sci-bot hijack of cells for virus replication

Steven Avery

Administrator
2020 · DOI: 10.1080/21505594.2020.1726594
The roles of nucleic acid editing in adaptation of zoonotic viruses to humans
2023 · DOI: 10.1016/j.coviro.2023.101326
Searching for "virus hijack host cell cycle transcription translation machinery replication"
Viperin triggers ribosome collision-dependent translation inhibition to restrict viral replication
2022 · DOI: 10.1016/j.molcel.2022.02.031
Hijacking the translation apparatus by RNA viruses
As invading viruses do not harbor functional ribosomes in their virions, successful amplification of the viral genomes requires that viral mRNAs compete with cellular mRNAs for the host cell translation apparatus. Several RNA viruses have evolved remarkable strategies to recruit the host translation...
2002 · DOI: 10.1083/jcb.200205044
The roles of nucleic acid editing in adaptation of zoonotic viruses to humans
2023 · DOI: 10.1016/j.coviro.2023.101326
Searching for "viruses hijack host cell nucleus replication transcription DNA viruses"
Searching for "virus manipulation host cell cytoskeleton hijacking transport pathways"
Virus DNA Replication and the Host DNA Damage Response
Viral DNA genomes have limited coding capacity and therefore harness cellular factors to facilitate replication of their genomes and generate progeny virions. Studies of viruses and how they interact with cellular processes have historically provided seminal insights into basic biology and disease m...
2018 · DOI: 10.1146/annurev-virology-092917-043534
How SARS-CoV-2 and Other Viruses Build an Invasion Route to Hijack the Host Nucleocytoplasmic Trafficking System
The host nucleocytoplasmic trafficking system is often hijacked by viruses to accomplish their replication and to suppress the host immune response. Viruses encode many factors that interact with the host nuclear transport receptors (NTRs) and the nucleoporins of the nuclear pore complex (NPC) to ac...
2021 · DOI: 10.3390/cells10061424
Rerouting the traffic from a virus perspective
Viruses are important human and animal pathogens causing disease that affect global health and the economy. One outcome of many virus infections is the regulation of cellular trafficking machinery. Viral proteins recruit and interact with cellular trafficking proteins to divert the normal traffickin...
2017 · DOI: 10.2741/4575
Searching for "virus hijack host autophagy apoptosis cell death pathways replication"
Searching for "virus hijack host lipid metabolism replication membrane remodeling"
Virus Impact on Lipids and Membranes
Viruses manipulate cellular lipids and membranes at each stage of their life cycle. This includes lipid-receptor interactions, the fusion of viral envelopes with cellular membranes during endocytosis, the reorganization of cellular membranes to form replication compartments, and the envelopment and ...
2019 · DOI: 10.1146/annurev-virology-092818-015748
Autophagy in Viral Replication and Pathogenesis
Autophagy is a catabolic process that is important for the removal of damaged organelles and long-lived proteins for the maintenance of cellular homeostasis. It can also serve as innate immunity to remove intracellular microbial pathogens. A growing list of viruses has been shown to affect this cell...
2010 · DOI: 10.1007/s10059-010-0014-2
Lipids and RNA virus replication
Most viruses rely heavily on their host machinery to successfully replicate their genome and produce new virus particles. Recently, the interaction of positive-strand RNA viruses with the lipid biosynthetic and transport machinery has been the subject of intense investigation. In this review, we wil...
2014 · DOI: 10.1016/j.coviro.2014.09.005
Searching for "virus hijack immune evasion host interferon response scientific paper"
Searching for ""viruses hijack" OR "viral hijacking" host cell machinery review"
Viral hijacking of cellular metabolism
This review discusses the current state of the viral metabolism field and gaps in knowledge that will be important for future studies to investigate. We discuss metabolic rewiring caused by viruses, the influence of oncogenic viruses on host cell metabolism, and the use of viruses as guides to ident...
2019 · DOI: 10.1186/s12915-019-0678-9
Viral Subversion of the Immune System
This review describes the diverse array of pathways and molecular targets that are used by viruses to elude immune detection and destruction. These include targeting of pathways for major histocompatibility complex-restricted antigen presentation, apoptosis, cytokine-mediated signaling, and humoral ...
2000 · DOI: 10.1146/annurev.immunol.18.1.861
Now I have a substantial body of evidence. Let me also get some more articles focusing on specific viruses and their hijacking mechanisms.
Searching for "HIV hijack host cell CD4 T cell replication mechanisms"
Searching for "influenza virus hijack host nuclear machinery replication"
Influenza A replication and host nuclear compartments: Many changes and many questions
It is over 40 years since investigations showed that influenza A, one of the rare nuclear replicating RNA viruses, induces marked remodeling of the host nuclear architecture. Influenza modifies and/or hijacks host nuclear machinery in order to replicate, express viral proteins and interfere with hos...
2008 · DOI: 10.1016/j.jcv.2008.08.017
Nuclear import of the influenza A virus transcriptional machinery
Unusually for an RNA virus, influenza A viruses transcribe and replicate their genomes in the nuclei of infected cells. As a result the viral ribonucleoprotein complexes (RNPs), and their newly synthesised protein subunits, must interact with the host nuclear import machinery. In this review we disc...
2012 · DOI: 10.1016/j.vaccine.2012.04.085
Formatting citations in IEEE ... 10.1080/21505594.2020.1726594, 10.1083/jcb.200205044, 10.1016/j.molcel.2022.02.031, 10.1146/annurev-virology-092917-043534, 10.3390/cells10061424, 10.2741/4575, 10.1146/annurev-virology-092818-015748, 10.1007/s10059-010-0014-2, 10.1016/j.coviro.2014.09.005, 10.1186/s12915-019-0678-9, 10.1146/annurev.immunol.18.1.861, 10.1016/j.jcv.2008.08.017, 10.1016/j.vaccine.2012.04.085
Formatting citations in IEEE ... 10.1146/annurev.immunol.18.1.861, 10.1016/j.jcv.2008.08.017, 10.1016/j.vaccine.2012.04.085, 10.1080/21505594.2020.1726594, 10.3390/cells10061424, 10.1186/s12915-019-0678-9
Formatting citations in IEEE ... 10.3390/cells10061424
How SARS-CoV-2 and Other Viruses Build an Invasion Route to Hijack the Host Nucleocytoplasmic Trafficking System
The host nucleocytoplasmic trafficking system is often hijacked by viruses to accomplish their replication and to suppress the host immune response. Viruses encode many factors that interact with the host nuclear transport receptors (NTRs) and the nucleoporins of the nuclear pore complex (NPC) to ac...
2021 · DOI: 10.3390/cells10061424
Formatting citations in IEEE ... 10.3390/cells10061424
 

Steven Avery

Administrator
The citation tool seems to have an issue with the Cells journal format. Let me proceed with my comprehensive answer.

Yes, there is extensive scientific literature that has demonstrated and provided evidence that human viruses hijack host cell functions for replication. This concept is one of the fundamental tenets of virology, and numerous peer-reviewed papers have systematically described the molecular mechanisms by which viruses usurp cellular machinery. Below is a detailed synthesis of the evidence.

Scientific Evidence That Human Viruses Hijack Cell Functions for Replication
The notion that viruses are obligate intracellular parasites that must exploit host cellular machinery to replicate is well-established in the scientific literature. Since viruses lack their own ribosomes, energy-producing systems, and many biosynthetic enzymes, they must commandeer host cell processes to produce viral proteins, replicate their genomes, assemble new virions, and spread. A large body of research, spanning decades, has systematically identified and characterized the multiple cellular pathways that viruses hijack.

1. Hijacking of Host Translation Machinery
Since viruses do not possess functional ribosomes, they must compete with cellular mRNAs for the host cell's translation apparatus. Bushell and Sarnow [1] demonstrated that several families of RNA viruses have evolved strategies to recruit the host translation initiation factors, particularly the cap-binding complex eIF4F, effectively usurping limiting initiation factors from the host. Their review showed that viruses like poliovirus and hepatitis C virus use internal ribosome entry sites (IRESs) to bypass the need for certain host initiation factors, thereby hijacking the translation machinery.

More recently, Hsu et al. [2] provided evidence that the host antiviral protein viperin restricts viral replication by synthesizing ddhCTP, a nucleoside derivative that induces ribosome collisions, leading to translation inhibition. This work illuminates the host-virus arms race at the level of translation control.

2. Hijacking of Host Nuclear Transport Machinery
Many viruses, including influenza A virus, HIV, SARS-CoV-2, and human papillomavirus, must access the host nucleus to replicate. Sajidah et al. [3] reviewed how viruses hijack the host nucleocytoplasmic trafficking system by encoding factors that interact with nuclear transport receptors (NTRs) and nucleoporins of the nuclear pore complex (NPC) to access the nucleus.

Specifically, Hutchinson and Fodor [4] described how influenza A virus—unusually for an RNA virus—transcribes and replicates its genome in the nucleus. The virus exploits host nuclear import pathways to allow regulated assembly of viral ribonucleoprotein complexes (RNPs) in the nucleus, with the import machinery itself acting as a determinant of host tropism. Josset et al. [5] further showed that influenza A virus induces marked remodeling of host nuclear architecture, modifying and hijacking host nuclear machinery to replicate and express viral proteins.
 

Steven Avery

Administrator
3. Hijacking of Host DNA Damage and Repair Pathways
DNA viruses with limited coding capacity must harness cellular factors to replicate their genomes. Weitzman and Fradet-Turcotte [6] provided comprehensive evidence that the replicative life cycles of many DNA viruses (e.g., adenoviruses, herpesviruses, papillomaviruses) engage components of the host DNA damage and repair machinery. These viruses have evolved numerous strategies to navigate the cellular DNA damage response, selectively harnessing or abrogating distinct components to facilitate their own genome replication.

4. Hijacking of Host Lipid Metabolism and Membranes
Viruses manipulate cellular lipids and membranes at every stage of their life cycle. Ketter and Randall [7] reviewed how viruses manipulate lipid signaling and metabolism to benefit their replication, including lipid-receptor interactions, membrane fusion during entry, reorganization of cellular membranes to form replication compartments, and viral envelopment and egress. Konan and Sanchez-Felipe [8] specifically showed that positive-strand RNA viruses (e.g., Flaviviridae, Picornaviridae) employ multifaceted strategies to hijack host machinery involved in lipid biosynthesis and transport, as they rely heavily on cytosolic membranes for efficient genome replication.

5. Hijacking of Host Autophagy Pathways
Autophagy—a catabolic process that can serve as innate immunity to remove intracellular pathogens—is also exploited by viruses. Sir and Ou [9] demonstrated that a growing list of viruses affect this cellular pathway. Some viruses suppress autophagy for their survival, while others enhance or exploit it to benefit their replication.

6. Hijacking of Host Metabolism
Thaker et al. [10] reviewed how viral infection triggers metabolic reprogramming in host cells to facilitate optimal virus production. They showed that viruses promote anabolism for generation of macromolecules needed for virion replication and assembly, with metabolic phenotypes often mirroring changes seen in cancer cells (e.g., the Warburg effect—increased glycolytic metabolism).

7. Hijacking of Host Immune Pathways
Tortorella et al. [11] documented the diverse array of pathways and molecular targets used by viruses to elude immune detection and destruction. These include targeting pathways for MHC-restricted antigen presentation, apoptosis, cytokine-mediated signaling, and humoral immune responses.

8. Hijacking of Host Cellular Trafficking Machinery
Cruz and Buchkovich [12] showed that viral proteins recruit and interact with cellular trafficking proteins to divert the normal trafficking of key proteins or induce the formation of novel membrane structures. These alterations increase replication efficiency by mislocalizing immune regulators or restriction factors and by creating platforms for replication and assembly.
 

Steven Avery

Administrator
9. Systemic Framework: Orchestrated Network Hijacking
Dai et al. [13] synthesized the evidence into a comprehensive framework, identifying five key cellular processes that viruses hijack to guide replication: autophagy, programmed cell death (apoptosis), immune response, cell cycle alteration, and lipid metabolic reprogramming. Their review systematically described how viruses orchestrate these hijacking efforts across host networks.
 

Steven Avery

Administrator
Conclusion
There is overwhelming scientific evidence—from numerous peer-reviewed papers spanning multiple decades—that human viruses hijack host cell functions for replication. The concept has been demonstrated at the molecular level across diverse viral families, cellular pathways, and experimental systems. This body of work represents a cornerstone of modern virology and has informed the development of antiviral therapies that target virus-host interactions.
 

Steven Avery

Administrator
References
[1]M. Bushell and P. Sarnow, "Hijacking the translation apparatus by RNA viruses," The Journal of Cell Biology, vol. 158, no. 3, pp. 395–399, Aug. 2002
DOI: 10.1083/jcb.200205044
[2]J. C.-C. Hsu et al., "Viperin triggers ribosome collision-dependent translation inhibition to restrict viral replication," Molecular Cell, vol. 82, no. 9, pp. 1631-1642.e6, May 2022
DOI: 10.1016/j.molcel.2022.02.031
[3]E. S. Sajidah, K. Lim, and R. W. Wong, "How SARS-CoV-2 and Other Viruses Build an Invasion Route to Hijack the Host Nucleocytoplasmic Trafficking System," Cells, vol. 10, no. 6, p. 1424, Jun. 2021
DOI: 10.3390/cells10061424
[4]E. C. Hutchinson and E. Fodor, "Nuclear import of the influenza A virus transcriptional machinery," Vaccine, vol. 30, no. 51, pp. 7353–7358, Dec. 2012
DOI: 10.1016/j.vaccine.2012.04.085
[5]L. Josset, E. Frobert, and M. Rosa-Calatrava, "Influenza A replication and host nuclear compartments: Many changes and many questions," Journal of Clinical Virology, vol. 43, no. 4, pp. 381–390, Dec. 2008
DOI: 10.1016/j.jcv.2008.08.017
[6]M. D. Weitzman and A. Fradet-Turcotte, "Virus DNA Replication and the Host DNA Damage Response," Annual Review of Virology, vol. 5, no. 1, pp. 141–164, Sep. 2018
DOI: 10.1146/annurev-virology-092917-043534
[7]E. Ketter and G. Randall, "Virus Impact on Lipids and Membranes," Annual Review of Virology, vol. 6, no. 1, pp. 319–340, Sep. 2019
DOI: 10.1146/annurev-virology-092818-015748
[8]K. V. Konan and L. Sanchez-Felipe, "Lipids and RNA virus replication," Current Opinion in Virology, vol. 9, pp. 45–52, Dec. 2014
DOI: 10.1016/j.coviro.2014.09.005
[9]D. Sir and J. James Ou, "Autophagy in Viral Replication and Pathogenesis," Molecules and Cells, vol. 29, no. 1, pp. 1–8, Jan. 2010
DOI: 10.1007/s10059-010-0014-2
[10]S. K. Thaker, J. Ch'ng, and H. R. Christofk, "Viral hijacking of cellular metabolism," BMC Biology, vol. 17, no. 1, Jul. 2019
DOI: 10.1186/s12915-019-0678-9
[11]D. Tortorella, B. E. Gewurz, M. H. Furman, D. J. Schust, and H. L. Ploegh, "Viral Subversion of the Immune System," Annual Review of Immunology, vol. 18, no. 1, pp. 861–926, Apr. 2000
DOI: 10.1146/annurev.immunol.18.1.861
[12]L. Cruz and N. J. Buchkovich, "Rerouting the traffic from a virus perspective," Frontiers in Bioscience, vol. 22, no. 11, pp. 1845–1866, 2017
DOI: 10.2741/4575
[13]X. Dai, O. Hakizimana, X. Zhang, A. C. Kaushik, and J. Zhang, "Orchestrated efforts on host network hijacking: Processes governing virus replication," Virulence, vol. 11, no. 1, pp. 183–198, Feb. 2020
DOI: 10.1080/21505594.2020.1726594
 
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