Indiana vesiculovirus

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Indiana vesiculovirus
Vesicular stomatitis virus (VSV) EM 18 lores.jpg
TEM micrograph of Indiana vesiculovirus particles
Virus classification OOjs UI icon edit-ltr.svg
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Negarnaviricota
Class: Monjiviricetes
Order: Mononegavirales
Family: Rhabdoviridae
Genus: Vesiculovirus
Species:
Indiana vesiculovirus
Synonyms [1]
  • Vesicular stomatitis Indiana virus
  • Vesicular stomatitis virus

Indiana vesiculovirus, formerly Vesicular stomatitis Indiana virus (VSIV or VSV) is a virus in the family Rhabdoviridae ; the well-known Rabies lyssavirus belongs to the same family. VSIV can infect insects, cattle, horses and pigs. It has particular importance to farmers in certain regions of the world where it infects cattle. This is because its clinical presentation is identical to the very important foot and mouth disease virus. [2]

Contents

The virus is zoonotic and leads to a flu-like illness in infected humans.

It is also a common laboratory virus used to study the properties of viruses in the family Rhabdoviridae, as well as to study viral evolution. [3]

Properties

Indiana vesiculovirus is the prototypic member of the genus Vesiculovirus of the family Rhabdoviridae. VSIV is an arbovirus, and its replication occurs in the cytoplasm. Natural VSIV infections encompass two steps, cytolytic infections of mammalian hosts and transmission by insects. In insects, infections are noncytolytic persistent. One confirmed vector of the virus is the phlebotomine sand fly Lutzomyia shannoni . [4] The genome of VSIV is on a single molecule of negative-sense RNA that has 11,161 nucleotides in length, [5] that encodes five major proteins: G protein (G), large protein (L), phosphoprotein (P), matrix protein (M) and nucleoprotein (N):

The VSIV G protein, aka VSVG, enables viral entry. It mediates viral attachment to an LDL receptor (LDLR) or an LDLR family member present on the host cell. [6] Following binding, the VSIV-LDLR complex is rapidly endocytosed. It then mediates fusion of the viral envelope with the endosomal membrane. VSIV enters the cell through partially clathrin-coated vesicles; virus-containing vesicles contain more clathrin and clathrin adaptor than conventional vesicles. Virus-containing vesicles recruit components of the actin machinery for their interaction, thus inducing its own uptake. VSIV G does not follow the same path as most vesicles because transport of the G protein from the ER to the plasma membrane is interrupted by incubation at 15 °C. Under this condition, the molecules accumulate in both the ER and a subcellular vesicle fraction of low density called the lipid-rich vesicle fraction. The material in the lipid-rich vesicle fraction appears to be a post-ER intermediate in the transport process to the plasma membrane (PM). After infection, the VSIV G gene is expressed and is commonly studied as a model for N-linked glycosylation in the endoplasmic reticulum (ER). It is translated into the rough ER where the Glc 3-Man 9-GlcNac 2 oligosaccharide is added by a dolichol-containing protein, to an NXS motif on VSIV G. Sugars are removed gradually as the protein travels to the Golgi apparatus, and it becomes resistant to endoglycosidase H. [7] When synthesized in polarized epithelial cells, the envelope glycoprotein VSV G is targeted to the basolateral PM. VSVG is also a common coat protein for lentiviral vector expression systems used to introduce genetic material into in vitro systems or animal models, mainly because of its extremely broad tropism.[ citation needed ]

The VSIV L protein is encoded by half the genome, and combines with the phosphoprotein to catalyze replication of the mRNA.

The VSIV M protein is encoded by an mRNA that is 831 nucleotides long and translates to a 229 amino acid-protein. The predicted M protein sequence does not contain any long hydrophobic or nonpolar domains that might promote membrane association. The protein is rich in basic amino acids and contains a highly basic amino terminal domain.[ citation needed ]

The VSV N protein is required to initiate genome synthesis. [8] [9]

Vesicular stomatitis

Clinical signs and diagnosis

The main sign in animals is oral disease appearing as mucosal vesicles and ulcers in the mouth, but also on the udder and around the coronary band. Animals may show systemic signs such as anorexia, lethargy and pyrexia (fever). Disease usually resolves within two weeks, and animals usually recover completely. [2]

Cases of human infection with vesicular stomatitis virus have been described. Most of these cases have been among laboratory workers, veterinarians, and livestock handlers. In most cases, VSV infection has resulted in a short 3 to 5 day illness characterized by fever, headache, myalgia, weakness and occasionally vesicular lesions of the mouth. [10] Serological testing is most commonly performed with an ELISA or complement fixation, and viral isolation can also be attempted. [2]

Treatment and control

No specific treatment is available, but some animals may require supportive fluids or antibiotics for secondary infections. [2]

Control relies on biosecurity protocols, quarantine, isolation and disinfection to ensure the viral disease does not enter a country or herd. [2]

Medical applications

Oncolytic therapy

In healthy human cells the virus cannot reproduce, likely because of the interferon response, which allows the cells to adequately respond to viral infection. The same cannot be said of interferon non-responsive cancer cells, a quality which allows VSIV to grow and lyse oncogenic cells preferentially. [11]

Recently, attenuated VSIV with a mutation in its M protein has been found to have oncolytic properties. Research is ongoing, and has shown VSIV to reduce tumor size and spread in melanoma, lung cancer, colon cancer and certain brain tumors in laboratory models of cancer. [12]

Anti-HIV therapy

VSIV was modified to attack HIV-infected T-cells. The modified virus was called a "trojan horse" virus NIH Press Release - Trojan Horse Virus Controls HIV Infection - 09/04/1997

Ebola vaccine

Recombinant VSIV has undergone phase 1 trials as a vaccine for Ebola virus. [13]

Recombinant VSIV expressing the Ebola virus glycoprotein has undergone phase III trials in Africa as a vaccine for Ebola virus disease. The vaccine was shown to be 76-100% effective in preventing Ebola virus disease. [14] [15] (see also rVSV-ZEBOV vaccine) In December 2019, Merck & Co.'s rVSV-ZEBOV vaccine Ervebo was approved by the Food and Drug Administration to treat individuals 18 and older. [16]

Other Uses

Replication competent rVSV has also been created expressing proteins of Lassa fever and Marburg virus. [17]

Other applications

The VSIV G protein is routinely used in biomedical research to pseudotype retroviral and lentiviral vectors, conferring the ability to transduce a broad range of mammalian cell types with genes of interest. [18]

The VSIV G protein has also been used in cytological studies of trafficking in the endomembrane system. Immunoelectron microscopy suggests that VSIV G protein moves from cis to trans Golgi bodies without being transported between them in vesicles, supporting the cisternal maturation model of Golgi trafficking. [19]

VSV is often used to perform quantitative and computational studies on viral genome replication and transcription. [8] [20] Such studies help build a better understanding of viral behavior in the presence and absence of innate immune response.[ citation needed ]

In 2020, a possible vaccine against COVID-19, the disease caused by SARS-CoV-2, was developed based on modified VSV. The modification involved replacing the VSV's surface protein genes with those for SARS-CoV-2's spike proteins. [21] [22]

See also

Related Research Articles

<i>Rhabdoviridae</i> Family of viruses in the order Mononegavirales

Rhabdoviridae is a family of negative-strand RNA viruses in the order Mononegavirales. Vertebrates, invertebrates, plants, fungi and protozoans serve as natural hosts. Diseases associated with member viruses include rabies encephalitis caused by the rabies virus, and flu-like symptoms in humans caused by vesiculoviruses. The name is derived from Ancient Greek rhabdos, meaning rod, referring to the shape of the viral particles. The family has 40 genera, most assigned to three subfamilies.

<span class="mw-page-title-main">Defective interfering particle</span>

Defective interfering particles (DIPs), also known as defective interfering viruses, are spontaneously generated virus mutants in which a critical portion of the particle's genome has been lost due to defective replication or non-homologous recombination. The mechanism of their formation is presumed to be as a result of template-switching during replication of the viral genome, although non-replicative mechanisms involving direct ligation of genomic RNA fragments have also been proposed. DIPs are derived from and associated with their parent virus, and particles are classed as DIPs if they are rendered non-infectious due to at least one essential gene of the virus being lost or severely damaged as a result of the defection. A DIP can usually still penetrate host cells, but requires another fully functional virus particle to co-infect a cell with it, in order to provide the lost factors.

<i>Adenoviridae</i> Family of viruses

Adenoviruses are medium-sized, nonenveloped viruses with an icosahedral nucleocapsid containing a double-stranded DNA genome. Their name derives from their initial isolation from human adenoids in 1953.

<span class="mw-page-title-main">Mumps virus</span> Viral agent that causes mumps

The mumps virus (MuV) is the virus that causes mumps. MuV contains a single-stranded, negative-sense genome made of ribonucleic acid (RNA). Its genome is about 15,000 nucleotides in length and contains seven genes that encode nine proteins. The genome is encased by a capsid that is in turn surrounded by a viral envelope. MuV particles, called virions, are pleomorphic in shape and vary in size from 100 to 600 nanometers in diameter. One serotype and twelve genotypes that vary in their geographic distribution are recognized. Humans are the only natural host of the mumps virus.

<i>Murine respirovirus</i> Sendai virus, virus of rodents

Murine respirovirus, formerly Sendai virus (SeV) and previously also known as murine parainfluenza virus type 1 or hemagglutinating virus of Japan (HVJ), is an enveloped, 150-200 nm–diameter, negative sense, single-stranded RNA virus of the family Paramyxoviridae. It typically infects rodents and it is not pathogenic for humans or domestic animals

<span class="mw-page-title-main">VAPA</span> Protein-coding gene in humans

VAMP-Associated Protein A is a protein that in humans is encoded by the VAPA gene. Together with VAPB and VAPC it forms the VAP protein family. They are integral endoplasmic reticulum membrane proteins of the type II and are ubiquitous among eukaryotes.

Pseudotyping is the process of producing viruses or viral vectors in combination with foreign viral envelope proteins. The result is a pseudotyped virus particle, also called a pseudovirus. With this method, the foreign viral envelope proteins can be used to alter host tropism or increase or decrease the stability of the virus particles. Pseudotyped particles do not carry the genetic material to produce additional viral envelope proteins, so the phenotypic changes cannot be passed on to progeny viral particles. In some cases, the inability to produce viral envelope proteins renders the pseudovirus replication incompetent. In this way, the properties of dangerous viruses can be studied in a lower risk setting.

<span class="mw-page-title-main">Marburg virus</span> Species of filamentous virus responsible for hemorrhagic fever

Marburg virus (MARV) is a hemorrhagic fever virus of the Filoviridae family of viruses and a member of the species Marburg marburgvirus, genus Marburgvirus. It causes Marburg virus disease in primates, a form of viral hemorrhagic fever. The virus is considered to be extremely dangerous. The World Health Organization (WHO) rates it as a Risk Group 4 Pathogen. In the United States, the National Institute of Allergy and Infectious Diseases ranks it as a Category A Priority Pathogen and the Centers for Disease Control and Prevention lists it as a Category A Bioterrorism Agent. It is also listed as a biological agent for export control by the Australia Group.

<span class="mw-page-title-main">Vesiculovirus matrix proteins</span>

The family of vesiculovirus matrix proteins consists of several matrix proteins of the vesicular stomatitis virus, also known as VSIV or VSV. The matrix (M) protein of the virus causes many of the cytopathic effects of VSV, including an inhibition of host gene expression and the induction of cell rounding. It has been shown that M protein also induces apoptosis in the absence of other viral components. It is thought that the activation of apoptotic pathways causes the inhibition of host gene expression and cell rounding by M protein.

<span class="mw-page-title-main">Lentiviral vector in gene therapy</span>

Lentiviral vectors in gene therapy is a method by which genes can be inserted, modified, or deleted in organisms using lentiviruses.

<i>Zaire ebolavirus</i> Species of virus affecting humans and animals

Zaire ebolavirus, more commonly known as Ebola virus, is one of six known species within the genus Ebolavirus. Four of the six known ebolaviruses, including EBOV, cause a severe and often fatal hemorrhagic fever in humans and other mammals, known as Ebola virus disease (EVD). Ebola virus has caused the majority of human deaths from EVD, and was the cause of the 2013–2016 epidemic in western Africa, which resulted in at least 28,646 suspected cases and 11,323 confirmed deaths.

rVSV-ZEBOV vaccine Vaccine against Ebola virus disease

Recombinant vesicular stomatitis virus–Zaire Ebola virus (rVSV-ZEBOV), also known as Ebola Zaire vaccine live and sold under the brand name Ervebo, is an Ebola vaccine for adults that prevents Ebola caused by the Zaire ebolavirus. When used in ring vaccination, rVSV-ZEBOV has shown a high level of protection. Around half the people given the vaccine have mild to moderate adverse effects that include headache, fatigue, and muscle pain.

<span class="mw-page-title-main">Ebola vaccine</span> Any of several vaccines to prevent Ebola

Ebola vaccines are vaccines either approved or in development to prevent Ebola. As of 2022, there are only vaccines against the Zaire ebolavirus. The first vaccine to be approved in the United States was rVSV-ZEBOV in December 2019. It had been used extensively in the Kivu Ebola epidemic under a compassionate use protocol. During the early 21st century, several vaccine candidates displayed efficacy to protect nonhuman primates against lethal infection.

David Mahan Knipe is the Higgins Professor of Microbiology and Molecular Genetics in the Department of Microbiology at the Harvard Medical School in Boston, Massachusetts and co-chief editor of the reference book Fields Virology. He returned to the Chair of the Program in Virology at Harvard Medical School in 2019, having previously held the position from 2004 through 2016 and served as interim Co-Chair of the Microbiology and Immunobiology Department from 2016 through 2018.

<span class="mw-page-title-main">Negative-strand RNA virus</span> Phylum of viruses

Negative-strand RNA viruses are a group of related viruses that have negative-sense, single-stranded genomes made of ribonucleic acid. They have genomes that act as complementary strands from which messenger RNA (mRNA) is synthesized by the viral enzyme RNA-dependent RNA polymerase (RdRp). During replication of the viral genome, RdRp synthesizes a positive-sense antigenome that it uses as a template to create genomic negative-sense RNA. Negative-strand RNA viruses also share a number of other characteristics: most contain a viral envelope that surrounds the capsid, which encases the viral genome, −ssRNA virus genomes are usually linear, and it is common for their genome to be segmented.

<span class="mw-page-title-main">Sean Whelan (scientist)</span> British-American virologist

Sean Whelan is a British-American virologist. He is known for identifying the cellular protein used as a receptor by Ebola virus, for defining the entry pathway that rabies virus uses to enter neurons, and for identifying the ribosome as a possible target for antiviral drugs. In July 2019, he was announced as the new Chair of the Department of Molecular Microbiology at Washington University School of Medicine in St Louis, Missouri. In February 2020, Whelan was recognized as the LGBTQ+ Scientist of the Year 2020 by the National Organization of Gay and Lesbian Scientists and Technical Professionals.

West Caucasian bat lyssavirus (WCBL) is a member of genus Lyssavirus, family Rhabdoviridae and order Mononegavirales. This virus was first isolated from Miniopterus schreibersii, in the western Caucasus Mountains of southeastern Europe in 2002. WCBL is the most divergent form of Lyssavirus, and is found in Miniopterus bats (insectivorous), Rousettus aegyptiacus, and Eidolon helvum. The latter two are both fruit bats. The virus is fragile as it can be inactivated by UV light and chemicals, such as ether, chloroform, and bleach. WCBL has not been known to infect humans thus far.

<i>Orthornavirae</i> Kingdom of viruses

Orthornavirae is a kingdom of viruses that have genomes made of ribonucleic acid (RNA), those genomes encoding an RNA-dependent RNA polymerase (RdRp). The RdRp is used to transcribe the viral RNA genome into messenger RNA (mRNA) and to replicate the genome. Viruses in this kingdom also share a number of characteristics involving evolution, including high rates of genetic mutations, recombinations, and reassortments.

<span class="mw-page-title-main">Viral vector vaccine</span> Type of vaccine

A viral vector vaccine is a vaccine that uses a viral vector to deliver genetic material (DNA) that can be transcribed by the recipient's host cells as mRNA coding for a desired protein, or antigen, to elicit an immune response. As of April 2021, six viral vector vaccines, four COVID-19 vaccines and two Ebola vaccines, have been authorized for use in humans.

Endothelial cell tropism or endotheliotropism is a type of tissue tropism or host tropism that characterizes an pathogen's ability to recognize and infect an endothelial cell. Pathogens, such as viruses, can target a specific tissue type or multiple tissue types. Like other cells, the endothelial cell possesses several features that supports a productive viral infection a cell including, cell surface receptors, immune responses, and other virulence factors. Endothelial cells are found in various tissue types such as in the capillaries, veins, and arteries in the human body. As endothelial cells line these blood vessels and critical networks that extend access to various human organ systems, the virus entry into these cells can be detrimental to virus spread across the host system and affect clinical course of disease. Understanding the mechanisms of how viruses attach, enter, and control endothelial functions and host responses inform infectious disease understanding and medical countermeasures.

References

  1. "ICTV Taxonomy history: Indiana vesiculovirus" (html). International Committee on Taxonomy of Viruses (ICTV). Retrieved 6 February 2019.
  2. 1 2 3 4 5 "Vesicular Stomatitis Virus". reviewed and published by WikiVet, accessed 12 October 2011.
  3. Norkin LC (2010). Virology: Molecular Biology and Pathogenesis. Washington DC: American Society for Microbiology Press. ISBN   978-1-55581-453-3.
  4. Mann RS, Kaufman PE, Butler JF (2009). "A Sand Fly, Lutzomyia shannoni Dyar (Insecta: Diptera: Psychodidae: Phlebotomine)". EENY-421. Entomology and Nematology. Florida Cooperative Extension Service. University of Florida IFAS.
  5. "VSV complete genome" . Retrieved 30 May 2013.
  6. Finkelshtein D, Werman A, Novick D, Barak S, Rubinstein M. LDL receptor and its family members serve as the cellular receptors for vesicular stomatitis virus. Proc Natl Acad Sci U S A. 2013 Apr 30;110(18):7306–11.
  7. Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P (2002). "Transport from the ER through the Golgi Apparatus". Molecular Biology of the Cell (Fourth ed.). New York: Garland Science.
  8. 1 2 Timm C, Gupta A, Yin J (August 2015). "Robust kinetics of an RNA virus: Transcription rates are set by genome levels". Biotechnology and Bioengineering. 112 (8): 1655–62. doi:10.1002/bit.25578. PMC   5653219 . PMID   25726926.
  9. Davis NL, Wertz GW (March 1982). "Synthesis of vesicular stomatitis virus negative-strand RNA in vitro: dependence on viral protein synthesis". Journal of Virology. 41 (3): 821–32. doi:10.1128/JVI.41.3.821-832.1982. PMC   256819 . PMID   6284973.
  10. Quiroz E, Moreno N, Peralta PH, Tesh RB. A human case of encephalitis associated with vesicular stomatitis virus (Indiana serotype) infection. Am J Trop Med Hyg. 1988;39(3):312–314. doi:10.4269/ajtmh.1988.39.312
  11. Stojdl DF, Lichty B, Knowles S, Marius R, Atkins H, Sonenberg N, Bell JC (July 2000). "Exploiting tumor-specific defects in the interferon pathway with a previously unknown oncolytic virus". Nature Medicine. 6 (7): 821–5. doi:10.1038/77558. PMID   10888934. S2CID   8492631.
  12. Ozduman K, Wollmann G, Piepmeier JM, van den Pol AN (February 2008). "Systemic vesicular stomatitis virus selectively destroys multifocal glioma and metastatic carcinoma in brain". The Journal of Neuroscience. 28 (8): 1882–93. doi:10.1523/JNEUROSCI.4905-07.2008. PMC   6671450 . PMID   18287505.
  13. Agnandji ST, Huttner A, Zinser ME, Njuguna P, Dahlke C, Fernandes JF, et al. (April 2016). "Phase 1 Trials of rVSV Ebola Vaccine in Africa and Europe". The New England Journal of Medicine. 374 (17): 1647–60. doi:10.1056/NEJMoa1502924. PMC   5490784 . PMID   25830326.
  14. Henao-Restrepo AM, Longini IM, Egger M, Dean NE, Edmunds WJ, Camacho A, et al. (August 2015). "Efficacy and effectiveness of an rVSV-vectored vaccine expressing Ebola surface glycoprotein: interim results from the Guinea ring vaccination cluster-randomised trial". Lancet. 386 (9996): 857–66. doi:10.1016/S0140-6736(15)61117-5. hdl: 10144/575218 . PMID   26248676. S2CID   40830730.
  15. Henao-Restrepo AM, Camacho A, Longini IM, Watson CH, Edmunds WJ, Egger M, et al. (February 2017). "Efficacy and effectiveness of an rVSV-vectored vaccine in preventing Ebola virus disease: final results from the Guinea ring vaccination, open-label, cluster-randomised trial (Ebola Ça Suffit!)". Lancet. 389 (10068): 505–518. doi:10.1016/S0140-6736(16)32621-6. PMC   5364328 . PMID   28017403.
  16. Commissioner, Office of the (2020-03-24). "First FDA-approved vaccine for the prevention of Ebola virus disease, marking a critical milestone in public health preparedness and response". FDA. Retrieved 2021-10-20.
  17. Garbutt M, Liebscher R, Wahl-Jensen V, Jones S, Möller P, Wagner R, et al. (May 2004). "Properties of replication-competent vesicular stomatitis virus vectors expressing glycoproteins of filoviruses and arenaviruses". Journal of Virology. 78 (10): 5458–65. doi:10.1128/jvi.78.10.5458-5465.2004. PMC   400370 . PMID   15113924.
  18. Cronin J, Zhang XY, Reiser J (August 2005). "Altering the tropism of lentiviral vectors through pseudotyping". Current Gene Therapy. 5 (4): 387–98. doi:10.2174/1566523054546224. PMC   1368960 . PMID   16101513.
  19. Mironov AA, Beznoussenko GV, Nicoziani P, Martella O, Trucco A, Kweon HS, et al. (December 2001). "Small cargo proteins and large aggregates can traverse the Golgi by a common mechanism without leaving the lumen of cisternae". The Journal of Cell Biology. 155 (7): 1225–38. doi:10.1083/jcb.200108073. PMC   2199327 . PMID   11756473.
  20. Lim KI, Lang T, Lam V, Yin J (September 2006). "Model-based design of growth-attenuated viruses". PLOS Computational Biology. 2 (9): e116. Bibcode:2006PLSCB...2..116L. doi:10.1371/journal.pcbi.0020116. PMC   1557587 . PMID   16948530.
  21. SciTechDaily: Researchers Created a Virus That Mimics SARS-CoV-2, the COVID-19 Coronavirus – Here’s Why. Source: Washington University School of Medicine. August 19, 2020
  22. James Brett Case, Paul W. Rothlauf, Rita E. Chen, Zhuoming Liu, Haiyan Zhao, Arthur S. Kim, Louis-Marie Bloyet, Qiru Zeng, Stephen Tahan, Lindsay Droit, Ma. Xenia G. Ilagan, Michael A. Tartell, Gaya Amarasinghe, Jeffrey P. Henderson, Shane Miersch, Mart Ustav, Sachdev Sidhu, Herbert W. Virgin, David Wang, Siyuan Ding, Davide Corti, Elitza S. Theel, Daved H. Fremont, Michael S. Diamond and Sean P. J. Whelan: Neutralizing Antibody and Soluble ACE2 Inhibition of a Replication-Competent VSV-SARS-CoV-2 and a Clinical Isolate of SARS-CoV-2, Cell Host and Microbe, 1 July 2020, doi:10.1016/j.chom.2020.06.021