4b) isolate at 5 or 7 weeks of age, respectively. Evaluation of clinical protection, reduction of challenge virus shedding, and transmission to vaccinated contact birds was done on the basis of clinical signs/mortality, detection, and quantitation of challenge virus in oronasal and cloacal swabs (regularly between 1 and 14 days postchallenge). Measurement of seroconversion to AIV nucleoprotein was used as an indicator of infection and replication of challenge virus. Our results demonstrated that rHVT-H5 vaccination could prevent the development of clinical disease and suppress shedding very efficiently, resulting in the lack of challenge virus transmission to vaccinated contact chickens, regardless the type of birds. Single immunization with the tested rHVT-H5 vaccine proved to be effective to stop HPAIV H5N8 (2.3.4.4b) transmission within vaccinated poultry population under experimental conditions.

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Jóźwik, A., J. Manteufel, H. J. Selbitz, and U. Truyen. "Vaccination against porcine parvovirus protects against disease, but does not prevent infection and virus shedding after challenge infection with a heterologous virus strain." Journal of General Virology 90, no. 10 (October 1, 2009): 2437–41. http://dx.doi.org/10.1099/vir.0.012054-0.

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The demonstration of field isolates of porcine parvovirus (PPV) that differ genetically and antigenically from vaccine strains of PPV raises the question of whether the broadly used inactivated vaccines can still protect sows against the novel viruses. Ten specific-pathogen-free primiparous sows were assigned to three groups and were vaccinated with one of two vaccines based on the old vaccine strains, or served as non-vaccinated controls. After insemination, all sows were challenged with the prototype genotype 2 virus, PPV-27a, on gestation day 41; fetuses were delivered on gestation day 90 and examined for virus infection. The fetuses of the vaccinated sows were protected against disease, but both the vaccinated and the non-vaccinated sows showed a marked increase in antibody titres after challenge infection, indicating replication of the challenge virus. All sows (vaccinated and non-vaccinated) shed the challenge virus for at least 10 days after infection, with no difference in the pattern or duration of virus shedding.

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Metcalfe, Lucy, Mathieu Chevalier, Marie-Pascale Tiberghien, Edmond Jolivet, Milan Huňady, Sioned Timothy, and Corinne Philippe-Reversat. "Efficacy of a live intranasal vaccine against parainfluenza type 3 and bovine respiratory syncytial virus in young calves with maternally derived antibodies." Veterinary Record Open 7, no. 1 (November 2020): e000429. http://dx.doi.org/10.1136/vetreco-2020-000429.

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Trial designTwo randomised controlled vaccination trials with artificial challenges were carried out in addition to a serological survey of levels of maternally derived antibodies (MDA) to parainfluenza type 3 virus (PI3V) and bovine respiratory syncytial virus (BRSV) in European calves.ParticipantsTen-day-old calves with and without MDA were included in the two vaccine trials.InterventionsIntranasal administration of a bivalent modified live (PI3V/BRSV) vaccine followed by artificial challenge approximately three months post vaccination.ObjectiveThe study aimed to assess the efficacy of a modified live respiratory vaccine, Bovalto Respi Intranasal (Boehringer Ingelheim). In order to assess the interference of MDA, both seropositive and seronegative calves were used.RandomisationPI3V and BRSV serological status was determined seven days before vaccination; calves without maternal antibodies became the MDA− vaccinates. Calves with MDA were ranked according to individual titres and allocated alternately to MDA+ vaccinate and MDA+ control groups.BlindingTreatment was carried out by the unblinded study director. Animal care and veterinary examinations were conducted by personnel unaware of the treatments received. The serological survey used blood samples obtained from calves on commercial farms in five European countries, Germany, Spain, Italy, Ireland and the UK, to determine the levels of MDA to PI3V and BRSV in calves approximately two weeks of age.ResultsA total of 36 calves were included in the two challenge studies and 32 of these completed the challenge studies. Twenty-one calves were included in the PI3V challenge study, with six of six MDA− and six of seven MDA+ vaccinated calves and five of five MDA+ unvaccinated control calves being challenged with PI3V. Fifteen calves were included in the BRSV challenge study, with five of five MDA− and five of five MDA+ vaccinated calves and five of five MDA+ unvaccinated control calves being challenged with BRSV.OutcomeFor both challenges, clinical scores and nasal shedding were significantly higher in control animals compared with vaccinates (PI3V challenge: clinical scores P=0.001, nasal shedding P=0.001; BRSV challenge: clinical scores P=0.016, nasal shedding P=0.002) and not significantly different between MDA+ and MDA− vaccinated animals for both challenges (P>0.05). A total of 254 samples from six countries were tested in the serological survey of MDA.ConclusionThe results of the challenge studies demonstrated the efficacy of the vaccine in the presence of BRSV and PI3V MDA under laboratory conditions. The field assessment confirmed that the MDA titres in the MDA+ calves corresponded to those typically found on farms.

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Boyden, Alexander, Kevin Legge, and Thomas Waldschmidt. "Regulation of influenza virus-induced germinal center reactions (130.9)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 130.9. http://dx.doi.org/10.4049/jimmunol.182.supp.130.9.

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Abstract Previous work from our laboratory has demonstrated a steady state environment within primary splenic germinal center (GC) reactions as measured by the ratio of non-switched (IgM+) to switched (IgM-) GC B cells, following i.p. challenge with SRBC or protein Ags precipitated in alum. Since both of these experimental antigens induce a Th2-biased response, we sought to analyze the GC reaction after challenge with influenza virus, a natural pathogen that induces B cell activation under Th1 conditions. BALB/c mice were challenged i.p. or i.n. with the H1N1 PR8 virus and splenocytes subjected to multi-parameter flow cytometric analysis. After i.p. challenge, we again observed a steady ratio of IgM+ to switched GC B cells in the spleen. Surprisingly, an intense GC response was found in the spleen following respiratory (i.n.) challenge, with loss of a steady state environment at later time points. To evaluate the degree to which Tregs contribute to control of GC responses during influenza infection, mice were treated with anti-GITR or anti-CD25 mAb prior to and during viral challenge. Treg disruption resulted in a marked abrogation of GC homeostasis in the spleen, leading to exaggerated numbers of switched GC B cells.

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Weingartl, Hana M., Yohannes Berhane, Jeff L. Caswell, Sheena Loosmore, Jean-Christophe Audonnet, James A. Roth, and Markus Czub. "Recombinant Nipah Virus Vaccines Protect Pigs against Challenge." Journal of Virology 80, no. 16 (August 15, 2006): 7929–38. http://dx.doi.org/10.1128/jvi.00263-06.

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ABSTRACT Nipah virus (NiV), of the family Paramyxoviridae, was isolated in 1999 in Malaysia from a human fatality in an outbreak of severe human encephalitis, when human infections were linked to transmission of the virus from pigs. Consequently, a swine vaccine able to abolish virus shedding is of veterinary and human health interest. Canarypox virus-based vaccine vectors carrying the gene for NiV glycoprotein (ALVAC-G) or the fusion protein (ALVAC-F) were used to intramuscularly immunize four pigs per group, either with 108 PFU each or in combination. Pigs were boosted 14 days postvaccination and challenged with 2.5 × 105 PFU of NiV two weeks later. The combined ALVAC-F/G vaccine induced the highest levels of neutralization antibodies (2,560); despite the low neutralizing antibody levels in the F vaccinees (160), all vaccinated animals appeared to be protected against challenge. Virus was not isolated from the tissues of any of the vaccinated pigs postchallenge, and a real-time reverse transcription (RT)-PCR assay detected only small amounts of viral RNA in several samples. In challenge control pigs, virus was isolated from a number of tissues (104.4 PFU/g) or detected by real-time RT-PCR. Vaccination of the ALVAC-F/G vaccinees appeared to stimulate both type 1 and type 2 cytokine responses. Histopathological findings indicated that there was no enhancement of lesions in the vaccinees. No virus shedding was detected in vaccinated animals, in contrast to challenge control pigs, from which virus was isolated from the throat and nose (102.9 PFU/ml). Based on the data presented, the combined ALVAC-F/G vaccine appears to be a very promising vaccine candidate for swine.

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Parer, I., WR Sobey, D. Conolly, and R. Morton. "Sire Transmission of Acquired-Resistance to Myxomatosis." Australian Journal of Zoology 43, no. 5 (1995): 459. http://dx.doi.org/10.1071/zo9950459.

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Male rabbits that had recovered from myxomatosis transmitted to their offspring some factor that increased by 22% the offspring's probability of survival to myxoma virus challenge. The degree of protection transmitted differed between sires challenged with different myxoma strains and between sires challenged with myxoma virus and those challenged with Shope's fibroma virus (SFV). We suggest that future tests of the resistance of wild rabbits should be designed to minimise or eliminate the sire effect.

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Hartlage, Alex S., Piyush Dravid, Christopher M. Walker, and Amit Kapoor. "Adenovirus-vectored T cell vaccine for hepacivirus shows reduced effectiveness against a CD8 T cell escape variant in rats." PLOS Pathogens 17, no. 3 (March 18, 2021): e1009391. http://dx.doi.org/10.1371/journal.ppat.1009391.

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There is an urgent need for a vaccine to prevent chronic infection by hepatitis C virus (HCV) and its many genetic variants. The first human vaccine trial, using recombinant viral vectors that stimulate pan-genotypic T cell responses against HCV non-structural proteins, failed to demonstrate efficacy despite significant preclinical promise. Understanding the factors that govern HCV T cell vaccine success is necessary for design of improved immunization strategies. Using a rat model of chronic rodent hepacivirus (RHV) infection, we assessed the impact of antigenic variation and immune escape upon success of a conceptually analogous RHV T cell vaccine. Naïve Lewis rats were vaccinated with a recombinant human adenovirus expressing RHV non-structural proteins (NS)3-5B and later challenged with a viral variant containing immune escape mutations within major histocompatibility complex (MHC) class I-restricted epitopes (escape virus). Whereas 7 of 11 (64%) rats cleared infection caused by wild-type RHV, only 3 of 12 (25%) were protected against heterologous challenge with escape virus. Uncontrolled replication of escape virus was associated with durable CD8 T cell responses targeting escaped epitopes alone. In contrast, clearance of escape virus correlated with CD4 T cell helper immunity and maintenance of CD8 T cell responses against intact viral epitopes. Interestingly, clearance of wild-type RHV infection after vaccination conferred enhanced protection against secondary challenge with escape virus. These results demonstrate that the efficacy of an RHV T cell vaccine is reduced when challenge virus contains escape mutations within MHC class I-restricted epitopes and that failure to sustain CD8 T cell responses against intact epitopes likely underlies immune failure in this setting. Further investigation of the immune responses that yield protection against diverse RHV challenges in this model may facilitate design of broadly effective HCV vaccines.

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Islam, AFMF, SW Walkden-brown, PJ Groves, and GJ Underwood. "Effects of vaccine dose, virus challenge dose and interval from vaccination to challenge on protection of broiler chickens against Marek's disease virus challenge." Australian Veterinary Journal 85, no. 9 (September 2007): 348–55. http://dx.doi.org/10.1111/j.1751-0813.2007.00195.x.

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Nimesh, Saurabh. "Ebola Virus Disease: A Challenge for Humans." Acta Scientific Pharmaceutical Sciences 3, no. 7 (June 20, 2019): 81–87. http://dx.doi.org/10.31080/asps.2019.03.0317.

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Boivin, Guy, and Bruno Lina. "Influenza virus epidemiology: a permanent vaccine challenge." Virologie 23, no. 5 (October 2019): 271–76. http://dx.doi.org/10.1684/vir.2019.0788.

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Ma, Wenjun. "Swine influenza virus: Current status and challenge." Virus Research 288 (October 2020): 198118. http://dx.doi.org/10.1016/j.virusres.2020.198118.

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Al-Hajjar, Sami. "Zika virus: The challenge of congenital infection." International Journal of Pediatrics and Adolescent Medicine 3, no. 3 (September 2016): 89–90. http://dx.doi.org/10.1016/j.ijpam.2016.08.001.

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Chang, Hui-Wen, Lawrence J. Tartaglia, James B. Whitney, So-Yon Lim, Srisowmya Sanisetty, Christy L. Lavine, Michael S. Seaman, et al. "Generation and Evaluation of Clade C Simian-Human Immunodeficiency Virus Challenge Stocks." Journal of Virology 89, no. 4 (December 3, 2014): 1965–74. http://dx.doi.org/10.1128/jvi.03279-14.

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ABSTRACTThe development of a panel of mucosally transmissible simian-human immunodeficiency virus (SHIV) challenge stocks from multiple virus clades would facilitate preclinical evaluation of candidate HIV-1 vaccines and therapeutics. The majority of SHIV stocks that have been generated to date have been derived from clade B HIV-1envsequences from viruses isolated during chronic infection and typically required serial animal-to-animal adaptation for establishing mucosal transmissibility and pathogenicity. To capture essential features of mucosal transmission of clade C viruses, we produced a series of SHIVs with early clade C HIV-1envsequences from acutely HIV-1-infected individuals from South Africa. SHIV-327c and SHIV-327cRM expressedenvsequences that were 99.7 to 100% identical to the original HIV-1 isolate and did not requirein vivopassaging for mucosal infectivity. These challenge stocks infected rhesus monkeys efficiently by both intrarectal and intravaginal routes, replicated to high levels during acute infection, and established chronic setpoint viremia in 13 of 17 (76%) infected animals. The SHIV-327cRM challenge stock was also titrated for both single, high-dose intrarectal challenges and repetitive, low-dose intrarectal challenges in rhesus monkeys. These SHIV challenge stocks should facilitate the preclinical evaluation of vaccines and other interventions aimed at preventing clade C HIV-1 infection.IMPORTANCEWe describe the development of two related clade C SHIV challenge stocks. These challenge stocks should prove useful for preclinical testing of vaccines and other interventions aimed at preventing clade C HIV-1 infection.

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Moser, Charlotte A., Tully J. Speaker, and Paul A. Offit. "Effect of Water-Based Microencapsulation on Protection against EDIM Rotavirus Challenge in Mice." Journal of Virology 72, no. 5 (May 1, 1998): 3859–62. http://dx.doi.org/10.1128/jvi.72.5.3859-3862.1998.

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ABSTRACT We determined the capacity of microcapsules formed by the combination of sodium alginate, an aqueous anionic polymer, and spermine hydrochloride, an aqueous cationic amine, to enhance protection against rotavirus challenge in mice. Adult BALB/c mice were orally inoculated with either free or microencapsulated rotavirus (simian rotavirus strain RRV) and challenged 6 or 16 weeks later with murine rotavirus strain EDIM. Virus-specific humoral immune responses were determined at the time of challenge and 4 days after challenge by intestinal fragment culture. We found that spermine-alginate microcapsules enhanced protection against challenge 16 weeks after immunization but not 6 weeks after immunization. Quantities of virus-specific immunoglobulin A produced by small intestinal lamina propria lymphocytes were correlated with the degree of protection against challenge afforded by spermine-alginate microcapsules. Possible mechanisms by which microcapsules enhance protection against rotavirus challenge are discussed.

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Tamura, S., Y. Ito, H. Asanuma, Y. Hirabayashi, Y. Suzuki, T. Nagamine, C. Aizawa, and T. Kurata. "Cross-protection against influenza virus infection afforded by trivalent inactivated vaccines inoculated intranasally with cholera toxin B subunit." Journal of Immunology 149, no. 3 (August 1, 1992): 981–88. http://dx.doi.org/10.4049/jimmunol.149.3.981.

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Abstract Cross-protection against influenza virus infection was examined in mice, immunized intranasally with a nasal site-restricted volume of inactivated vaccines together with cholera toxin B subunit (CTB) as an adjuvant. The mice were challenged with either a small or a large volume of mouse-adapted virus suspension, each of which gave virgin mice either a predominant upper or lower respiratory tract infection. A single dose of a monovalent influenza A H3N2 virus vaccine with CTB provided complete cross-protection against the small-volume challenge with a drift virus within the same subtype, but a slight cross-protection against the large-volume challenge. A second dose of another drift virus vaccine increased the efficacy of cross-protection against the large-volume challenge. Similar cross-protection against H1N1, H3N2, or B type drift virus challenge was provided in the mice having received a primary dose of a mixture of H1N1, H3N2, and B virus vaccines with CTB and a second dose of another trivalent vaccine. The degree of cross-protection against the small- and the large-volume infection paralleled mainly the amount of cross-reacting IgA antibodies to challenge virus hemagglutinin in the nasal wash and that of cross-reacting IgG antibodies in the bronchoalveolar wash, respectively. On the other hand, in mice immunized subcutaneously with the trivalent vaccines having no cross-reacting IgA antibodies, the efficacy of cross-protection was not so high as that of nasal vaccination. These results suggest that the nasal inoculation of trivalent vaccines with CTB provides cross-protection against a broader range of viruses than does the current parenteral vaccination.

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A, Ortiz-Plata. "Virus in Human Health." Virology & Immunology Journal 4, no. 2 (July 2, 2020): 1–4. http://dx.doi.org/10.23880/vij-16000247.

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Virus discovery as submicroscopic entities, data from the end of the 19th century, which marked the beginning of a new research discipline, the viruses study. Since then, the presence of viruses has been found in cancer and in multiple diseases whose origin was unknown. Viruses have shown their great potential in triggering infections, causing pandemics at a high cost to society as the Spanish Flu in 1918. The challenge of acting at the health emergency due to the outbreak of diseases caused by new viruses, has led to research with the application of new technologies, in order to find strategies, diagnostic methods, treatment and development of vaccines.

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Martínez, David A., Manuel F. Chamorro, Thomas Passler, Laura Huber, Paul H. Walz, Merrilee Thoresen, Gage Raithel, Scott Silvis, Ricardo Stockler, and Amelia R. Woolums. "Local and Systemic Antibody Responses in Beef Calves Vaccinated with a Modified-Live Virus Bovine Respiratory Syncytial Virus (BRSV) Vaccine at Birth following BRSV Infection." Veterinary Sciences 10, no. 1 (December 29, 2022): 20. http://dx.doi.org/10.3390/vetsci10010020.

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Abstract:

Maternal antibodies interfere with BRSV vaccine responses and efficacy in young calves. The objective of this study was to determine if vaccination before the complete absorption of colostral antibodies results in adequate immune priming and clinical protection of beef calves. Within 6 h of life, calves were randomly assigned to 2 different treatment groups. Group Vacc (n = 25) received a single dose of a modified-live virus (MLV) BRSV vaccine intranasally (IN) and group Control (n = 25) received 2 mL of 0.9% saline IN. At approximately 3 months of age, all calves were experimentally challenged with BRSV. Serum and nasal secretion samples were collected before and after challenge for BRSV real-time RT-PCR and antibody testing. Respiratory signs were not observed before challenge. After challenge, respiratory scores were similar between groups. On the challenge day, >40% of calves in each group were febrile. The mean serum and nasal BRSV-specific antibody titers indicated natural BRSV exposure before the experimental challenge in both groups. All calves tested positive for BRSV and had a similar duration of shedding after challenge. Based on these results, vaccination at birth does not offer advantages for immune priming or clinical protection for beef calves in BRSV-endemic cow-calf herds.

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Liu, Jian-xing, Ying Zhang, Miao An, Qing-guang Wu, Ya Zhao, Xiong Li, and Geng Li. "Diversity of Th1/Th2 immunity in mice with acute lung injury induced by the H1N1 influenza virus and lipopolysaccharides." Journal of Infection in Developing Countries 13, no. 06 (June 30, 2019): 536–44. http://dx.doi.org/10.3855/jidc.10338.

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Abstract:

Introduction: The polarization of T helper (Th) cells plays an important role in the inflammatory response, pathogen removal, and tissue damage processes of infectious acute lung injury (ALI). However, Th cell polarization in viral- or bacterial-mediated ALI is not well defined. Herein, an influenza virus (A/FM/1/47, H1N1) and lipopolysaccharide (LPS) were chosen to induce ALI in mice, and the resultant diversity of Th-cell polarization was explored. Methodology: BALB/c mice were challenged intranasally with the influenza virus or LPS. Edema of the lung, infiltration of inflammatory cells (macrophages, neutrophils, and lymphocytes), oxidative stress, and signature cytokines of Th1 and Th2 cells were detected at 2 days post virus or LPS challenge. Results: The mice exhibited increased capillary permeability accompanied by lung edema and protein-rich alveolar exudation after virus or LPS challenge. Additionally, excessive infiltration of inflammatory cells, robust oxidative stress, and cytokine production were observed in both mouse groups. However, there was conspicuous disparity in the inflammatory cell infiltration and cytokines between the virus- and LPS-challenged mice, where the infiltration in virus-challenged mice was mainly of macrophages and accompanied by robust Th1 cytokine elevation, whereas the infiltration in LPS-challenged mice was primarily of neutrophils and accompanied by robust Th2 cytokine elevation. Conclusions: The Th cell polarization was skewed depending on whether ALI was induced by the influenza virus or LPS. The polarization in the virus-challenged mice was primarily toward a Th1 response, whereas that in the LPS-challenged mice was mainly toward Th2.

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Journal articles on the topic 'Virus challenge'

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