Abstract
Mitochondrial movement and distribution throughout the cytoplasm is crucial for maintaining cell homeostasis. Mitochondria are dynamic organelles but can be functionally disrupted during infection. Here, we show that the ubiquitous human pathogens HHV-1 and HHV-2 induce changes in the mitochondrial morphology and distribution in the early and late phases of productive infection in human keratinocytes (HaCaT cells). We observed a decrease in the mitochondrial potential at 2 h postinfection and a decrease in cell vitality at 24 h postinfection. Moreover, we found that mitochondria migrated to the perinuclear area, where HHV-1 and HHV-2 antigens were also observed, mainly in the early stages of infection. Positive results of real-time PCR showed a high level of HHV-1 and HHV-2 DNA in HaCaT cells and culture medium. Our data demonstrate that HHV-1 and HHV-2 cause mitochondrial dysfunction in human keratinocytes.
Highlights
Human herpesviruses types 1 and 2 (HHV-1 and HHV-2) belong to the subfamily Alphaherpesvirinae of the family Herpesviridae
HHV-1 and HHV-2 use mucosal epithelial cells, including epidermal keratinocytes, as the primary portal of entry, and infection spreads through the epithelium
After episodic reactivation from latency established in neurons, newly replicating viruses infect epithelial cells, often leading to recurrent herpetic lesions
Summary
Human herpesviruses types 1 and 2 (HHV-1 and HHV-2) belong to the subfamily Alphaherpesvirinae of the family Herpesviridae. There are two main processes responsible for mitochondrial homeostasis: fission and fusion. These are crucial for maintenance of a proper number of functional mitochondria. The most important protein participating in the defragmentation of the mitochondrial network in the cell is dynamin-related protein 1 (Drp1), which has GTPase activity. Murata et al [10] have shown that, in Vero cells, mitochondria are recruited to the site of viral replication and morphogenesis. Little is known about the role of mitochondria in skin cells, which function as the primary barrier and, on the other hand, constitute a very important replication site. In the present study we investigated the effect of HHV-1 and HHV-2 infection on cell vitality, apoptosis, mitochondrial network rearrangement, and mitochondrial potential in human keratinocytes in vitro
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