62 results match your criteria marv vp40


Lipid-specific oligomerization of the Marburg virus matrix protein VP40 is regulated by two distinct interfaces for virion assembly.

J Biol Chem 2021 May 18:100796. Epub 2021 May 18.

Department of Medicinal Chemistry & Molecular Pharmacology, Purdue University, West Lafayette IN 47906. Electronic address:

Marburg virus (MARV) is a lipid-enveloped virus harboring a negative sense RNA genome, which has caused sporadic outbreaks of viral hemorrhagic fever in Sub-Saharan Africa. MARV assembles and buds from the host cell plasma where MARV matrix protein (mVP40) dimers associate with anionic lipids at the plasma membrane inner leaflet and undergo a dynamic and extensive self-oligomerization into the structural matrix layer. The MARV matrix layer confers the virion filamentous shape and stability but how host lipids modulate mVP40 oligomerization is mostly unknown. Read More

View Article and Full-Text PDF

Compound FC-10696 Inhibits Egress of Marburg Virus.

Antimicrob Agents Chemother 2021 Jun 17;65(7):e0008621. Epub 2021 Jun 17.

University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Marburg virus (MARV) VP40 protein (mVP40) directs egress and spread of MARV, in part, by recruiting specific host WW domain-containing proteins via its conserved PPxY late (L) domain motif to facilitate efficient virus-cell separation. We reported previously that small-molecule compounds targeting the viral PPxY/host WW domain interaction inhibited VP40-mediated egress and spread. Here, we report on the antiviral potency of novel compound FC-10696, which emerged from extensive structure-activity relationship (SAR) of a previously described series of PPxY inhibitors. Read More

View Article and Full-Text PDF

Ubiquitin Ligase SMURF2 Interacts with Filovirus VP40 and Promotes Egress of VP40 VLPs.

Viruses 2021 02 12;13(2). Epub 2021 Feb 12.

Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

Filoviruses Ebola (EBOV) and Marburg (MARV) are devastating high-priority pathogens capable of causing explosive outbreaks with high human mortality rates. The matrix proteins of EBOV and MARV, as well as eVP40 and mVP40, respectively, are the key viral proteins that drive virus assembly and egress and can bud independently from cells in the form of virus-like particles (VLPs). The matrix proteins utilize proline-rich Late (L) domain motifs (e. Read More

View Article and Full-Text PDF
February 2021

Angiomotin Counteracts the Negative Regulatory Effect of Host WWOX on Viral PPxY-Mediated Egress.

J Virol 2021 Feb 3. Epub 2021 Feb 3.

Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, 3800 Spruce Street, Philadelphia, PA, USA

family members Ebola (EBOV) and Marburg (MARV) viruses and family member Lassa virus (LASV) are emerging pathogens that can cause hemorrhagic fever and high rates of mortality in humans. A better understanding of the interplay between these viruses and the host will inform about the biology of these pathogens, and may lead to the identification of new targets for therapeutic development. Notably, expression of the filovirus VP40 and LASV Z matrix proteins alone drives assembly and egress of virus-like particles (VLPs). Read More

View Article and Full-Text PDF
February 2021

Modified vaccinia Ankara vaccine expressing Marburg virus-like particles protects guinea pigs from lethal Marburg virus infection.

NPJ Vaccines 2020 2;5:78. Epub 2020 Sep 2.

GeoVax Inc., Atlanta, GA USA.

We introduce a new vaccine platform against Marburg virus (MARV) combining the advantages of the immunogenicity of a highly attenuated vaccine vector (Modified Vaccinia Ankara, MVA) with the authentic conformation of virus-like particles (VLPs). Our vaccine, MVA-MARV-VLP, expresses the minimal components of MARV VLPs: the envelope glycoprotein GP and the matrix protein VP40. Electron microscopy confirmed self-assembly and budding of VLPs from infected cells. Read More

View Article and Full-Text PDF
September 2020

High-Throughput Screening Assay to Identify Small Molecule Inhibitors of Marburg Virus VP40 Protein.

ACS Infect Dis 2020 10 16;6(10):2783-2799. Epub 2020 Sep 16.

Center for Microbial Pathogenesis, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia 30302-3965, United States.

Marburg virus (MARV) causes sporadic outbreaks of severe disease with high case fatality rates in humans. To date, neither therapeutics nor prophylactic approaches have been approved for MARV disease. The MARV matrix protein VP40 (mVP40) plays central roles in virus assembly and budding. Read More

View Article and Full-Text PDF
October 2020

Mutation of Hydrophobic Residues in the C-Terminal Domain of the Marburg Virus Matrix Protein VP40 Disrupts Trafficking to the Plasma Membrane.

Viruses 2020 04 24;12(4). Epub 2020 Apr 24.

Department of Medicinal Chemistry and Molecular Pharmacology and the Purdue Institute for Inflammation, Immunology and Infectious Disease, Purdue University, West Lafayette, IN 47907, USA.

Marburg virus (MARV) is a lipid-enveloped negative sense single stranded RNA virus, which can cause a deadly hemorrhagic fever. MARV encodes seven proteins, including VP40 (mVP40), a matrix protein that interacts with the cytoplasmic leaflet of the host cell plasma membrane. VP40 traffics to the plasma membrane inner leaflet, where it assembles to facilitate the budding of viral particles. Read More

View Article and Full-Text PDF

Impact of Měnglà Virus Proteins on Human and Bat Innate Immune Pathways.

J Virol 2020 06 16;94(13). Epub 2020 Jun 16.

Center for Microbial Pathogenesis, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, USA

Měnglà virus (MLAV), identified in bats, is a phylogenetically distinct member of the family Because the filoviruses Ebola virus (EBOV) and Marburg virus (MARV) modulate host innate immunity, MLAV VP35, VP40, and VP24 proteins were compared with their EBOV and MARV homologs for innate immune pathway modulation. In human and cells, MLAV VP35 behaved like EBOV and MARV VP35s, inhibiting virus-induced activation of the interferon beta (IFN-β) promoter and interferon regulatory factor 3 (IRF3) phosphorylation. MLAV VP35 also interacted with PACT, a host protein engaged by EBOV VP35 to inhibit RIG-I signaling. Read More

View Article and Full-Text PDF

Modular mimicry and engagement of the Hippo pathway by Marburg virus VP40: Implications for filovirus biology and budding.

PLoS Pathog 2020 01 6;16(1):e1008231. Epub 2020 Jan 6.

Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.

Ebola (EBOV) and Marburg (MARV) are members of the Filoviridae family, which continue to emerge and cause sporadic outbreaks of hemorrhagic fever with high mortality rates. Filoviruses utilize their VP40 matrix protein to drive virion assembly and budding, in part, by recruitment of specific WW-domain-bearing host proteins via its conserved PPxY Late (L) domain motif. Here, we screened an array of 115 mammalian, bacterially expressed and purified WW-domains using a PPxY-containing peptide from MARV VP40 (mVP40) to identify novel host interactors. Read More

View Article and Full-Text PDF
January 2020

Analysis of the multifunctionality of Marburg virus VP40.

J Gen Virol 2018 12 5;99(12):1614-1620. Epub 2018 Nov 5.

1​Institut für Virologie, Philipps-Universität Marburg, 35043 Marburg, Germany.

The Marburg virus (MARV) matrix protein, VP40, is a multifunctional protein that is essential for the assembly and release of viral particles, inhibition of the interferon response and viral transcription/replication. VP40 is assumed to be present as soluble monomers and membrane-bound higher-order oligomers. To investigate the functional relevance of oligomerization and lipid binding of VP40 we constructed mutants with impaired VP40-VP40 or VP40-lipid interactions and tested their capacity to bind the plasma membrane, to form virus-like particles (VLPs) and to inhibit viral RNA synthesis. Read More

View Article and Full-Text PDF
December 2018

A Fluorescently Labeled Marburg Virus Glycoprotein as a New Tool to Study Viral Transport and Assembly.

J Infect Dis 2018 11;218(suppl_5):S318-S326

Institut für Virologie, Philipps-Universität Marburg, Marburg, Germany.

The single surface glycoprotein (GP) of filoviruses is indispensable for recognition of its cellular receptor and infection of target cells. To study the intracellular trafficking of GP by using live-cell imaging, the mucin-like domain of Marburg virus (MARV) GP was replaced by the fluorophore mCherry (GP∆MLD_mCherry). Intracellular distribution, surface transport, and recruitment of GP∆MLD_mCherry into virus-like particles were similar to observations for wild-type GP. Read More

View Article and Full-Text PDF
November 2018

Pan-Filovirus Serum Neutralizing Antibodies in a Subset of Congolese Ebolavirus Infection Survivors.

J Infect Dis 2018 11;218(12):1929-1936

Department of Epidemiology, School of Public Health, University of California, Los Angeles.

One year after a Zaire ebolavirus (EBOV) outbreak occurred in the Boende Health Zone of the Democratic Republic of the Congo during 2014, we sought to determine the breadth of immune response against diverse filoviruses including EBOV, Bundibugyo (BDBV), Sudan (SUDV), and Marburg (MARV) viruses. After assessing the 15 survivors, 5 individuals demonstrated some degree of reactivity to multiple ebolavirus species and, in some instances, Marburg virus. All 5 of these survivors had immunoreactivity to EBOV glycoprotein (GP) and EBOV VP40, and 4 had reactivity to EBOV nucleoprotein (NP). Read More

View Article and Full-Text PDF
November 2018

Marburg virus-like particles by co-expression of glycoprotein and matrix protein in insect cells induces immune responses in mice.

Virol J 2017 10 25;14(1):204. Epub 2017 Oct 25.

Key Laboratory of Jilin Province for Zoonosis Prevention and Control, Institute of Military Veterinary, Academy of Military Medical Sciences, Changchun, China.

Background: Marburg virus (MARV) causes severe haemorrhagic fever in humans and nonhuman primates and has a high mortality rate. However, effective drugs or licensed vaccines are not currently available to control the outbreak and spread of this disease.

Methods: In this study, we generated MARV virus-like particles (VLPs) by co-expressing the glycoprotein (GP) and matrix protein (VP40) using the baculovirus expression system. Read More

View Article and Full-Text PDF
October 2017

Intracellular Crosslinking of Filoviral Nucleoproteins with Xintrabodies Restricts Viral Packaging.

Front Immunol 2017 27;8:1197. Epub 2017 Sep 27.

Department of Virology and Immunology, Texas Biomedical Research Institute, San Antonio, TX, United States.

Viruses assemble large macromolecular repeat structures that become part of the infectious particles or virions. Ribonucleocapsids (RNCs) of negative strand RNA viruses are a prime example where repetition of nucleoprotein (NP) along the genome creates a core polymeric helical scaffold that accommodates other nucleocapsid proteins including viral polymerase. The RNCs are transported through the cytosol for packaging into virions through association with viral matrix proteins at cell membranes. Read More

View Article and Full-Text PDF
September 2017

Deep-sequencing of Marburg virus genome during sequential mouse passaging and cell-culture adaptation reveals extensive changes over time.

Sci Rep 2017 06 13;7(1):3390. Epub 2017 Jun 13.

Special Pathogens Program, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada.

Marburg virus (MARV) has caused outbreaks of filoviral hemorrhagic fever since its discovery in 1967. The largest and deadliest outbreak occurred in Angola in 2005, with 252 cases and 227 deaths. In 2014, we developed a mouse-adapted MARV, Angola variant through serial passaging in mice. Read More

View Article and Full-Text PDF

Marburg virus-like particles produced in insect cells induce neutralizing antibodies in rhesus macaques.

J Med Virol 2017 12 1;89(12):2069-2074. Epub 2017 Sep 1.

Key Laboratory of Jilin Province for Zoonosis Prevention and Control, Institute of Military Veterinary, Academy of Military Medical Sciences, Changchun, China.

Marburg virus (MARV), which is one of the most virulent agents in the world, causes lethal haemorrhagic fever in humans and nonhuman primates (NHPs) with a mortality rate of up to 90%. Currently, there is no effective treatment or approved vaccine for MARV for human use to control disease outbreak and spread. Virus-like particles (VLPs), which are morphologically identical to the native infectious virus particle, are efficacious as vaccines against many viruses, including human papilloma virus (HPV), porcine circovirus (PCV) type 2 and hepatitis B virus (HBV). Read More

View Article and Full-Text PDF
December 2017

Detection of lipid-induced structural changes of the Marburg virus matrix protein VP40 using hydrogen/deuterium exchange-mass spectrometry.

J Biol Chem 2017 04 6;292(15):6108-6122. Epub 2017 Feb 6.

From the Department of Chemistry and Biochemistry, The Eck Institute for Global Health and The Boler-Parseghian Center for Rare and Neglected Diseases, University of Notre Dame, Notre Dame, Indiana 46556,

Marburg virus (MARV) is a lipid-enveloped virus from the family containing a negative sense RNA genome. One of the seven MARV genes encodes the matrix protein VP40, which forms a matrix layer beneath the plasma membrane inner leaflet to facilitate budding from the host cell. MARV VP40 (mVP40) has been shown to be a dimeric peripheral protein with a broad and flat basic surface that can associate with anionic phospholipids such as phosphatidylserine. Read More

View Article and Full-Text PDF

Chaperone-Mediated Autophagy Protein BAG3 Negatively Regulates Ebola and Marburg VP40-Mediated Egress.

PLoS Pathog 2017 01 11;13(1):e1006132. Epub 2017 Jan 11.

Department of Pathobiology, School Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.

Ebola (EBOV) and Marburg (MARV) viruses are members of the Filoviridae family which cause outbreaks of hemorrhagic fever. The filovirus VP40 matrix protein is essential for virus assembly and budding, and its PPxY L-domain motif interacts with WW-domains of specific host proteins, such as Nedd4 and ITCH, to facilitate the late stage of virus-cell separation. To identify additional WW-domain-bearing host proteins that interact with VP40, we used an EBOV PPxY-containing peptide to screen an array of 115 mammalian WW-domain-bearing proteins. Read More

View Article and Full-Text PDF
January 2017

Novel activities by ebolavirus and marburgvirus interferon antagonists revealed using a standardized in vitro reporter system.

Virology 2017 01 6;501:147-165. Epub 2016 Dec 6.

Viral Special Pathogens Branch, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, United States. Electronic address:

Filoviruses are highly lethal in humans and nonhuman primates, likely due to potent antagonism of host interferon (IFN) responses early in infection. Filoviral protein VP35 is implicated as the major IFN induction antagonist, while Ebola virus (EBOV) VP24 or Marburg virus (MARV) VP40 are known to block downstream IFN signaling. Despite progress elucidating EBOV and MARV antagonist function, those for most other filoviruses, including Reston (RESTV), Sudan (SUDV), Taï Forest (TAFV), Bundibugyo (BDBV) and Ravn (RAVV) viruses, remain largely neglected. Read More

View Article and Full-Text PDF
January 2017

ITCH E3 Ubiquitin Ligase Interacts with Ebola Virus VP40 To Regulate Budding.

J Virol 2016 10 29;90(20):9163-71. Epub 2016 Sep 29.

Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA

Unlabelled: Ebola virus (EBOV) and Marburg virus (MARV) belong to the Filoviridae family and can cause outbreaks of severe hemorrhagic fever, with high mortality rates in humans. The EBOV VP40 (eVP40) and MARV VP40 (mVP40) matrix proteins play a central role in virion assembly and egress, such that independent expression of VP40 leads to the production and egress of virus-like particles (VLPs) that accurately mimic the budding of infectious virus. Late (L) budding domains of eVP40 recruit host proteins (e. Read More

View Article and Full-Text PDF
October 2016

An active site mutation increases the polymerase activity of the guinea pig-lethal Marburg virus.

J Gen Virol 2016 10 22;97(10):2494-2500. Epub 2016 Jul 22.

German Center for Infection Research (DZIF), Institut für Virologie, Philipps-Universität, Hans-Meerwein-Str. 2, 35043 Marburg, Germany.

Marburg virus (MARV) causes severe, often fatal, disease in humans and transient illness in rodents. Sequential passaging of MARV in guinea pigs resulted in selection of a lethal virus containing 4 aa changes. A D184N mutation in VP40 (VP40D184N), which leads to a species-specific gain of viral fitness, and three mutations in the active site of viral RNA-dependent RNA polymerase L, which were investigated in the present study for functional significance in human and guinea pig cells. Read More

View Article and Full-Text PDF
October 2016

Human Survivors of Disease Outbreaks Caused by Ebola or Marburg Virus Exhibit Cross-Reactive and Long-Lived Antibody Responses.

Clin Vaccine Immunol 2016 08 5;23(8):717-24. Epub 2016 Aug 5.

Molecular and Translational Sciences, United States Army Medical Research Institute of Infectious Diseases, Frederick, Maryland, USA Virology Division, United States Army Medical Research Institute of Infectious Diseases, Frederick, Maryland, USA

A detailed understanding of serological immune responses to Ebola and Marburg virus infections will facilitate the development of effective diagnostic methods, therapeutics, and vaccines. We examined antibodies from Ebola or Marburg survivors 1 to 14 years after recovery from disease, by using a microarray that displayed recombinant nucleoprotein (NP), viral protein 40 (VP40), envelope glycoprotein (GP), and inactivated whole virions from six species of filoviruses. All three outbreak cohorts exhibited significant antibody responses to antigens from the original infecting species and a pattern of additional filoviruses that varied by outbreak. Read More

View Article and Full-Text PDF

Virus-Like Particle Vaccination Protects Nonhuman Primates from Lethal Aerosol Exposure with Marburgvirus (VLP Vaccination Protects Macaques against Aerosol Challenges).

Viruses 2016 Apr 8;8(4):94. Epub 2016 Apr 8.

United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, MD 21702, USA.

Marburg virus (MARV) was the first filovirus to be identified following an outbreak of viral hemorrhagic fever disease in Marburg, Germany in 1967. Due to several factors inherent to filoviruses, they are considered a potential bioweapon that could be disseminated via an aerosol route. Previous studies demonstrated that MARV virus-like particles (VLPs) containing the glycoprotein (GP), matrix protein VP40 and nucleoprotein (NP) generated using a baculovirus/insect cell expression system could protect macaques from subcutaneous (SQ) challenge with multiple species of marburgviruses. Read More

View Article and Full-Text PDF

Effects of Filovirus Interferon Antagonists on Responses of Human Monocyte-Derived Dendritic Cells to RNA Virus Infection.

J Virol 2016 05 29;90(10):5108-5118. Epub 2016 Apr 29.

Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA

Unlabelled: Dendritic cells (DCs) are major targets of filovirus infection in vivo Previous studies have shown that the filoviruses Ebola virus (EBOV) and Marburg virus (MARV) suppress DC maturation in vitro Both viruses also encode innate immune evasion functions. The EBOV VP35 (eVP35) and the MARV VP35 (mVP35) proteins each can block RIG-I-like receptor signaling and alpha/beta interferon (IFN-α/β) production. The EBOV VP24 (eVP24) and MARV VP40 (mVP40) proteins each inhibit the production of IFN-stimulated genes (ISGs) by blocking Jak-STAT signaling; however, this occurs by different mechanisms, with eVP24 blocking nuclear import of tyrosine-phosphorylated STAT1 and mVP40 blocking Jak1 function. Read More

View Article and Full-Text PDF

Investigation of the Lipid Binding Properties of the Marburg Virus Matrix Protein VP40.

J Virol 2015 Dec 30;90(6):3074-85. Epub 2015 Dec 30.

Department of Chemistry and Biochemistry, Eck Institute for Global Health, and Boler-Parseghian Center for Rare and Neglected Diseases, University of Notre Dame, Notre Dame, Indiana, USA Department of Biochemistry and Molecular Biology, Indiana University School of Medicine-South Bend, South Bend, Indiana, USA

Unlabelled: Marburg virus (MARV), which belongs to the virus family Filoviridae, causes hemorrhagic fever in humans and nonhuman primates that is often fatal. MARV is a lipid-enveloped virus that during the replication process extracts its lipid coat from the plasma membrane of the host cell it infects. MARV carries seven genes, one of which encodes its matrix protein VP40 (mVP40), which regulates the assembly and budding of the virions. Read More

View Article and Full-Text PDF
December 2015

Crystal Structure of Marburg Virus VP40 Reveals a Broad, Basic Patch for Matrix Assembly and a Requirement of the N-Terminal Domain for Immunosuppression.

J Virol 2016 02 9;90(4):1839-48. Epub 2015 Dec 9.

Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, USA Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California, USA

Unlabelled: Marburg virus (MARV), a member of the filovirus family, causes severe hemorrhagic fever with up to 90% lethality. MARV matrix protein VP40 is essential for assembly and release of newly copied viruses and also suppresses immune signaling in the infected cell. Here we report the crystal structure of MARV VP40. Read More

View Article and Full-Text PDF
February 2016

A Single Amino Acid Change in the Marburg Virus Matrix Protein VP40 Provides a Replicative Advantage in a Species-Specific Manner.

J Virol 2016 02 18;90(3):1444-54. Epub 2015 Nov 18.

Institut für Virologie, Philipps-Universität Marburg, Marburg, Germany German Center for Infection Research (DZIF), Institut für Virologie, Philipps-Universität Marburg, Marburg, Germany

Unlabelled: Marburg virus (MARV) induces severe hemorrhagic fever in humans and nonhuman primates but only transient nonlethal disease in rodents. However, sequential passages of MARV in rodents boosts infection leading to lethal disease. Guinea pig-adapted MARV contains one mutation in the viral matrix protein VP40 at position 184 (VP40D184N). Read More

View Article and Full-Text PDF
February 2016

Lloviu virus VP24 and VP35 proteins function as innate immune antagonists in human and bat cells.

Virology 2015 Nov 6;485:145-52. Epub 2015 Aug 6.

Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States. Electronic address:

Lloviu virus (LLOV) is a new member of the filovirus family that also includes Ebola virus (EBOV) and Marburg virus (MARV). LLOV has not been cultured; however, its genomic RNA sequence indicates the coding capacity to produce homologs of the EBOV and MARV VP24, VP35, and VP40 proteins. EBOV and MARV VP35 proteins inhibit interferon (IFN)-alpha/beta production and EBOV VP35 blocks activation of the antiviral kinase PKR. Read More

View Article and Full-Text PDF
November 2015

Amino Acid Residue at Position 79 of Marburg Virus VP40 Confers Interferon Antagonism in Mouse Cells.

J Infect Dis 2015 Oct 29;212 Suppl 2:S219-25. Epub 2015 Apr 29.

Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York.

Marburg viruses (MARVs) cause highly lethal infections in humans and nonhuman primates. Mice are not generally susceptible to MARV infection; however, if the strain is first adapted to mice through serial passaging, it becomes able to cause disease in this animal. A previous study correlated changes accrued during mouse adaptation in the VP40 gene of a MARV strain known as Ravn virus (RAVV) with an increased capacity to inhibit interferon (IFN) signaling in mouse cell lines. Read More

View Article and Full-Text PDF
October 2015

Homologous and heterologous protection of nonhuman primates by Ebola and Sudan virus-like particles.

PLoS One 2015 20;10(3):e0118881. Epub 2015 Mar 20.

Integrated Biotherapeutics, Inc., Gaithersburg, Maryland, United States of America.

Filoviruses cause hemorrhagic fever resulting in significant morbidity and mortality in humans. Several vaccine platforms that include multiple virus-vectored approaches and virus-like particles (VLPs) have shown efficacy in nonhuman primates. Previous studies have shown protection of cynomolgus macaques against homologous infection for Ebola virus (EBOV) and Marburg virus (MARV) following a three-dose vaccine regimen of EBOV or MARV VLPs, as well as heterologous protection against Ravn Virus (RAVV) following vaccination with MARV VLPs. Read More

View Article and Full-Text PDF
December 2015