Previous studies have established that chlorella viruses encode K؉ channels with different structural and functional properties. In the current study, we exploit the different sensitivities of these channels to Cs ؉ to determine if the membrane depolarization observed during virus infection is caused by the activities of these channels. Infection of Chlorella NC64A with four viruses caused rapid membrane depolarization of similar amplitudes, but with different kinetics. Depolarization was fastest after infection with virus SC-1A (half time [t 1/2 ], about 9 min) and slowest with virus NY-2A (t 1/2 , about 12 min). Cs ؉ inhibited membrane depolarization only in viruses that encode a Cs ؉ -sensitive K ؉ channel. Collectively, the results indicate that membrane depolarization is an early event in chlorella virus-host interactions and that it is correlated with viral-channel activity. This suggestion was supported by investigations of thin sections of Chlorella cells, which show that channel blockers inhibit virus DNA release into the host cell. Together, the data indicate that the channel is probably packaged in the virion, presumably in its internal membrane. We hypothesize that fusion of the virus internal membrane with the host plasma membrane results in an increase in K ؉ conductance and membrane depolarization; this depolarization lowers the energy barrier for DNA release into the host.

Because the distinct heterochromatic structure of rods focuses transmitting light to enable vision at low photon levels, the inability to phosphorylate KAP1 and the failure to relax heterochromatin could serve to maintain this structure and the functionality of rods in the presence of DSBs. Collectively, our findings show that the unique chromatin organization of adult rods renders them incapable to efficiently repair heterochromatic DSBs, providing evidence that heterochromatin affects mammalian DSB repair in vivo.

Infection of Chlorella NC64A cells by PBCV-1 produces a rapid depolarization of the host probably by incorporation of a viral-encoded K(+) channel (Kcv) into the host membrane. To examine the effect of an elevated conductance, we monitored the virus-stimulated efflux of K(+) from the chlorella cells. The results indicate that all 8 chlorella viruses tested evoked a host specific K(+) efflux with a concomitant decrease in the intracellular K(+). This K(+) efflux is partially reduced by blockers of the Kcv channel. Qualitatively these results support the hypothesis that depolarization and K(+) efflux are at least partially mediated by Kcv. The virus-triggered K(+) efflux occurs in the same time frame as host cell wall degradation and ejection of viral DNA. Therefore, it is reasonable to postulate that loss of K(+) and associated water fluxes from the host lower the pressure barrier to aid ejection of DNA from the virus particles into the host.

Originally published at: Rahn, Carolin. Water-filtered infrared A reduces chlamydial infectivity in vitro without causing ex vivo eye damage in pig and mouse models. 2016, University of Zurich, Vetsuisse Faculty. We demonstrated a significant wIRA-dependent reduction of chlamydial infectivity in HCjE cells.Moreover, we observed that wIRA treatment of HCjE prior to infection was sufficient to inhibit chlamydial infectivity and that visible light enhances the effect of wIRA. Irradiation did not reduce cell

Previous experiments established that when the unicellular green alga Chlorella NC64A is inoculated with two viruses, usually only one virus replicates in a single cell. That is, the viruses mutually exclude one another. In the current study, we explore the possibility that virus-induced host membrane depolarization, at least partially caused by a virus-encoded K+ channel (Kcv), is involved in this mutual exclusion. Two chlorella viruses, PBCV-1 and NY-2A, were chosen for the study because (i) they can be distinguished by real-time PCR and (ii) they exhibit differential sensitivity to Cs+, a well-known K+ channel blocker. PBCV-1-induced host membrane depolarization, Kcv channel activity and plaque formation are only slightly affected by Cs+, whereas all three NY-2A-induced events are strongly inhibited by Cs+. The addition of one virus 5–15 min before the other results primarily in replication of the first virus. However, if virus NY-2A-induced membrane depolarization of the host is blocked by Cs+, PBCV-1 is not excluded. We conclude that virus-induced membrane depolarization is at least partially responsible for the exclusion phenomenon.