Abstract
Recent discoveries on virus-driven hijacking and compartmentalization of the cellular glycolytic and fermentation pathways to support robust virus replication put the spotlight on the energy requirement of viral processes. The active recruitment of glycolytic enzymes in combination with fermentation enzymes by the viral replication proteins emphasizes the advantages of producing ATP locally within viral replication structures. This leads to a paradigm shift in our understanding of how viruses take over host metabolism to support the virus’s energy needs during the replication process. This review highlights our current understanding of how a small plant virus, Tomato bushy stunt virus, exploits a conserved energy-generating cellular pathway during viral replication. The emerging picture is that viruses not only rewire cellular metabolic pathways to obtain the necessary resources from the infected cells but the fast replicating viruses might have to actively hijack and compartmentalize the energy-producing enzymes to provide a readily available source of ATP for viral replication process.
Highlights
In spite of their small genomes, positive-strand (+)RNA viruses are among the most successful and wide-spread pathogens of humans, animals, and plants
The metabolic process that converts glucose to ethanol in yeast and plants and lactic acid in animals even in the presence of oxygen is known as aerobic glycolysis or Warburg effect
We propose that aerobic glycolysis might be less exposed to feedback regulation when sequestered into the viral replication compartments or replication organelles (VROs) than when present in the cytosol
Summary
In spite of their small genomes, positive-strand (+)RNA viruses are among the most successful and wide-spread pathogens of humans, animals, and plants. The abundant plant-infecting (+)RNA viruses only have a limited coding capacity of 4-to-12 genes. These viruses heavily depend on co-opted cellular factors and rewire several cellular pathways to support their replication in infected hosts [1,2,3,4]. Plant viruses use viral-coded proteins together with co-opted host factors to build viral replication compartments or replication organelles (VROs) inside the infected cells. Numerous interactions among viral components and host cellular proteins and lipids are needed that lead to their retargeting and sequestration within the VROs. Altogether, during successful infections, virus–host interactions create a subcellular environment suitable for virus replication [4,5,6,7,8]. TBSV is highly suitable for studies on virus–host interactions considering a large number of protein–protein interactions and network of interactions identified between TBSV and the host cell, based on budding yeast (Saccharomyces cerevisiae) [6,9,10,11]
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