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Relevant bibliographies by topics / Virus trafficking

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Academic literature on the topic 'Virus trafficking'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Virus trafficking"

1

Brandenburg, Boerries, and Xiaowei Zhuang. "Virus trafficking – learning from single-virus tracking." Nature Reviews Microbiology 5, no. 3 (March 2007): 197–208. http://dx.doi.org/10.1038/nrmicro1615.

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Spiropoulou, C. F., C. S. Goldsmith, T. R. Shoemaker, C. J. Peters, and R. W. Compans. "Sin nombre virus glycoprotein trafficking." Virology 308, no. 1 (March 2003): 48–63. http://dx.doi.org/10.1016/s0042-6822(02)00092-2.

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Wozniak, Ann L., Abby Long, Kellyann N. Jones-Jamtgaard, and Steven A. Weinman. "Hepatitis C virus promotes virion secretion through cleavage of the Rab7 adaptor protein RILP." Proceedings of the National Academy of Sciences 113, no. 44 (October 17, 2016): 12484–89. http://dx.doi.org/10.1073/pnas.1607277113.

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Hepatitis C virus (HCV) is an enveloped RNA virus that modifies intracellular trafficking processes. The mechanisms that HCV and other viruses use to modify these events are poorly understood. In this study, we observed that two different RNA viruses, HCV and Sendai, cause inhibition of ras-related protein Rab-7 (Rab7)-dependent endosome–lysosome fusion. In both cases, viral infection causes cleavage of the Rab7 adaptor protein RILP (Rab interacting lysosomal protein), which is responsible for linking Rab7 vesicles to dynein motor complexes. RILP cleavage results in the generation of a cleaved RILP fragment (cRILP) missing the N terminus of the molecule. Although RILP localizes in a perinuclear fashion, cRILP moves to the cell periphery. Both knockdown of RILP and expression of cRILP reproduced the HCV-induced trafficking defect, and restoring full-length RILP reversed the trafficking effects of virus. For the first 3 d after electroporation of HCV RNA, intracellular virus predominates over secreted virus, but the quantity of intracellular virus then rapidly declines as secreted virus dominates. The transition from the intracellular-predominant to the secretion-predominant phenotype corresponds to the time course of cRILP generation. Expressing cRILP directly prevents intracellular virus accumulation at early times without affecting net virus production. The ability of cRILP to promote virus secretion could be prevented by a kinesin inhibitor. HCV thus modifies cellular trafficking by cleaving RILP, which serves to redirect Rab7-containing vesicles to a kinesin-dependent trafficking mode promoting virion secretion. Cleavage of a Rab adaptor protein is thus a mechanism by which viruses modify trafficking patterns of infected cells.

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Jiang, Bingfu, and Eberhard Hildt. "Intracellular Trafficking of HBV Particles." Cells 9, no. 9 (September 2, 2020): 2023. http://dx.doi.org/10.3390/cells9092023.

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The human hepatitis B virus (HBV), that is causative for more than 240 million cases of chronic liver inflammation (hepatitis), is an enveloped virus with a partially double-stranded DNA genome. After virion uptake by receptor-mediated endocytosis, the viral nucleocapsid is transported towards the nuclear pore complex. In the nuclear basket, the nucleocapsid disassembles. The viral genome that is covalently linked to the viral polymerase, which harbors a bipartite NLS, is imported into the nucleus. Here, the partially double-stranded DNA genome is converted in a minichromosome-like structure, the covalently closed circular DNA (cccDNA). The DNA virus HBV replicates via a pregenomic RNA (pgRNA)-intermediate that is reverse transcribed into DNA. HBV-infected cells release apart from the infectious viral parrticle two forms of non-infectious subviral particles (spheres and filaments), which are assembled by the surface proteins but lack any capsid and nucleic acid. In addition, naked capsids are released by HBV replicating cells. Infectious viral particles and filaments are released via multivesicular bodies; spheres are secreted by the classic constitutive secretory pathway. The release of naked capsids is still not fully understood, autophagosomal processes are discussed. This review describes intracellular trafficking pathways involved in virus entry, morphogenesis and release of (sub)viral particles.

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Mouland, Andrew J., Hongbin Xu, Hongyi Cui, Winfried Krueger, Trent P. Munro, Melanie Prasol, Johanne Mercier, et al. "RNA Trafficking Signals in Human Immunodeficiency Virus Type 1." Molecular and Cellular Biology 21, no. 6 (March 15, 2001): 2133–43. http://dx.doi.org/10.1128/mcb.21.6.2133-2143.2001.

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ABSTRACT Intracellular trafficking of retroviral RNAs is a potential mechanism to target viral gene expression to specific regions of infected cells. Here we show that the human immunodeficiency virus type 1 (HIV-1) genome contains two sequences similar to the hnRNP A2 response element (A2RE), a cis-acting RNA trafficking sequence that binds to the trans-acting trafficking factor, hnRNP A2, and mediates a specific RNA trafficking pathway characterized extensively in oligodendrocytes. The two HIV-1 sequences, designated A2RE-1, within the major homology region of the gag gene, and A2RE-2, in a region of overlap between the vpr andtat genes, both bind to hnRNP A2 in vitro and are necessary and sufficient for RNA transport in oligodendrocytes in vivo. A single base change (A8G) in either sequence reduces hnRNP A2 binding and, in the case of A2RE-2, inhibits RNA transport. A2RE-mediated RNA transport is microtubule and hnRNP A2 dependent. Differentially labelledgag and vpr RNAs, containing A2RE-1 and A2RE-2, respectively, coassemble into the same RNA trafficking granules and are cotransported to the periphery of the cell. tat RNA, although it contains A2RE-2, is not transported as efficiently asvpr RNA. An A2RE/hnRNP A2-mediated trafficking pathway for HIV RNA is proposed, and the role of RNA trafficking in targeting HIV gene expression is discussed.

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Mankouri, Jamel, Cheryl Walter, Hazel Stewart, Matthew Bentham, Wei Sun Park, Won Do Heo, Mitsunori Fukuda, Stephen Griffin, and Mark Harris. "Release of Infectious Hepatitis C Virus from Huh7 Cells Occurs via atrans-Golgi Network-to-Endosome Pathway Independent of Very-Low-Density Lipoprotein Secretion." Journal of Virology 90, no. 16 (May 25, 2016): 7159–70. http://dx.doi.org/10.1128/jvi.00826-16.

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ABSTRACTThe release of infectious hepatitis C virus (HCV) particles from infected cells remains poorly characterized. We previously demonstrated that virus release is dependent on the endosomal sorting complex required for transport (ESCRT). Here, we show a critical role oftrans-Golgi network (TGN)-endosome trafficking during the assembly, but principally the secretion, of infectious virus. This was demonstrated by both small interfering RNA (siRNA)-mediated silencing of TGN-associated adaptor proteins and a panel of dominant negative (DN) Rab GTPases involved in TGN-endosome trafficking steps. Importantly, interfering with factors critical for HCV release did not have a concomitant effect on secretion of triglycerides, ApoB, or ApoE, indicating that particles are likely released from Huh7 cells via pathways distinct from that of very-low-density lipoprotein (VLDL). Finally, we show that HCV NS2 perturbs TGN architecture, redistributing TGN membranes to closely associate with HCV core protein residing on lipid droplets. These findings support the notion that HCV hijacks TGN-endosome trafficking to facilitate particle assembly and release. Moreover, although essential for assembly and infectivity, the trafficking of mature virions is seemingly independent of host lipoproteins.IMPORTANCEThe mechanisms by which infectious hepatitis C virus particles are assembled and released from the cell are poorly understood. We show that the virus subverts host cell trafficking pathways to effect the release of virus particles and disrupts the structure of the Golgi apparatus, a key cellular organelle involved in secretion. In addition, we demonstrate that the mechanisms used by the virus to exit the cell are distinct from those used by the cell to release lipoproteins, suggesting that the virus effects a unique modification to cellular trafficking pathways.

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Hsiao, Jye-Chian, Li-Wei Chu, Yung-Tsun Lo, Sue-Ping Lee, Tzu-Jung Chen, Cheng-Yen Huang, Yueh-Hsin Ping, and Wen Chang. "Intracellular Transport of Vaccinia Virus in HeLa Cells Requires WASH-VPEF/FAM21-Retromer Complexes and Recycling Molecules Rab11 and Rab22." Journal of Virology 89, no. 16 (June 3, 2015): 8365–82. http://dx.doi.org/10.1128/jvi.00209-15.

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ABSTRACTVaccinia virus, the prototype of theOrthopoxvirusgenus in the familyPoxviridae, infects a wide range of cell lines and animals. Vaccinia mature virus particles of the WR strain reportedly enter HeLa cells through fluid-phase endocytosis. However, the intracellular trafficking process of the vaccinia mature virus between cellular uptake and membrane fusion remains unknown. We used live imaging of single virus particles with a combination of various cellular vesicle markers, to track fluorescent vaccinia mature virus particle movement in cells. Furthermore, we performed functional interference assays to perturb distinct vesicle trafficking processes in order to delineate the specific route undertaken by vaccinia mature virus prior to membrane fusion and virus core uncoating in cells. Our results showed that vaccinia virus traffics to early endosomes, where recycling endosome markers Rab11 and Rab22 are recruited to participate in subsequent virus trafficking prior to virus core uncoating in the cytoplasm. Furthermore, we identified WASH-VPEF/FAM21-retromer complexes that mediate endosome fission and sorting of virus-containing vesicles prior to virus core uncoating in the cytoplasm.IMPORTANCEVaccinia mature virions of the WR strain enter HeLa cells through fluid phase endocytosis. We previously demonstrated that virus-containing vesicles are internalized into phosphatidylinositol 3-phosphate positive macropinosomes, which are then fused with Rab5-positive early endosomes. However, the subsequent process of sorting the virion-containing vesicles prior to membrane fusion remains unclear. We dissected the intracellular trafficking pathway of vaccinia mature virions in cells up to virus core uncoating in cytoplasm. We show that vaccinia mature virions first travel to early endosomes. Subsequent trafficking events require the important endosome-tethered protein VPEF/FAM21, which recruits WASH and retromer protein complexes to the endosome. There, the complex executes endosomal membrane fission and cargo sorting to the Rab11-positive and Rab22-positive recycling pathway, resulting in membrane fusion and virus core uncoating in the cytoplasm.

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Counihan, Natalie A., Stephen M. Rawlinson, and Brett D. Lindenbach. "Trafficking of Hepatitis C Virus Core Protein during Virus Particle Assembly." PLoS Pathogens 7, no. 10 (October 20, 2011): e1002302. http://dx.doi.org/10.1371/journal.ppat.1002302.

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Gilbert, Joanna M., Ilya G. Goldberg, and Thomas L. Benjamin. "Cell Penetration and Trafficking of Polyomavirus." Journal of Virology 77, no. 4 (February 15, 2003): 2615–22. http://dx.doi.org/10.1128/jvi.77.4.2615-2622.2003.

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ABSTRACT The murine polyomavirus (Py) enters mouse fibroblasts and kidney epithelial cells via an endocytic pathway that is caveola-independent (as well as clathrin-independent). In contrast, uptake of simian virus 40 into the same cells is dependent on caveola. Following the initial uptake of Py, both microtubules and microfilaments play roles in trafficking of the virus to the nucleus. Colcemid, which disrupts microtubules, inhibits the ability of Py to reach the nucleus and replicate. Paclitaxel, which stabilizes microtubules and prevents microtubule turnover, has no effect, indicating that intact but not dynamic microtubules are required for Py infectivity. Compounds that disrupt actin filaments enhance Py uptake while stabilization of actin filaments impedes Py infection. Virus particles are seen in association with actin in cells treated with microfilament-disrupting or filament-stabilizing agents at levels comparable to those in untreated cells, suggesting that a dynamic state of the microfilament system is important for Py infectivity.

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Miao, Congrong, Gertrud U. Radu, Hayat Caidi, Ralph A. Tripp, Larry J. Anderson, and Lia M. Haynes. "Treatment with respiratory syncytial virus G glycoprotein monoclonal antibody or F(ab′)2 components mediates reduced pulmonary inflammation in mice." Journal of General Virology 90, no. 5 (May 1, 2009): 1119–23. http://dx.doi.org/10.1099/vir.0.009308-0.

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Therapeutic treatment with a non-neutralizing monoclonal antibody (mAb) (131-2G) specific to respiratory syncytial virus (RSV) G glycoprotein mediates virus clearance and decreases leukocyte trafficking and interferon gamma (IFN-γ) production in the lungs of RSV-infected mice. Its F(ab′)2 component only mediates decreased leukocyte trafficking and IFN-γ production without reducing virus replication. Thus, this mAb has two independent actions that could facilitate treatment and/or prevention of RSV infection by reducing both virus replication and virus-induced pulmonary inflammation.

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Dissertations / Theses on the topic "Virus trafficking"

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Read, Eliot Keith Curtis. "Investigating influenza A virus RNA trafficking." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609127.

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Xiao, Wu. "Intracellular trafficking of adeno-associated virus type 2." [Gainesville, Fla.] : University of Florida, 2002. http://purl.fcla.edu/fcla/etd/UFE1001195.

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Muenzner, Julia. "Viral subversion of host cell membrane trafficking." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267890.

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Enveloped viruses acquire their membrane coat from the plasma membrane or intracellular organelles and rely on cellular machinery to facilitate envelopment and egress of virus progeny. This thesis examines egress-related interactions between host cell factors and proteins of two different enveloped viruses: hepatitis D virus (HDV) and herpes simplex virus 1 (HSV-1). HDV is a small RNA virus causing fulminant hepatitis or severely aggravating cirrhosis and hepatocellular carcinoma. HSV-1 is a large DNA virus infecting epithelial and neuronal cells. Infection with HSV-1 not only triggers the development of recurring sores on oral or genital mucosa, but can also cause severe disease in neonates and immunocompromised patients. The interaction between the large antigen of HDV (HDAg-L) and the N-terminal domain (NTD) of clathrin, a protein crucial for endocytosis and intracellular vesicular trafficking, was examined by structural, biochemical and biophysical techniques. Co-crystal structures of NTD bound to HDAg-L peptides derived from different HDV genotypes revealed that HDV interacts with multiple binding sites on NTD promiscuously, prompting re-evaluation of the binding between cellular peptides and NTD. Surprisingly, co-crystal structures and pull-down capture assays showed that cellular peptides containing clathrin-binding motifs can also bind multiple sites on the surface of NTD simultaneously. In addition, the structures of viral and cellular peptides bound to NTD enabled the molecular characterization of the fourth peptide binding site on NTD, the “Royle box”, and led to the identification of a novel binding mode at the “arrestin box” peptide binding site on NTD. The work in this thesis therefore not only identifies the molecular basis of HDV:clathrin interactions, but also furthers our understanding of basic clathrin biology. Even though many HSV-1 proteins have been implicated in the envelopment and egress of viral particles, only few interactions between HSV-1 and cellular proteins promoting these processes have been described. Therefore, the HSV-1 proteins gE, UL21 and UL56 were selected and characterized bioinformatically and/or biochemically. Cellular proteins interacting with UL56 were identified by yeast two-hybrid screening and quantitative mass spectrometry. Co-immunoprecipitation and pull-down experiments confirmed the Golgi-trafficking protein GOPC, components of the mammalian trafficking protein particle complex, and the ubiquitin ligase NEDD4 as novel binding partners of UL56, thereby suggesting exciting new avenues for the investigation of cellular mechanisms contributing to HSV-1 envelopment and egress.

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Price, Philip John Ritchie. "Leukocyte trafficking during infection with modified vaccinia virus Ankara." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-173737.

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Berka, Ursula, Martin Volker Hamann, and Dirk Lindemann. "Early Events in Foamy Virus - Host Interaction and Intracellular Trafficking." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-127078.

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Here we review viral and cellular requirements for entry and intracellular trafficking of foamy viruses (FVs) resulting in integration of viral sequences into the host cell genome. The virus encoded glycoprotein harbors all essential viral determinants, which are involved in absorption to the host membrane and triggering the uptake of virus particles. However, only recently light was shed on some details of FV’s interaction with its host cell receptor(s). Latest studies indicate glycosaminoglycans of cellular proteoglycans, particularly heparan sulfate, to be of utmost importance. In a species-specific manner FVs encounter endogenous machineries of the target cell, which are in some cases exploited for fusion and further egress into the cytosol. Mostly triggered by pH-dependent endocytosis, viral and cellular membranes fuse and release naked FV capsids into the cytoplasm. Intact FV capsids are then shuttled along microtubules and are found to accumulate nearby the centrosome where they can remain in a latent state for extended time periods. Depending on the host cell cycle status, FV capsids finally disassemble and, by still poorly characterized mechanisms, the preintegration complex gets access to the host cell chromatin. Host cell mitosis finally allows for viral genome integration, ultimately starting a new round of viral replication.

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Lindemann, Dirk, Ursula Berka, and Martin Volker Hamann. "Early Events in Foamy Virus - Host Interaction and Intracellular Trafficking." MDPI, 2013. https://tud.qucosa.de/id/qucosa%3A28912.

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Here we review viral and cellular requirements for entry and intracellular trafficking of foamy viruses (FVs) resulting in integration of viral sequences into the host cell genome. The virus encoded glycoprotein harbors all essential viral determinants, which are involved in absorption to the host membrane and triggering the uptake of virus particles. However, only recently light was shed on some details of FV’s interaction with its host cell receptor(s). Latest studies indicate glycosaminoglycans of cellular proteoglycans, particularly heparan sulfate, to be of utmost importance. In a species-specific manner FVs encounter endogenous machineries of the target cell, which are in some cases exploited for fusion and further egress into the cytosol. Mostly triggered by pH-dependent endocytosis, viral and cellular membranes fuse and release naked FV capsids into the cytoplasm. Intact FV capsids are then shuttled along microtubules and are found to accumulate nearby the centrosome where they can remain in a latent state for extended time periods. Depending on the host cell cycle status, FV capsids finally disassemble and, by still poorly characterized mechanisms, the preintegration complex gets access to the host cell chromatin. Host cell mitosis finally allows for viral genome integration, ultimately starting a new round of viral replication.

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Lindemann, Dirk, Ursula Berka, and Martin Volker Hamann. "Early Events in Foamy Virus - Host Interaction and Intracellular Trafficking." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-178848.

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Here we review viral and cellular requirements for entry and intracellular trafficking of foamy viruses (FVs) resulting in integration of viral sequences into the host cell genome. The virus encoded glycoprotein harbors all essential viral determinants, which are involved in absorption to the host membrane and triggering the uptake of virus particles. However, only recently light was shed on some details of FV’s interaction with its host cell receptor(s). Latest studies indicate glycosaminoglycans of cellular proteoglycans, particularly heparan sulfate, to be of utmost importance. In a species-specific manner FVs encounter endogenous machineries of the target cell, which are in some cases exploited for fusion and further egress into the cytosol. Mostly triggered by pH-dependent endocytosis, viral and cellular membranes fuse and release naked FV capsids into the cytoplasm. Intact FV capsids are then shuttled along microtubules and are found to accumulate nearby the centrosome where they can remain in a latent state for extended time periods. Depending on the host cell cycle status, FV capsids finally disassemble and, by still poorly characterized mechanisms, the preintegration complex gets access to the host cell chromatin. Host cell mitosis finally allows for viral genome integration, ultimately starting a new round of viral replication.

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Gao, William Ning Da. "Viral and cellular proteins involved in vaccinia virus egress." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/280280.

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Vaccinia virus (VACV) is a large double-stranded DNA virus with a cytoplasmic site of replication. It has a complex life cycle that produces two distinct infectious virion forms, Intracellular Mature Virions (IMVs) and Extracellular Enveloped Virions (EEVs). The host cell microtubule trafficking machinery is hijacked by the virus at three distinct positions of the viral life cycle. After virus entry, the virus cores are transported to pre-nuclear sites where they form viral factories that ultimately produce fully functional and infectious IMVs. A small proportion of IMVs are further transported to sites of wrapping, where they are enveloped by a host-derived double membrane to form Intracellular Enveloped Virions (IEVs). The IEVs are then transported to the cell periphery to facilitate efficient viral spread. The viral proteins A36, F12 and E2 together with the kinesin-1 microtubule motor protein are thought to be involved in IEV egress from the site of wrapping to the cell periphery, although the exact mechanism of movement is unclear. Until recently, A36 was the only known protein to interact with the kinesin-1 motor through kinesin light chain (KLC), but F12 has also been shown to interact with KLC through E2. The precise mechanism of how the IEV interacts with and activates the kinesin-1 motor protein is unclear, and this study explores the interactions of IEV proteins with KLCs in detail, mapping interactions between KLC and A36 or F12/E2. A36, F12 and E2 also show no sequence or predicted structural homology to any other known proteins, and structural studies were performed in an attempt solve their 3D structure. The CRISPR-Cas9 targeted genome editing tool was also utilised to knockout different KLC isoforms in multiple cell lines to assess their contribution to IEV egress as well as cellular trafficking. These studies will provide insight into the mechanisms behind the spatial and temporal control of kinesin motor activity in the cell.

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Haines, Felicity Jade. "Trafficking of GP64 and Virus Egress in AcNPV-infected insect cells." Thesis, Oxford Brookes University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432736.

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Dudleenamjil, Enkhmart. "BPV Entry and Trafficking in EBTr Cells." BYU ScholarsArchive, 2009. https://scholarsarchive.byu.edu/etd/2301.

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Bovine Parvovirus (BPV) belongs to the genus Bocavirus, family Parvoviridae. BPV is the leading etiologic agent among the pathogens that cause primary gastroenteritis of cattle. Many of the intracellular events associated with virus replication are unknown. In this research project, we investigated BPV internalization into the host cell and trafficking in the cytosol. Preliminarily, EBTr cells had abundant clathrin, virus attached to purified clathrin, and EM micrographs revealed virus in endocytic vacuoles. Assays detecting virus infectivity (i.e. viral protein synthesis), virus production (completion of the replication cycle), and quantitative PCR (qPCR) to detect viral transcripts were used to evaluate virus uptake and subsequent trafficking events in the presence of selective inhibitors. Cell toxicity mediated by the drugs was evaluated by the MTT test. Virucidal effects of the drugs were assessed. A control virus was used to verify the inhibitor technology. Immunofluoresceinated virus particles were found in clathrin-rich early endosomes. Clathrin-mediated endocytosis (CME) was examined by clathrin polymerization inhibiting agent (chloropromazine), lysosomotropic agents (ammonium chloride and chloroquine), a vacuolar ATPase inhibitor (bafilomycin A1), and a blocker of transition between endosomes (brefeldin A). Caveosome pathway inhibitors included phorbol 12-myristate 13-acetate (a suppressor of caveolae formation), nystatin and methyl-beta-cyclodextrin (lipid raft blockers), and genistein (a tyrosine kinase phosphorylation inhibitor). Trafficking of BPV was investigated using specific inhibitors of proteasomal activity, actin-myosin function, and microtubule-dynein function. The proteasomal protease suppressor (lactacystin), and a proteasomal chymotrypsin inhibitor (epoxomicin) were used. The role of actin was probed by cytochlasin D, latrunculin A, and ML-7. The microtubule inhibitors nocodazole, vanadate, and EHNA were used to probe microtubule function. The inhibitors of CME reduced virus production and reduced infectivity, a result confirmed by qPCR. The blockers of caveolin-mediated entry did not interfere with virus production nor virus infectivity. Proteasome activity blockage did not affect the virus replication. But the virus cycle was affected by actin blockage and by microtubule blockage detected by qPCR. Taken together these data indicate that BPV uptake is mediated by clathrin coated pits and is acid-dependent. Further processing of BPV in the cytosol does not require proteasomal enzymes. Actin-associated vesicular transport appears to be essential to virus replication and trafficking to the nucleus appears to be mediated by microtubules.

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Books on the topic "Virus trafficking"

1

Membrane Trafficking in Viral Replication (Current Topics in Microbiology and Immunology). Springer, 2004.

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Book chapters on the topic "Virus trafficking"

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Nir, Shlomo, Nejat Düzgüneş, Dick Hoekstra, João Ramalho-Santos, and Maria C. Pedroso de Lima. "Mass action model of virus fusion." In Trafficking of Intracellular Membranes:, 155–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79547-3_9.

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Pedroso de Lima, Maria C., João Ramalho-Santos, Nejat Düzgünes, Diana Flasher, and Shlomo Nir. "Entry of Enveloped Viruses Into Host Cells: Fusion Activity of the Influenza Virus Hemagglutinin." In Trafficking of Intracellular Membranes:, 131–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79547-3_8.

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Morozov, Sergey Yu. "CURRENT VIEWS ON HOST COMPONENTS INVOLVED IN PLANT VIRUS INTERCELLULAR TRAFFICKING." In Virus Diseases and Crop Biosecurity, 107–19. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/978-1-4020-5298-9_10.

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Baktash, Yasmine, and Glenn Randall. "Live Cell Imaging of Hepatitis C Virus Trafficking in Hepatocytes." In Methods in Molecular Biology, 263–74. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8976-8_18.

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Spapens, Toine. "Is COVID-19 a Crime? A Criminological Perspective." In The New Common, 203–8. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65355-2_29.

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AbstractIs COVID-19 a crime? The answer to that question seems relatively straightforward. Although the virus may be viewed as a “villain,” we cannot treat it as a criminal. However, how the virus impacts societies and government responses to the crisis raises serious criminological questions. In this chapter, I briefly address three. I will start by looking at the effects of COVID-19 and particularly the lockdowns on criminal activities. My second question is whether we should rethink our response to crimes that may facilitate future pandemics, particularly wildlife trafficking. Finally, I will discuss some examples of systemic inequalities, which affect the impact of the virus on societies. Given the current state of affairs, I will raise questions and ideas for future research, rather than provide clear-cut answers.

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Chou, Yi-ying, and Timothée Lionnet. "Single-Molecule Sensitivity RNA FISH Analysis of Influenza Virus Genome Trafficking." In Methods in Molecular Biology, 195–211. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8678-1_10.

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Block, Timothy M., Xuanyong Lu, Anand Mehta, Jason Park, Baruch S. Blumberg, and Raymond Dwek. "Role of Glycan Processing in Hepatitis B Virus Envelope Protein Trafficking." In Advances in Experimental Medicine and Biology, 207–16. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5383-0_20.

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Chu, Hin, Jaang-Jiun Wang, and Paul Spearman. "Human Immunodeficiency Virus Type-1 Gag and Host Vesicular Trafficking Pathways." In Current Topics in Microbiology and Immunology, 67–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02175-6_4.

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Nelson, Richard S., and Aart J. E. van Bel. "The Mystery of Virus Trafficking Into, Through and Out of Vascular Tissue." In Progress in Botany, 476–533. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80446-5_17.

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Kalicharran, Kishna, and Samuel Dales. "Involvement of Microtubules and the Microtubule-Associated Protein TAU in Trafficking of JHM Virus and Components within Neurons." In Advances in Experimental Medicine and Biology, 57–61. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1899-0_8.

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