Journal articles: 'Viral traffic'

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Luethy, Lauren N., and Julie K. Pfeiffer. "Viral Infection Brings Mitochondrial Traffic to a Standstill." Cell Host & Microbe 11, no. 5 (May 2012): 420–21. http://dx.doi.org/10.1016/j.chom.2012.05.001.

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Enserink, M. "AVIAN INFLUENZA: Keeping Track of Viral Air Traffic." Science 310, no. 5747 (October 21, 2005): 428. http://dx.doi.org/10.1126/science.310.5747.428.

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Morse, Stephen S. "Emerging Viruses: Defining the Rules for Viral Traffic." Perspectives in Biology and Medicine 34, no. 3 (1991): 387–409. http://dx.doi.org/10.1353/pbm.1991.0038.

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Roman, Laura M., and Henrik Garoff. "Revelation through exploitation: the viral model for intracellular traffic." Trends in Biochemical Sciences 10, no. 11 (November 1985): 428–32. http://dx.doi.org/10.1016/0968-0004(85)90024-6.

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Lidsky, Peter V., Stanleyson Hato, Maryana V. Bardina, Alexei G. Aminev, Ann C. Palmenberg, Eugene V. Sheval, Vladimir Y. Polyakov, Frank J. M. van Kuppeveld, and Vadim I. Agol. "Nucleocytoplasmic Traffic Disorder Induced by Cardioviruses." Journal of Virology 80, no. 6 (March 15, 2006): 2705–17. http://dx.doi.org/10.1128/jvi.80.6.2705-2717.2006.

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ABSTRACT Some picornaviruses, for example, poliovirus, increase bidirectional permeability of the nuclear envelope and suppress active nucleocytoplasmic transport. These activities require the viral protease 2Apro. Here, we studied nucleocytoplasmic traffic in cells infected with encephalomyocarditis virus (EMCV; a cardiovirus), which lacks the poliovirus 2Apro-related protein. EMCV similarly enhanced bidirectional nucleocytoplasmic traffic. By using the fluorescent “Timer” protein, which contains a nuclear localization signal, we showed that the cytoplasmic accumulation of nuclear proteins in infected cells was largely due to the nuclear efflux of “old” proteins rather than impaired active nuclear import of newly synthesized molecules. The nuclear envelope of digitonin-treated EMCV-infected cells permitted rapid efflux of a nuclear marker protein. Inhibitors of poliovirus 2Apro did not prevent the EMCV-induced efflux. Extracts from EMCV-infected cells and products of in vitro translation of viral RNAs contained an activity increasing permeability of the nuclear envelope of uninfected cells. This activity depended on the expression of the viral leader protein. Mutations disrupting the zinc finger motif of this protein abolished its efflux-inducing ability. Inactivation of the L protein phosphorylation site (Thr47→Ala) resulted in a delayed efflux, while a phosphorylation-mimicking (Thr47→Asp) replacement did not significantly impair the efflux-inducing ability. Such activity of extracts from EMCV-infected cells was suppressed by the protein kinase inhibitor staurosporine. As evidenced by electron microscopy, cardiovirus infection resulted in alteration of the nuclear pores, but it did not trigger degradation of the nucleoporins known to be degraded in the poliovirus-infected cells. Thus, two groups of picornaviruses, enteroviruses and cardioviruses, similarly alter the nucleocytoplasmic traffic but achieve this by strikingly different mechanisms.

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Suikkanen, Sanna, Tuula Aaltonen, Marjukka Nevalainen, Outi Välilehto, Laura Lindholm, Matti Vuento, and Maija Vihinen-Ranta. "Exploitation of Microtubule Cytoskeleton and Dynein during Parvoviral Traffic toward the Nucleus." Journal of Virology 77, no. 19 (October 1, 2003): 10270–79. http://dx.doi.org/10.1128/jvi.77.19.10270-10279.2003.

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ABSTRACT Canine parvovirus (CPV), a model virus for the study of parvoviral entry, enters host cells by receptor-mediated endocytosis, escapes from endosomal vesicles to the cytosol, and then replicates in the nucleus. We examined the role of the microtubule (MT)-mediated cytoplasmic trafficking of viral particles toward the nucleus. Immunofluorescence and immunoelectron microscopy showed that capsids were transported through the cytoplasm into the nucleus after cytoplasmic microinjection but that in the presence of MT-depolymerizing agents, viral capsids were unable to reach the nucleus. The nuclear accumulation of capsids was also reduced by microinjection of an anti-dynein antibody. Moreover, electron microscopy and light microscopy experiments demonstrated that viral capsids associate with tubulin and dynein in vitro. Coprecipitation studies indicated that viral capsids interact with dynein. When the cytoplasmic transport process was studied in living cells by microinjecting fluorescently labeled capsids into the cytoplasm of cells containing fluorescent tubulin, capsids were found in close contact with MTs. These results suggest that intact MTs and the motor protein dynein are required for the cytoplasmic transport of CPV capsids and contribute to the accumulation of the capsid in the nucleus.

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Haupt, Sophie, Graham H. Cowan, Angelika Ziegler, Alison G. Roberts, Karl J. Oparka, and Lesley Torrance. "Two Plant–Viral Movement Proteins Traffic in the Endocytic Recycling Pathway." Plant Cell 17, no. 1 (December 17, 2004): 164–81. http://dx.doi.org/10.1105/tpc.104.027821.

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Shimizu, Kenta, Kumiko Yoshimatsu, Takaaki Koma, Shumpei P. Yasuda, and Jiro Arikawa. "Role of nucleocapsid protein of hantaviruses in intracellular traffic of viral glycoproteins." Virus Research 178, no. 2 (December 2013): 349–56. http://dx.doi.org/10.1016/j.virusres.2013.09.022.

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Ikonen, E., R. G. Parton, F. Lafont, and K. Simons. "Analysis of the role of p200-containing vesicles in post-Golgi traffic." Molecular Biology of the Cell 7, no. 6 (June 1996): 961–74. http://dx.doi.org/10.1091/mbc.7.6.961.

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p200 is a cytoplasmic protein that associates with vesicles budding from the trans-golgi network (TGN). The protein was identified by a monoclonal antibody AD7. We have used this antibody to analyze whether p200 functions in exocytic transport from the TGN to the apical or basolateral plasma membrane in Madin-Darby canine kidney cells. We found that transport of the viral marker proteins, influenza hemagglutinin (HA) to the apical surface or vesicular stomatitis virus glycoprotein (VSV G) to the basolateral surface in streptolysin O-permeabilized cells was not affected when p200 was depleted from both the membranes and the cytosol. When vesicles isolated from perforated cells were analyzed by equilibrium density gradient centrifugation, the p200 immunoreactive membranes did not comigrate with either the apical vesicle marker HA or the basolateral vesicle marker VSV G. Immunoelectron microscopy of perforated and double-labeled cells showed that the p200 positive vesicular profiles were not labeled by antibodies to HA or VSV G when the viral proteins were accumulated in the TGN. Furthermore, the p200-decorated vesicles were more electron dense than those labeled with the viral antibodies. Together, these results suggest that p200 does not function in the transport pathways that carry HA from the TGN to the apical surface or VSV G from the TGN to the basolateral surface.

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Jing, Peng, Farzin Haque, Dan Shu, Carlo Montemagno, and Peixuan Guo. "One-Way Traffic of a Viral Motor Channel for Double-Stranded DNA Translocation." Nano Letters 10, no. 9 (September 8, 2010): 3620–27. http://dx.doi.org/10.1021/nl101939e.

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Rosas-Acosta, Germán, Sharon C. Braunagel, and Max D. Summers. "Effects of Deletion and Overexpression of the Autographa californica Nuclear Polyhedrosis Virus FP25KGene on Synthesis of Two Occlusion-Derived Virus Envelope Proteins and Their Transport into Virus-Induced Intranuclear Membranes." Journal of Virology 75, no. 22 (November 15, 2001): 10829–42. http://dx.doi.org/10.1128/jvi.75.22.10829-10842.2001.

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ABSTRACT Partial deletions within Autographa californica open reading frame 61 (FP25K) alter the expression and accumulation profile of several viral proteins and the transport of occlusion-derived virus (ODV)-E66 to intranuclear membranes during infection (S. C. Braunagel et al., J. Virol. 73:8559–8570, 1999). Here we show the effects of a full deletion and overexpression of FP25K on the transport and expression of two ODV envelope proteins, ODV-E66 (E66) and ODV-E25 (E25). Deletion and overexpression of FP25K substantially altered the levels of expression of E66 during infection. Compared with cells infected with wild-type (wt) virus, the levels of E66 were reduced fivefold in cells infected with a viral mutant lacking FP25K (ΔFP25K) and were slightly increased in cells infected with a viral mutant overexpressing FP25K (FP25Kpolh). In contrast, no significant changes were observed in the levels of E25 among wt-, ΔFP25K-, and FP25Kpolh-infected cells. The changes observed in the levels of E66 among the different viral mutants were not accompanied by changes in either the time of synthesis, membrane association, protein turnover, or steady-state transcript abundance. Deletion of FP25K also substantially altered the transport and localization of E66 during infection. In cells infected with the ΔFP25K mutant virus, E66 accumulated in localized regions at the nuclear periphery and the outer nuclear membrane and did not traffic to intranuclear membranes. In contrast, in cells infected with the FP25Kpolh mutant virus E66 trafficked to intranuclear membranes. For comparison, E25 was normally transported to intranuclear membranes in both ΔFP25K- and FP25Kpolh-infected cells. Altogether these studies suggest that FP25K affects the synthesis of E66 at a posttranscriptional level, probably by altering the translation of E66; additionally, the block in transport of E66 at the nuclear envelope in ΔFP25K-infected cells suggests that the pathway of E66 trafficking to the inner nuclear membrane and intranuclear microvesicles is specifically regulated and must be influenced by factors that do not control the traffic of E25.

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Hauri, H. P., F. Kappeler, H. Andersson, and C. Appenzeller. "ERGIC-53 and traffic in the secretory pathway." Journal of Cell Science 113, no. 4 (February 15, 2000): 587–96. http://dx.doi.org/10.1242/jcs.113.4.587.

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The ER-Golgi intermediate compartment (ERGIC) marker ERGIC-53 is a mannose-specific membrane lectin operating as a cargo receptor for the transport of glycoproteins from the ER to the ERGIC. Lack of functional ERGIC-53 leads to a selective defect in secretion of glycoproteins in cultured cells and to hemophilia in humans. Beyond its interest as a transport receptor, ERGIC-53 is an attractive probe for studying numerous aspects of protein trafficking in the secretory pathway, including traffic routes, mechanisms of anterograde and retrograde traffic, retention of proteins in the ER, and the function of the ERGIC. Understanding these fundamental processes of cell biology will be crucial for the elucidation and treatment of many inherited and acquired diseases, such as cystic fibrosis, Alzheimer's disease and viral infections.

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Genoves, A., V. Pallas, and J. A. Navarro. "Contribution of Topology Determinants of a Viral Movement Protein to Its Membrane Association, Intracellular Traffic, and Viral Cell-to-Cell Movement." Journal of Virology 85, no. 15 (May 18, 2011): 7797–809. http://dx.doi.org/10.1128/jvi.02465-10.

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Martínez, José L., and Carlos F. Arias. "Role of the Guanine Nucleotide Exchange Factor GBF1 in the Replication of RNA Viruses." Viruses 12, no. 6 (June 24, 2020): 682. http://dx.doi.org/10.3390/v12060682.

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The guanine nucleotide exchange factor GBF1 is a well-known factor that can activate different ADP-ribosylation factor (Arf) proteins during the regulation of different cellular vesicular transport processes. In the last decade, it has become increasingly evident that GBF1 can also regulate different steps of the replication cycle of RNA viruses belonging to different virus families. GBF1 has been shown not only to facilitate the intracellular traffic of different viral and cellular elements during infection, but also to modulate the replication of viral RNA, the formation and maturation of viral replication complexes, and the processing of viral proteins through mechanisms that do not depend on its canonical role in intracellular transport. Here, we review the various roles that GBF1 plays during the replication of different RNA viruses.

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DiGiuseppe, Stephen, Malgorzata Bienkowska-Haba, and Martin Sapp. "Human Papillomavirus Entry: Hiding in a Bubble." Journal of Virology 90, no. 18 (July 13, 2016): 8032–35. http://dx.doi.org/10.1128/jvi.01065-16.

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Incoming human papillomavirus (HPV) utilize vesicular transport to traffic from the plasma membrane to the trans-Golgi network. Following nuclear envelope breakdown during mitosis, the viral DNA associates with condensed chromosomes utilizing spindle microtubules for delivery. Most intriguingly, the viral DNA resides in a transport vesicle until mitosis is completed and the nuclear envelope has reformed. This finding provides support for the transient existence of nuclear membrane-bound vesicles. Due to their transient nature, it also points to the existence of a cell pathway for the disposal of vesicles ending up fortuitously or purposefully in the nucleus.

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Dharan, Adarsh, Silvana Opp, Omar Abdel-Rahim, Sevnur Komurlu Keceli, Sabrina Imam, Felipe Diaz-Griffero, and Edward M. Campbell. "Bicaudal D2 facilitates the cytoplasmic trafficking and nuclear import of HIV-1 genomes during infection." Proceedings of the National Academy of Sciences 114, no. 50 (November 27, 2017): E10707—E10716. http://dx.doi.org/10.1073/pnas.1712033114.

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Numerous viruses, including HIV-1, exploit the microtubule network to traffic toward the nucleus during infection. Although numerous studies have observed a role for the minus-end microtubule motor dynein in HIV-1 infection, the mechanism by which the viral core containing the viral genome associates with dynein and induces its perinuclear trafficking has remained unclear. Here, we report that the dynein adapter protein bicaudal D2 (BICD2) is able to interact with HIV-1 viral cores in target cells. We also observe that BICD2 can bind in vitro-assembled capsid tubes through its CC3 domain. We observe that BICD2 facilitates infection by promoting the trafficking of viral cores to the nucleus, thereby promoting nuclear entry of the viral genome and infection. Finally, we observe that depletion of BICD2 in the monocytic cell line THP-1 results in an induction of IFN-stimulated genes in these cells. Collectively, these results identify a microtubule adapter protein critical for trafficking of HIV-1 in the cytoplasm of target cells and evasion of innate sensing mechanisms in macrophages.

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Helle, Francois, Lynda Handala, Marine Bentz, Gilles Duverlie, and Etienne Brochot. "Intercellular Transmission of Naked Viruses through Extracellular Vesicles: Focus on Polyomaviruses." Viruses 12, no. 10 (September 26, 2020): 1086. http://dx.doi.org/10.3390/v12101086.

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Extracellular vesicles have recently emerged as a novel mode of viral transmission exploited by naked viruses to exit host cells through a nonlytic pathway. Extracellular vesicles can allow multiple viral particles to collectively traffic in and out of cells, thus enhancing the viral fitness and diversifying the transmission routes while evading the immune system. This has been shown for several RNA viruses that belong to the Picornaviridae, Hepeviridae, Reoviridae, and Caliciviridae families; however, recent studies also demonstrated that the BK and JC viruses, two DNA viruses that belong to the Polyomaviridae family, use a similar strategy. In this review, we provide an update on recent advances in understanding the mechanisms used by naked viruses to hijack extracellular vesicles, and we discuss the implications for the biology of polyomaviruses.

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Itaya, Asuka, Fengshan Ma, Yijun Qi, Yoshie Matsuda, Yali Zhu, Genqing Liang, and Biao Ding. "Plasmodesma-Mediated Selective Protein Traffic between “Symplasmically Isolated” Cells Probed by a Viral Movement Protein." Plant Cell 14, no. 9 (August 23, 2002): 2071–83. http://dx.doi.org/10.1105/tpc.003954.

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Dodd, Dana A., Thomas H. Giddings, and Karla Kirkegaard. "Poliovirus 3A Protein Limits Interleukin-6 (IL-6), IL-8, and Beta Interferon Secretion during Viral Infection." Journal of Virology 75, no. 17 (September 1, 2001): 8158–65. http://dx.doi.org/10.1128/jvi.75.17.8158-8165.2001.

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ABSTRACT During viral infections, the host secretory pathway is crucial for both innate and acquired immune responses. For example, the export of most proinflammatory and antiviral cytokines, which recruit lymphocytes and initiate antiviral defenses, requires traffic through the host secretory pathway. To investigate potential effects of the known inhibition of cellular protein secretion during poliovirus infection on pathogenesis, cytokine secretion from cells infected with wild-type virus and with 3A-2, a mutant virus carrying an insertion in viral protein 3A which renders the virus defective in the inhibition of protein secretion, was tested. We show here that cells infected with 3A-2 mutant virus secrete greater amounts of cytokines interleukin-6 (IL-6), IL-8, and beta interferon than cells infected with wild-type poliovirus. Increased cytokine secretion from the mutant-infected cells can be attributed to the reduced inhibition of host protein secretion, because no significant differences between 3A-2- and wild-type-infected cells were observed in the inhibition of viral growth, host cell translation, or the ability of wild-type- or 3A-2-infected cells to support the transcriptional induction of beta interferon mRNA. We surmise that the wild-type function of 3A in inhibiting ER-to-Golgi traffic is not required for viral replication in tissue culture but, by altering the amount of secreted cytokines, could have substantial effects on pathogenesis within an infected host. The global inhibition of protein secretion by poliovirus may reflect a general mechanism by which pathogens that do not require a functional protein secretory apparatus can reduce the native immune response and inflammation associated with infection.

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Kreiner, T., and H. P. Moore. "Membrane traffic between secretory compartments is differentially affected during mitosis." Cell Regulation 1, no. 5 (April 1990): 415–24. http://dx.doi.org/10.1091/mbc.1.5.415.

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Membrane traffic has been shown to be regulated during cell division. In particular, with the use of viral membrane proteins as markers, endoplasmic reticulum (ER)-to-Golgi transport in mitotic cells has been shown to be essentially blocked. However, the effect of mitosis on other steps in the secretory pathway is less clear, because an early block makes examination of following steps difficult. Here, we report studies on the functional characteristics of secretory pathways in mitotic mammalian tissue culture cells by the use of a variety of markers. Chinese hamster ovary cells were transfected with cDNAs encoding secretory proteins. Consistent with earlier results following viral membrane proteins, we found that the overall secretory pathway is nonfunctional in mitotic cells, and a major block to secretion is at the step between ER and Golgi: the overall rate of secretion of human growth hormone is reduced at least 10-fold in mitotic cells, and export of truncated vesicular stomatitis virus G protein from the ER is inhibited to about the same extent, as judged by acquisition of endoglycosidase H resistance. To ascertain the integrity of transport from the trans-Golgi to plasma membrane, we followed the secretion of sulfated glycosaminoglycan (GAG) chains, which are synthesized in the Golgi and thus are not subject to the earlier ER-to-Golgi block. GAG chains are valid markers for the pathway taken by constitutive secretory proteins; both protein secretion and GAG chain secretion are sensitive to treatment with n-ethyl-maleimide and monensin and are blocked at 19 degrees C. We found that the extent of GAG-chain secretion is not altered during mitosis, although the initial rate of secretion is reduced about twofold in mitotic compared with interphase cells. Thus, during mitosis, transport from the trans-Golgi to plasma membrane is much less hindered than ER-to-Golgi traffic. We conclude that transport steps are not affected to the same extent during mitosis.

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Youker, Robert T., Ujwal Shinde, Robert Day, and Gary Thomas. "At the crossroads of homoeostasis and disease: roles of the PACS proteins in membrane traffic and apoptosis." Biochemical Journal 421, no. 1 (June 12, 2009): 1–15. http://dx.doi.org/10.1042/bj20081016.

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The endomembrane system in mammalian cells has evolved over the past two billion years from a simple endocytic pathway in a single-celled primordial ancestor to complex networks supporting multicellular structures that form metazoan tissue and organ systems. The increased organellar complexity of metazoan cells requires additional trafficking machinery absent in yeast or other unicellular organisms to maintain organ homoeostasis and to process the signals that control proliferation, differentiation or the execution of cell death programmes. The PACS (phosphofurin acidic cluster sorting) proteins are one such family of multifunctional membrane traffic regulators that mediate organ homoeostasis and have important roles in diverse pathologies and disease states. This review summarizes our current knowledge of the PACS proteins, including their structure and regulation in cargo binding, their genetics, their roles in secretory and endocytic pathway traffic, interorganellar communication and how cell-death signals reprogramme the PACS proteins to regulate apoptosis. We also summarize our current understanding of how PACS genes are dysregulated in cancer and how viral pathogens ranging from HIV-1 to herpesviruses have evolved to usurp the PACS sorting machinery to promote virus assembly, viral spread and immunoevasion.

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Aicher, Sophie-Marie, Paul Monaghan, Christopher L. Netherton, and Philippa C. Hawes. "Unpicking the Secrets of African Swine Fever Viral Replication Sites." Viruses 13, no. 1 (January 8, 2021): 77. http://dx.doi.org/10.3390/v13010077.

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African swine fever virus (ASFV) is a highly contagious pathogen which causes a lethal haemorrhagic fever in domestic pigs and wild boar. The large, double-stranded DNA virus replicates in perinuclear cytoplasmic replication sites known as viral factories. These factories are complex, multi-dimensional structures. Here we investigated the protein and membrane compartments of the factory using super-resolution and electron tomography. Click IT chemistry in combination with stimulated emission depletion (STED) microscopy revealed a reticular network of newly synthesized viral proteins, including the structural proteins p54 and p34, previously seen as a pleomorphic ribbon by confocal microscopy. Electron microscopy and tomography confirmed that this network is an accumulation of membrane assembly intermediates which take several forms. At early time points in the factory formation, these intermediates present as small, individual membrane fragments which appear to grow and link together, in a continuous progression towards new, icosahedral virions. It remains unknown how these membranes form and how they traffic to the factory during virus morphogenesis.

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Aicher, Sophie-Marie, Paul Monaghan, Christopher L. Netherton, and Philippa C. Hawes. "Unpicking the Secrets of African Swine Fever Viral Replication Sites." Viruses 13, no. 1 (January 8, 2021): 77. http://dx.doi.org/10.3390/v13010077.

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African swine fever virus (ASFV) is a highly contagious pathogen which causes a lethal haemorrhagic fever in domestic pigs and wild boar. The large, double-stranded DNA virus replicates in perinuclear cytoplasmic replication sites known as viral factories. These factories are complex, multi-dimensional structures. Here we investigated the protein and membrane compartments of the factory using super-resolution and electron tomography. Click IT chemistry in combination with stimulated emission depletion (STED) microscopy revealed a reticular network of newly synthesized viral proteins, including the structural proteins p54 and p34, previously seen as a pleomorphic ribbon by confocal microscopy. Electron microscopy and tomography confirmed that this network is an accumulation of membrane assembly intermediates which take several forms. At early time points in the factory formation, these intermediates present as small, individual membrane fragments which appear to grow and link together, in a continuous progression towards new, icosahedral virions. It remains unknown how these membranes form and how they traffic to the factory during virus morphogenesis.

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Zafri, Niaz Mahmud, Sadia Afroj, Mohammad Ashraf Ali, Md Musleh Uddin Hasan, and Md Hamidur Rahman. "Effectiveness of containment strategies and local cognition to control vehicular traffic volume in Dhaka, Bangladesh during COVID-19 pandemic: Use of Google Map based real-time traffic data." PLOS ONE 16, no. 5 (May 27, 2021): e0252228. http://dx.doi.org/10.1371/journal.pone.0252228.

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Background To prevent the viral transmission from higher infected to lower infected area, controlling the vehicular traffic, consequently public movement on roads is crucial. Containment strategies and local cognition regarding pandemic might be helpful to control vehicular movement. This study aimed to ascertain the effectiveness of containment strategies and local cognition for controlling traffic volume during COVID-19 pandemic in Dhaka, Bangladesh. Method Six containment strategies were considered to explore their influence on traffic condition, including declaration of general holiday, closure of educational institution, deployment of force, restriction on religious gathering, closure of commercial activities, and closure of garments factories. Newspaper coverage and public concern about COVID-19 were considered as local cognition in this research. The month of Ramadan as a potential event was also taken into account considering it might have an impact on the overall situation. Average daily journey speed (ADJS) was calculated from real-time traffic data of Google Map to understand the vehicular traffic scenario of Dhaka. A multiple linear regression method was developed to comprehend the findings. Results The results showed that among the containment strategies, declaration of general holiday and closure of educational institutions could increase the ADJS significantly, thereby referring to less traffic movement. Besides, local cognition could not significantly affect the traffic condition, although the month of Ramadan could increase the ADJS significantly. Conclusion It is expected that these findings would provide new insights into decision-making and help to take appropriate strategies to tackle the future pandemic situation.

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Banerjee, Meenakshi, Yunjie Huang, Smita Joshi, Gabriel J. Popa, Michael D. Mendenhall, Qing Jun Wang, Beth A. Garvy, Thein Myint, and Sidney W. Whiteheart. "Platelets Endocytose Viral Particles and Are Activated via TLR (Toll-Like Receptor) Signaling." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 7 (July 2020): 1635–50. http://dx.doi.org/10.1161/atvbaha.120.314180.

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Objective: Thrombocytopenia is associated with many viral infections suggesting virions interact with and affect platelets. Consistently, viral particles are seen inside platelets, and platelet activation markers are detected in viremic patients. In this article, we sought mechanistic insights into these virion/platelet interactions by examining how platelets endocytose, traffic, and are activated by a model virion. Approach and Results: Using fluorescently tagged HIV-1 pseudovirions, 3-dimensional structured illumination microscopy, and transgenic mouse models, we probed the interactions between platelets and virions. Mouse platelets used known endocytic machinery, that is, dynamin, VAMP (vesicle-associated membrane protein)-3, and Arf6 (ADP-ribosylation factor 6), to take up and traffic HIV-1 pseudovirions. Endocytosed HIV-1 pseudovirions trafficked through early (Rab4 + ) and late endosomes (Rab7 + ), and then to an LC3 + (microtubule-associated protein 1A/1B-light chain 3) compartment. Incubation with virions induced IRAK4 (interleukin 1 receptor–associated kinase 4), Akt (protein kinase B), and IKK (IκB kinase) activation, granule secretion, and platelet-leukocyte aggregate formation. This activation required TLRs (Toll-like receptors) and MyD88 (myeloid differentiation primary response protein 88) but was less extensive and slower than activation with thrombin. In vivo, HIV-1 pseudovirions injection led to virion uptake and platelet activation, as measured by IKK activation, platelet-leukocyte aggregate formation, and mild thrombocytopenia. All were decreased in VAMP-3 −/− and, megakaryocyte/platelet-specific, Arf6 −/− mice. Similar platelet activation profiles (increased platelet-leukocyte aggregates, plasma platelet factor 4, and phospho-IκBα) were detected in newly diagnosed and antiretroviral therapy–controlled HIV-1 + patients. Conclusions: Collectively, our data provide mechanistic insights into the cell biology of how platelets endocytose and process virions. We propose a mechanism by which platelets sample the circulation and respond to potential pathogens that they take up.

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Lee, Grace E., John W. Murray, Allan W. Wolkoff, and Duncan W. Wilson. "Reconstitution of Herpes Simplex Virus Microtubule-Dependent Trafficking In Vitro." Journal of Virology 80, no. 9 (May 1, 2006): 4264–75. http://dx.doi.org/10.1128/jvi.80.9.4264-4275.2006.

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ABSTRACT Microtubule-mediated anterograde transport of herpes simplex virus (HSV) from the neuronal cell body to the axon terminal is crucial for the spread and transmission of the virus. It is therefore of central importance to identify the cellular and viral factors responsible for this trafficking event. In previous studies, we isolated HSV-containing cytoplasmic organelles from infected cells and showed that they represent the first and only destination for HSV capsids after they emerge from the nucleus. In the present study, we tested whether these cytoplasmic compartments were capable of microtubule-dependent traffic. Organelles containing green fluorescent protein-labeled HSV capsids were isolated and found to be able to bind rhodamine-labeled microtubules polymerized in vitro. Following the addition of ATP, the HSV-associated organelles trafficked along the microtubules, as visualized by time lapse microscopy in an imaging microchamber. The velocity and processivity of trafficking resembled those seen for neurotropic herpesvirus traffic in living axons. The use of motor-specific inhibitors indicated that traffic was predominantly kinesin mediated, consistent with the reconstitution of anterograde traffic. Immunocytochemical studies revealed that the majority of HSV-containing organelles attached to the microtubules contained the trans-Golgi network marker TGN46. This simple, minimal reconstitution of microtubule-mediated anterograde traffic should facilitate and complement molecular analysis of HSV egress in vivo.

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Zhang, Wei, and Michael J. Imperiale. "Requirement of the Adenovirus IVa2 Protein for Virus Assembly." Journal of Virology 77, no. 6 (March 15, 2003): 3586–94. http://dx.doi.org/10.1128/jvi.77.6.3586-3594.2003.

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ABSTRACT The adenovirus L1 52/55-kDa protein is required for viral DNA packaging and interacts with the viral IVa2 protein, which binds to the viral packaging sequence. Previous reports suggest that the IVa2 protein plays a role in viral DNA packaging and that this function of the IVa2 protein is serotype specific. To further examine the function of the IVa2 protein in viral DNA packaging, a mutant virus that does not express the IVa2 protein was constructed by introducing two stop codons at the beginning of the IVa2 open reading frame in a full-length bacterial clone of adenovirus type 5. The mutant virus, pm8002, was defective for growth in 293 cells, although it replicated its DNA and produced early and late viral proteins. Electron microscopic and gradient analyses revealed that the mutant virus did not assemble any viral particles in 293 cells. In 293-IVa2 cells, which express the IVa2 protein, infectious viruses were produced, although the titer of the mutant virus was lower than that of the wild-type virus, indicating that these cells may not fully complement the mutation. The mutant viral particles produced in 293-IVa2 cells were heterogeneous in size and shape, less stable, and did not traffic efficiently to the nucleus. Marker rescue experiments with a wild-type IVa2 DNA fragment confirmed that the only mutations present in pm8002 were in the IVa2 gene. The results indicate that the IVa2 protein is required for adenovirus assembly and suggest that virus particles may be assembled around the DNA rather than DNA being packaged into preformed capsids.

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Lehmann-Che, Jacqueline, Marie-Lou Giron, Olivier Delelis, Martin Löchelt, Patricia Bittoun, Joelle Tobaly-Tapiero, Hugues de Thé, and Ali Saïb. "Protease-Dependent Uncoating of a Complex Retrovirus." Journal of Virology 79, no. 14 (July 2005): 9244–53. http://dx.doi.org/10.1128/jvi.79.14.9244-9253.2005.

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ABSTRACT Although retrovirus egress and budding have been partly unraveled, little is known about early stages of the replication cycle. In particular, retroviral uncoating, a process during which incoming retroviral cores are altered to allow the integration of the viral genome into host chromosomes, is poorly understood. To get insights into these early events of the retroviral cycle, we have used foamy complex retroviruses as a model. In this report, we show that a protease-defective foamy retrovirus is noninfectious, although it is still able to bud and enter target cells efficiently. Similarly, a retrovirus mutated in an essential viral protease-dependent cleavage site in the central part of Gag is noninfectious. Following entry, wild-type and mutant retroviruses are able to traffic along microtubules towards the microtubule-organizing center (MTOC). However, whereas nuclear import of Gag and of the viral genome was observed for the wild-type virus as early as 8 hours postinfection, incoming capsids and genome from mutant viruses remained at the MTOC. Interestingly, a specific viral protease-dependent Gag cleavage product was detected only for the wild-type retrovirus early after infection, demonstrating that cleavage of Gag by the viral protease at this stage of the virus life cycle is absolutely required for productive infection, an unprecedented observation among retroviruses.

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Citovsky, Vitaly. "Tobacco mosaic virus: a pioneer to cell–to–cell movement." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1383 (March 29, 1999): 637–43. http://dx.doi.org/10.1098/rstb.1999.0415.

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Cell–to–cell movement of tobacco mosaic virus (TMV) is used to illustrate macromolecular traffic through plant intercellular connections, the plasmodesmata. This transport process is mediated by a specialized viral movement protein, P30. In the initially infected cell, P30 is produced by transcription of a subgenomic RNA derived from the invading virus. Presumably, P30 then associates with a certain proportion of the viral RNA molecules, sequestering them from replication and mediating their transport into neighbouring uninfected host cells. This nucleoprotein complex is targeted to plasmodesmata, possibly via interaction with the host cell cytoskeleton. Prior to passage through a plasmodesma, the plasmodesmal channel is dilated by the movement protein. It is proposed that targeting of P30–TMV RNA complexes to plasmodesmata involves binding to a specific cell wall–associated receptor molecule. In addition, a cell wall–associated protein kinase, phosphorylates P30 at its carboxy–terminus and minimizes P30–induced interference with plasmodesmatal permeability during viral infection.

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Pietiäinen, Vilja, Varpu Marjomäki, Paula Upla, Lucas Pelkmans, Ari Helenius, and Timo Hyypiä. "Echovirus 1 Endocytosis into Caveosomes Requires Lipid Rafts, Dynamin II, and Signaling Events." Molecular Biology of the Cell 15, no. 11 (November 2004): 4911–25. http://dx.doi.org/10.1091/mbc.e04-01-0070.

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Binding of echovirus 1 (EV1, a nonenveloped RNA virus) to the α2β1 integrin on the cell surface is followed by endocytic internalization of the virus together with the receptor. Here, video-enhanced live microscopy revealed the rapid uptake of fluorescently labeled EV1 into mobile, intracellular structures, positive for green fluorescent protein-tagged caveolin-1. Partial colocalization of EV1 with SV40 (SV40) and cholera toxin, known to traffic via caveosomes, demonstrated that the vesicles were caveosomes. The initiation of EV1 infection was dependent on dynamin II, cholesterol, and protein phosphorylation events. Brefeldin A, a drug that prevents SV40 transport, blocked the EV1 infection cycle, whereas drugs that disrupt the cellular cytoskeleton had no effect. In situ hybridization revealed the localization of viral RNA with endocytosed viral capsid proteins in caveosomes before initiation of viral replication. Thus, both the internalization of EV1 to caveosomes and subsequent events differ clearly from caveolar endocytosis of SV40 because EV1 uptake is fast and independent of actin and EV1 is not sorted further to sER from caveosomes. These results shed further light on the cell entry of nonenveloped viral pathogens and illustrate the use of viruses as probes to dissect caveolin-associated endocytic pathways.

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Martinez, Nathaniel W., Xiaoxiao Xue, Reem G. Berro, Geri Kreitzer, and Marilyn D. Resh. "Kinesin KIF4 Regulates Intracellular Trafficking and Stability of the Human Immunodeficiency Virus Type 1 Gag Polyprotein." Journal of Virology 82, no. 20 (August 6, 2008): 9937–50. http://dx.doi.org/10.1128/jvi.00819-08.

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ABSTRACT Retroviral Gag proteins are synthesized as soluble, myristoylated precursors that traffic to the plasma membrane and promote viral particle production. The intracellular transport of human immunodeficiency virus type 1 (HIV-1) Gag to the plasma membrane remains poorly understood, and cellular motor proteins responsible for Gag movement are not known. Here we show that disrupting the function of KIF4, a kinesin family member, slowed temporal progression of Gag through its trafficking intermediates and inhibited virus-like particle production. Knockdown of KIF4 also led to increased Gag degradation, resulting in reduced intracellular Gag protein levels; this phenotype was rescued by reintroduction of KIF4. When KIF4 function was blocked, Gag transiently accumulated in discrete, perinuclear, nonendocytic clusters that colocalized with endogenous KIF4, with Ubc9, an E2 SUMO-1 conjugating enzyme, and with SUMO. These studies identify a novel transit station through which Gag traffics en route to particle assembly and highlight the importance of KIF4 in regulating HIV-1 Gag trafficking and stability.

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Lee, Shu-Chuan, Chih-Hang Wu, and Chao-Wen Wang. "Traffic of a Viral Movement Protein Complex to the Highly Curved Tubules of the Cortical Endoplasmic Reticulum." Traffic 11, no. 7 (March 30, 2010): 912–30. http://dx.doi.org/10.1111/j.1600-0854.2010.01064.x.

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Gruhler, Albrecht, and Klaus Früh. "Control of MHC Class I Traffic from the Endoplasmic Reticulum by Cellular Chaperones and Viral Anti-Chaperones." Traffic 1, no. 4 (April 2000): 306–11. http://dx.doi.org/10.1034/j.1600-0854.2000.010403.x.

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Stewart, Corina M., Alexandra Phan, Yuxia Bo, Nicholas D. LeBlond, Tyler K. T. Smith, Geneviève Laroche, Patrick M. Giguère, et al. "Ebola virus triggers receptor tyrosine kinase-dependent signaling to promote the delivery of viral particles to entry-conducive intracellular compartments." PLOS Pathogens 17, no. 1 (January 29, 2021): e1009275. http://dx.doi.org/10.1371/journal.ppat.1009275.

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Filoviruses, such as the Ebola virus (EBOV) and Marburg virus (MARV), are causative agents of sporadic outbreaks of hemorrhagic fevers in humans. To infect cells, filoviruses are internalized via macropinocytosis and traffic through the endosomal pathway where host cathepsin-dependent cleavage of the viral glycoproteins occurs. Subsequently, the cleaved viral glycoprotein interacts with the late endosome/lysosome resident host protein, Niemann-Pick C1 (NPC1). This interaction is hypothesized to trigger viral and host membrane fusion, which results in the delivery of the viral genome into the cytoplasm and subsequent initiation of replication. Some studies suggest that EBOV viral particles activate signaling cascades and host-trafficking factors to promote their localization with host factors that are essential for entry. However, the mechanism through which these activating signals are initiated remains unknown. By screening a kinase inhibitor library, we found that receptor tyrosine kinase inhibitors potently block EBOV and MARV GP-dependent viral entry. Inhibitors of epidermal growth factor receptor (EGFR), tyrosine protein kinase Met (c-Met), and the insulin receptor (InsR)/insulin like growth factor 1 receptor (IGF1R) blocked filoviral GP-mediated entry and prevented growth of replicative EBOV in Vero cells. Furthermore, inhibitors of c-Met and InsR/IGF1R also blocked viral entry in macrophages, the primary targets of EBOV infection. Interestingly, while the c-Met and InsR/IGF1R inhibitors interfered with EBOV trafficking to NPC1, virus delivery to the receptor was not impaired in the presence of the EGFR inhibitor. Instead, we observed that the NPC1 positive compartments were phenotypically altered and rendered incompetent to permit viral entry. Despite their different mechanisms of action, all three RTK inhibitors tested inhibited virus-induced Akt activation, providing a possible explanation for how EBOV may activate signaling pathways during entry. In sum, these studies strongly suggest that receptor tyrosine kinases initiate signaling cascades essential for efficient post-internalization entry steps.

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Esteves, Eduardo, Nuno Rosa, Maria José Correia, Joel P. Arrais, and Marlene Barros. "New Targets forZikaVirus Determined by Human-Viral Interactomic: A Bioinformatics Approach." BioMed Research International 2017 (2017): 1–15. http://dx.doi.org/10.1155/2017/1734151.

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Identifying ZIKV factors interfering with human host pathways represents a major challenge in understanding ZIKV tropism and pathogenesis. The integration of proteomic, gene expression and Protein-Protein Interactions (PPIs) established between ZIKV and human host proteins predicted by the OralInt algorithm identified 1898 interactions with medium or high score (≥0.7). Targets implicated in vesicular traffic and docking were identified. New receptors involved in endocytosis pathways as ZIKV entry targets, using both clathrin-dependent (17 receptors) and independent (10 receptors) pathways, are described. New targets used by the ZIKV to undermine the host’s antiviral immune response are proposed based on predicted interactions established between the virus and host cell receptors and/or proteins with an effector or signaling role in the immune response such as IFN receptors and TLR. Complement and cytokines are proposed as extracellular potential interacting partners of the secreted form of NS1 ZIKV protein. Altogether, in this article, 18 new human targets for structural and nonstructural ZIKV proteins are proposed. These results are of great relevance for the understanding of viral pathogenesis and consequently the development of preventive (vaccines) and therapeutic targets for ZIKV infection management.

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Hughes, Heather C., and Israel Waismel-Manor. "The Macedonian Fake News Industry and the 2016 US Election." PS: Political Science & Politics 54, no. 1 (August 25, 2020): 19–23. http://dx.doi.org/10.1017/s1049096520000992.

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ABSTRACTDuring the 2016 US presidential election, Americans were exposed to an onslaught of disinformation on social media. Many of the most viral posts originated from Veles, a small town in central Macedonia. During fieldwork in Veles, where we interviewed several residents and disinformation creators, we found that the epicenter of this viral phenomenon was Mirko Ceselkoski, an autodidact social media expert, teacher, and mentor to Veles’ fake news operators. We interviewed Ceselkoski and registered and attended his online course—the same course numerous Veles residents took offline. Our research confirms (1) the pivotal role Ceselkoski had in the creation of this industry; (2) the economic motivation driving the fake news disseminators; and (3) the manner in which the mostly young people in their early twenties with little English fluency were able to generate so much traffic and disseminate so much disinformation.

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Vázquez-Calvo, Ángela, Flavia Caridi, Miguel Rodriguez-Pulido, Belén Borrego, Margarita Sáiz, Francisco Sobrino, and Miguel A. Martín-Acebes. "Modulation of foot-and-mouth disease virus pH threshold for uncoating correlates with differential sensitivity to inhibition of cellular Rab GTPases and decreases infectivity in vivo." Journal of General Virology 93, no. 11 (November 1, 2012): 2382–86. http://dx.doi.org/10.1099/vir.0.045419-0.

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The role of cellular Rab GTPases that govern traffic between different endosome populations was analysed on foot-and-mouth disease virus (FMDV) infection. Changes of viral receptor specificity did not alter Rab5 requirement for infection. However, a correlation between uncoating pH and requirement of Rab5 for infection was observed. A mutant FMDV with less acidic uncoating pH threshold was less sensitive to inhibition of Rab5, whereas another mutant with more acidic requirements was more sensitive to inhibition of Rab5. On the contrary, opposed correlations between uncoating pH and dependence of Rab function were observed upon expression of dominant-negative forms of Rab7 or 11. Modulation of uncoating pH also reduced FMDV virulence in suckling mice. These results are consistent with FMDV uncoating inside early endosomes and indicate that displacements from optimum pH for uncoating reduce viral fitness in vivo.

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Antinone, Sarah Elizabeth, and Gregory Allan Smith. "Retrograde Axon Transport of Herpes Simplex Virus and Pseudorabies Virus: a Live-Cell Comparative Analysis." Journal of Virology 84, no. 3 (November 18, 2009): 1504–12. http://dx.doi.org/10.1128/jvi.02029-09.

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ABSTRACT Upon entry, neuroinvasive herpesviruses traffic from axon terminals to the nuclei of neurons resident in peripheral ganglia, where the viral DNA is deposited. A detailed analysis of herpes simplex virus type 1 (HSV-1) transport dynamics in axons following entry is currently lacking. Here, time lapse fluorescence microscopy was used to compare the postentry viral transport of two neurotropic herpesviruses: HSV-1 and pseudorabies virus (PRV). HSV-1 capsid transport dynamics were indistinguishable from those of PRV and did not differ in neurons of human, mouse, or avian origin. Simultaneous tracking of capsids and tegument proteins demonstrated that the composition of actively transporting HSV-1 is remarkably similar to that of PRV. This quantitative assessment of HSV-1 axon transport following entry demonstrates that HSV-1 and PRV share a conserved mechanism for postentry retrograde transport in axons and provides the foundation for further studies of the retrograde transport process.

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Wendt, Lars Michael, Joachim Griesbaum, and Ralph Kölle. "Product advertising and viral stealth marketing in online videos." Aslib Journal of Information Management 68, no. 3 (May 16, 2016): 250–64. http://dx.doi.org/10.1108/ajim-11-2015-0174.

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Purpose – In the context of social media marketing, so called viral stealth videos (VSVs) often attract as much or even more attention than videos that directly advertise products (product advertising video (PAV)). However, beyond this, the product or brand-related impact of such videos is not so clear. In this context, the purpose of this paper is to investigate brand perception of PAVs and VSVs in YouTube. Design/methodology/approach – The research design is based on an examination of comments of six VSVs and six PAVs on YouTube. Therefore, the content of 1,080 posts was analyzed to capture the topic, the attitude toward the video and the pragmatic intent of posts. Findings – Results indicate that there are strong differences with regard to users ' perception of the two analyzed video type segments. The content of VSVs is clearly recognized as positive more often than the content of PAVs. In contrast, only PAVs evoke substantial brand awareness but receive rather mixed results with regards to brand assessment. Research limitations/implications – As a whole, the study is widely descriptive and of explorative value. Nevertheless, the research design can be estimated as a first step to measure the brand-related impact of online videos. Ideally, the data generated in the investigation should be combined with traffic and conversion data of the brands’ websites to get an encompassing picture of the marketing related impact of the investigated online videos. Practical implications – Seen from a marketers’ perspective, one can recommend PAVs over VSVs as there are hardly any brand-related impacts of VSVs visible in online communication. PAVs are perceived less positively but they are able to evoke brand awareness at least. Originality/value – According to the authors’ knowledge this investigation is one of only a few studies that analyzes real online communication in the context of video-based online marketing.

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Yudkina, Anna V., Anton V. Endutkin, Eugenia A. Diatlova, Nina A. Moor, Ivan P. Vokhtantsev, Inga R. Grin, and Dmitry O. Zharkov. "Displacement of Slow-Turnover DNA Glycosylases by Molecular Traffic on DNA." Genes 11, no. 8 (July 30, 2020): 866. http://dx.doi.org/10.3390/genes11080866.

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In the base excision repair pathway, the initiating enzymes, DNA glycosylases, remove damaged bases and form long-living complexes with the abasic DNA product, but can be displaced by AP endonucleases. However, many nuclear proteins can move along DNA, either actively (such as DNA or RNA polymerases) or by passive one-dimensional diffusion. In most cases, it is not clear whether this movement is disturbed by other bound proteins or how collisions with moving proteins affect the bound proteins, including DNA glycosylases. We have used a two-substrate system to study the displacement of human OGG1 and NEIL1 DNA glycosylases by DNA polymerases in both elongation and diffusion mode and by D4, a passively diffusing subunit of a viral DNA polymerase. The OGG1–DNA product complex was disrupted by DNA polymerase β (POLβ) in both elongation and diffusion mode, Klenow fragment (KF) in the elongation mode and by D4. NEIL1, which has a shorter half-life on DNA, was displaced more efficiently. Hence, both possibly specific interactions with POLβ and nonspecific collisions (KF, D4) can displace DNA glycosylases from DNA. The protein movement along DNA was blocked by very tightly bound Cas9 RNA-targeted nuclease, providing an upper limit on the efficiency of obstacle clearance.

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Weiler, Andrea M., Qingsheng Li, Lijie Duan, Masahiko Kaizu, Kim L. Weisgrau, Thomas C. Friedrich, Matthew R. Reynolds, Ashley T. Haase, and Eva G. Rakasz. "Genital Ulcers Facilitate Rapid Viral Entry and Dissemination following Intravaginal Inoculation with Cell-Associated Simian Immunodeficiency Virus SIVmac239." Journal of Virology 82, no. 8 (February 13, 2008): 4154–58. http://dx.doi.org/10.1128/jvi.01947-07.

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ABSTRACT Here we report the results of studies in the simian immunodeficiency virus (SIV)-rhesus macaque model of intravaginal transmission of human immunodeficiency virus type 1 in the setting of genital ulcerative diseases. We document preferential association of vRNA with induced ulcers during the first days of infection and show that allogeneic cells of the inoculum traffic from the vaginal lumen to lymphatic tissues. This surprisingly rapid systemic dissemination in this cell-associated SIV challenge model thus reveals the challenges of preventing transmission in the setting of genital ulcerative diseases and illustrates the utility of this animal model in tests of strategies aimed at reducing transmission under these conditions.

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Hirsch, Alec J., Guruprasad R. Medigeshi, Heather L. Meyers, Victor DeFilippis, Klaus Früh, Thomas Briese, W. Ian Lipkin, and Jay A. Nelson. "The Src Family Kinase c-Yes Is Required for Maturation of West Nile Virus Particles." Journal of Virology 79, no. 18 (September 15, 2005): 11943–51. http://dx.doi.org/10.1128/jvi.79.18.11943-11951.2005.

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ABSTRACT The role of cellular genes in West Nile virus (WNV) replication is not well understood. Examination of cellular transcripts upregulated during WNV infection revealed an increase in the expression of the src family kinase (SFK) c-Yes. WNV-infected cell lines treated with the SFK inhibitor PP2 demonstrated a 2- to 4-log decrease in viral titers, suggesting that SFK activity is required for completion of the viral replication cycle. RNA interference mediated knock-down of c-Yes, but not c-Src, and similarly reduced virus yield, specifically implicating c-Yes in WNV production. Interestingly, PP2 treatment did not reduce intracellular levels of either viral RNA or protein, suggesting that the drug does not act on the early stages of replication. However, endoglycosidase H (endoH) digestion of the viral envelope (E) glycoprotein revealed that the acquisition of endoH-resistant glycans by E, but not endogenous major histocompatibility complex class I, was reduced in PP2-treated cells, demonstrating that E specifically does not traffic beyond the endoplasmic reticulum in the absence of SFK activity. Electron microscopy further revealed that PP2-treated WNV-infected cells accumulated an increased number of virions in the ER compared to untreated cells. Therefore, we conclude that inhibition of SFK activity did not interfere with virus assembly but prevented transit of virions through the secretory pathway. These results identify c-Yes as a cellular protein that is involved in WNV assembly and egress.

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Breiner, Klaus M., and Heinz Schaller. "Cellular Receptor Traffic Is Essential for Productive Duck Hepatitis B Virus Infection." Journal of Virology 74, no. 5 (March 1, 2000): 2203–9. http://dx.doi.org/10.1128/jvi.74.5.2203-2209.2000.

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ABSTRACT We have investigated the mechanism of duck hepatitis B virus (DHBV) entry into susceptible primary duck hepatocytes (PDHs), using mutants of carboxypeptidase D (gp180), a transmembrane protein shown to act as the primary cellular receptor for avian hepatitis B virus uptake. The variant proteins were abundantly produced from recombinant adenoviruses and tested for the potential to functionally outcompete the endogenous wild-type receptor. Overexpression of wild-type gp180 significantly enhanced the efficiency of DHBV infection in PDHs but did not affect ongoing DHBV replication, an observation further supporting gp180 receptor function. A gp180 mutant deficient for endocytosis abolished DHBV infection, indicating endocytosis to be the route of hepadnaviral entry. With further gp180 variants, carrying mutations in the cytoplasmic domain and characterized by an accelerated turnover, the ability of gp180 to function as a DHBV receptor was found to depend on a wild-type-like sorting phenotype which largely avoids transport toward the endolysosomal compartment. Based on these data, we propose a model in which a distinct intracellular DHBV traffic to the endosome, but not beyond, is a prerequisite for completion of viral entry, i.e., for fusion and capsid release. Furthermore, the deletion of the two enzymatically active carboxypeptidase domains of gp180 did not lead to a loss of receptor function.

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Mayberry, Colleen L., and Melissa S. Maginnis. "Taking the Scenic Route: Polyomaviruses Utilize Multiple Pathways to Reach the Same Destination." Viruses 12, no. 10 (October 15, 2020): 1168. http://dx.doi.org/10.3390/v12101168.

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Members of the Polyomaviridae family differ in their host range, pathogenesis, and disease severity. To date, some of the most studied polyomaviruses include human JC, BK, and Merkel cell polyomavirus and non-human subspecies murine and simian virus 40 (SV40) polyomavirus. Although dichotomies in host range and pathogenesis exist, overlapping features of the infectious cycle illuminate the similarities within this virus family. Of particular interest to human health, JC, BK, and Merkel cell polyomavirus have all been linked to critical, often fatal, illnesses, emphasizing the importance of understanding the underlying viral infections that result in the onset of these diseases. As there are significant overlaps in the capacity of polyomaviruses to cause disease in their respective hosts, recent advancements in characterizing the infectious life cycle of non-human murine and SV40 polyomaviruses are key to understanding diseases caused by their human counterparts. This review focuses on the molecular mechanisms by which different polyomaviruses hijack cellular processes to attach to host cells, internalize, traffic within the cytoplasm, and disassemble within the endoplasmic reticulum (ER), prior to delivery to the nucleus for viral replication. Unraveling the fundamental processes that facilitate polyomavirus infection provides deeper insight into the conserved mechanisms of the infectious process shared within this virus family, while also highlighting critical unique viral features.

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Chen, Ping, Hui Chen, Maha Moussa, Jie Cheng, Tong Li, Jing Qin, Jeffrey D. Lifson, et al. "Recombinant Human Interleukin-15 and Anti-PD-L1 Combination Therapy Expands a CXCR3+PD1−/low CD8 T-Cell Subset in Simian Immunodeficiency Virus-Infected Rhesus Macaques." Journal of Infectious Diseases 221, no. 4 (September 28, 2019): 523–33. http://dx.doi.org/10.1093/infdis/jiz485.

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Abstract Background The PD1/PD-L1 pathway contributes to the pathogenesis of human immunodeficiency virus (HIV)/simian immunodeficiency virus (SIV) infection, and blockade of this pathway may have potential to restore immune function and promote viral control or elimination. In this study, we combined a checkpoint inhibitor anti-PD-L1 (Avelumab) and recombinant human interleukin-15 (rhIL-15) in SIV-infected rhesus macaques (RM). Methods The rhIL-15 was administered as continuous infusion in 2 cycles of 10 days in the context of weekly administration of anti-PD-L1 (Avelumab) in SIV-infected RM receiving combination antiretroviral therapy (cART). Safety, immunological parameters, and viral loads were monitored during the study. Results Administration of rhIL-15/anti-PD-L1 was safe and well tolerated. Treatment resulted in transient increases in proliferating (Ki67+) natural killer and CD8 T cells. In addition, treatment expanded a CXCR3+PD1−/low CD8 T-cell subset with the ability to secrete cytokines. Despite these effects, no changes in plasma viremia were observed after cART interruption. Conclusions Expansion of the CXCR3+PD1−/low CD8 T-cell subset with functional capacity and potential to traffic to sites of viral reservoirs in SIV-infected rhesus macaques had no demonstrable effect on plasma viremia after cART interruption.

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Yang, Jr-Ming, and Stephen J. Gould. "The cis-acting signals that target proteins to exosomes and microvesicles." Biochemical Society Transactions 41, no. 1 (January 29, 2013): 277–82. http://dx.doi.org/10.1042/bst20120275.

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Proteins bud from cells in small single-membraned vesicles (~50–250 nm) that have the same topology as the cell. Known variously as exosomes and microvesicles (EMVs), these extracellular organelles are enriched for specific proteins, lipids, carbohydrates and nucleic acids. EMV biogenesis plays critical roles in protein quality control and cell polarity, and, once released, EMVs can transmit signals and molecules to neighbouring cells via a non-viral pathway of intercellular vesicle traffic. In the present paper, we discuss the cis-acting targeting signals that target proteins to EMVs and mediate protein budding from the cell.

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Zins, S. R., C. D. S. Nelson, M. S. Maginnis, R. Banerjee, B. A. O'Hara, and W. J. Atwood. "The Human Alpha Defensin HD5 Neutralizes JC Polyomavirus Infection by Reducing Endoplasmic Reticulum Traffic and Stabilizing the Viral Capsid." Journal of Virology 88, no. 2 (November 6, 2013): 948–60. http://dx.doi.org/10.1128/jvi.02766-13.

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Carrington, Christine V. F., Jerome E. Foster, Oliver G. Pybus, Shannon N. Bennett, and Edward C. Holmes. "Invasion and Maintenance of Dengue Virus Type 2 and Type 4 in the Americas." Journal of Virology 79, no. 23 (December 15, 2005): 14680–87. http://dx.doi.org/10.1128/jvi.79.23.14680-14687.2005.

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ABSTRACT Dengue virus type 4 (DENV-4) was first reported in the Americas in 1981, where it caused epidemics of dengue fever throughout the region. In the same year, the region's first epidemic of dengue hemorrhagic fever was reported, caused by an Asian strain of dengue virus type 2 (DENV-2) that was distinct from the American subtype circulating previously. Despite the importance of these epidemics, little is known about the rates or determinants of viral spread among island and mainland populations or their directions of movement. We employed a Bayesian coalescent approach to investigate the transmission histories of DENV-2 and DENV-4 since their introduction in 1981 and a parsimony method to assess patterns of strain migration. For both viruses there was an initial invasion phase characterized by an exponential increase in the number of DENV lineages, after which levels of genetic diversity remained constant despite reported fluctuations in DENV-2 and DENV-4 activity. Strikingly, viral lineage numbers increased far more rapidly for DENV-4 than DENV-2, indicative of a more rapid rate of exponential population growth in DENV-4 or a higher rate of geographic dispersal, allowing this virus to move more effectively among localities. We propose that these contrasting dynamics may reflect underlying differences in patterns of host immunity. Despite continued gene flow along particular transmission routes, the overall extent of viral traffic was less than expected under panmixis. Hence, DENV in the Americas has a clear geographic structure that maintains viral diversity between outbreaks.

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Leblanc, P., S. Desset, F. Giorgi, A. R. Taddei, A. M. Fausto, M. Mazzini, B. Dastugue, and C. Vaury. "Life Cycle of an Endogenous Retrovirus,ZAM, in Drosophila melanogaster." Journal of Virology 74, no. 22 (November 15, 2000): 10658–69. http://dx.doi.org/10.1128/jvi.74.22.10658-10669.2000.

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ABSTRACT ZAM is an env-containing member of thegypsy family of retrotransposons that represents a possible retrovirus of invertebrates. In this paper, we tracedZAM mobilization to get information about a potential path a retroelement may take to reach the germ line of its host. In situ hybridization on whole-mount tissues and immunocytochemistry analyses with antibodies raised againstZAM Gag and Env proteins have shown that all components necessary to assemble ZAM viral particles, i.e., ZAM full-length RNAs and Gag and Env polypeptides, are coexpressed in a small set of follicle cells surrounding the oocyte. By electron microscopy, we have shown thatZAM viral particles are indeed detected in this somatic lineage of cells, which they leave and enter the closely apposed oocyte. Our data provide evidence that the vesicular traffic and yolk granules in the process of vitellogenesis play an important role in ZAM transfer to the oocyte. Our data support the possibility that vitellogenin transfer to the oocyte may help a retroelement pass to the germ line with no need of its envelope product.

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Peterson, C. W., J. Wang, P. Polacino, S. L. Hu, M. C. Holmes, and H. P. Kiem. "OA3-2 CCR5 gene edited cells traffic to viral reservoir tissues and undergo SHIV-dependent positive selection in nonhuman primates." Journal of Virus Eradication 2 (July 2016): 4. http://dx.doi.org/10.1016/s2055-6640(20)31014-1.

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Journal articles on the topic 'Viral traffic'

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