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Abstract
Kaposi sarcoma–associated herpesvirus (KSHV) can establish latent infection in host cells. The latently infected cells can survive and proliferate with a few viral genes expressed. However, in some Kaposi sarcoma cells, KSHV undergoes a productive life cycle and causes cell lysis. A new study (see the related article beginning on page 124) demonstrates that, after KSHV infection or introduction of viral plasmids into host cells, viral DNA is rapidly lost. Lytic virus production with ensuing infections could balance the loss of the viral plasmids to maintain the virus in cancer cells.
Authors
Chen-Yu Wang, Bill Sugden
Figure 1
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A model to explain one potential role for productive infections by KSHV in KS lesions. (I) KSHV (shown as an enveloped iscosahedral core) can infect cuboidal endothelial cells and (II) induce a spindle-shaped morphology in these cells. These infected spindle-shaped cells can proliferate, lose KSHV rapidly, and (III) revert to uninfected, cuboidal cells. (IV) The spindle-shaped cells also can support production of KSHV. (V) The released KSHV can infect more cells, inducing the change to the spindle shape and maintenance of the infected lesion.
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Copyright © 2019 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)
Copyright © 2019 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)