Vaccination with recombinant modified vaccinia virus Ankara protects against measles virus infection in the mouse and cotton rat model

Weidinger, Gerald; Ohlmann, Marion; Schlereth, Bernd; Sutter, Gerd; Niewiesk, Stefan

doi:10.1016/s0264-410x(00)00531-4

Cited by 31 publications

(16 citation statements)

References 19 publications

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“…The products of the reaction were subjected to reducing SDS-PAGE gels and silver stained as described in Materials and Methods. rats (CR) mimics natural infection (70)(71)(72)(73)(74)(75)(76)(77)(78)(79)(80)(81)(82)(83). MV replicates in CR lung tissue with peak titers occurring on day 4 or 5, and infection is overcome by day 8.…”

Section: Hpiv3 F-derived Hrc Peptides Inhibit Wt MV Entrymentioning

confidence: 99%

Prevention of Measles Virus Infection by Intranasal Delivery of Fusion Inhibitor Peptides

Mathieu

Huey

Jurgens

et al. 2015

J Virol

100

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Measles virus (MV) infection is undergoing resurgence and remains one of the leading causes of death among young children worldwide despite the availability of an effective measles vaccine. MV infects its target cells by coordinated action of the MV H and the fusion (F) envelope glycoprotein; upon receptor engagement by H, the prefusion F undergoes a structural transition, extending and inserting into the target cell membrane and then refolding into a postfusion structure that fuses the viral and cell membranes. By interfering with this structural transition of F, peptides derived from the heptad-repeat (HR) regions of F can potently inhibit MV infection at the entry stage. We show here that specific features of H's interaction with its receptors modulate the susceptibility of MV F to peptide fusion inhibitors. A higher concentration of inhibitory peptides is required to inhibit F-mediated fusion when H is engaged to its nectin-4 receptor than when H is engaged to its CD150 receptor. Peptide inhibition of F may be subverted by continued engagement of receptor by H, a finding that highlights the ongoing role of H-receptor interaction after F has been activated and that helps guide the design of more potent inhibitory peptides. Intranasal administration of these peptides results in peptide accumulation in the airway epithelium with minimal systemic levels of peptide and efficiently prevents MV infection in vivo in animal models. The results suggest an antiviral strategy for prophylaxis in vulnerable and/or immunocompromised hosts. IMPORTANCE Measles virus (MV) infection causes an acute illness that may be associated with infection of the central nervous system (CNS)and severe neurological disease. No specific treatment is available. We have shown that parenterally delivered fusion-inhibitory peptides protect mice from lethal CNS MV disease. Here we show, using established small-animal models of MV infection, that fusion-inhibitory peptides delivered intranasally provide effective prophylaxis against MV infection. Since the fusion inhibitors are stable at room temperature, this intranasal strategy is feasible even outside health care settings, could be used to protect individuals and communities in case of MV outbreaks, and could complement global efforts to control measles.

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Section: Hpiv3 F-derived Hrc Peptides Inhibit Wt MV Entrymentioning

confidence: 99%

Prevention of Measles Virus Infection by Intranasal Delivery of Fusion Inhibitor Peptides

Mathieu

Huey

Jurgens

et al. 2015

J Virol

100

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show abstract

“…As MVA can be easily grown to high titers in CEF, an approved tissue culture source for the production of human vaccines, considerable renewed interest in MVA originated from its usefulness as a safe yet efficacious viral vector (36,60,63). When tested in animal models, recombinant MVA vaccines protected against infectious disease or cancer (2,12,20,25,49,58,61,66,69,70), and first-candidate vaccines producing melanoma-associated tyrosinase (19) or human immunodeficiency virus antigen (24) are undergoing clinical testing. Moreover, use of MVA appeared advantageous when recombinant MVA and fully replication-competent vaccinia virus vectors were compared for protective capacities and immune responses elicited against foreign antigens (25,49,61).…”

mentioning

confidence: 99%

Replication of Modified Vaccinia Virus Ankara in Primary Chicken Embryo Fibroblasts Requires Expression of the Interferon Resistance Gene E3L

Hornemann

Harlin

Staib³

et al. 2003

J Virol

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“…8). Despite the small numbers of animals involved, the diminution in viral load (TCID 50 ) observed in cotton rats immunized with CVD 908-htrA(pGA3-mH) and CVD 1208(pMSIN-H) was statistically significant (P ϭ 0.04 and P ϭ 0.02, respectively). Results of this experiment (Fig.…”

Section: Vol 77 2003 Bacterial Vector Measles Dna Vaccines In Cottomentioning

confidence: 96%

“…inoculation of cotton rats with wild-type MV, virus replication ensues, allowing recovery of virus from lung tissue, bronchial cells, and draining lymph nodes, as well as from the spleen (31,51,52). Vaccine candidates that elicit sufficiently high titers of neutralizing antibodies and MV-specific T-cell responses can confer protection against subsequent challenge with wild-type virus (41,42,50,53).…”

mentioning

confidence: 99%

AttenuatedSalmonella entericaSerovar Typhi andShigella flexneri2a Strains Mucosally Deliver DNA Vaccines Encoding Measles Virus Hemagglutinin, Inducing Specific Immune Responses and Protection in Cotton Rats

Pasetti

Barry

Losonsky

et al. 2003

J Virol

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Vaccination with recombinant modified vaccinia virus Ankara protects against measles virus infection in the mouse and cotton rat model

Cited by 31 publications

References 19 publications

Prevention of Measles Virus Infection by Intranasal Delivery of Fusion Inhibitor Peptides

Prevention of Measles Virus Infection by Intranasal Delivery of Fusion Inhibitor Peptides

Replication of Modified Vaccinia Virus Ankara in Primary Chicken Embryo Fibroblasts Requires Expression of the Interferon Resistance Gene E3L

AttenuatedSalmonella entericaSerovar Typhi andShigella flexneri2a Strains Mucosally Deliver DNA Vaccines Encoding Measles Virus Hemagglutinin, Inducing Specific Immune Responses and Protection in Cotton Rats

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