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Corcoran et al., Interestingly, although induction of mitochondria biogenesis has been reported in HSV-1-infected neurons at 18 hpi, as determined by an increase in molecular markers, such as PGC1 and TFAM (Martin et al., 2014b), mitochondria function was impaired upon HSV-1 infection in neuronal cells, in which the motility and morphology of mitochondria were severely affected through a mechanism that involved increased intracellular Ca 2+ and reduced recruitment of kinesin-1, a protein necessary for mitochondria transport along microtubules (Kramer and Enquist, 2012)

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This limits the entry of pathogens and toxins but also impairs critical communication and transport processes (like hormone signaling and nutrient uptake)