Progeny Varicella-Zoster Virus Capsids Exit the Nucleus but Never Undergo Secondary Envelopment during Autophagic Flux Inhibition by Bafilomycin A1

Girsch, James H.; Walters, Katherine; Jackson, Wallen; Grose, Charles

There are complementary studies of the effects of Golgi apparatus inhibition on the infectious cycles of PRV and HSV-1. Brefeldin A inhibits protein transport from the endoplasmic reticulum (ER) to the cis-Golgi (42) . In the presence of brefeldin A, PRV crossed the INM and acquired an envelope, becoming a PEV (43) , but the passage of the PEVs through the ONM was blocked by brefeldin A. Monensin causes disassembly and vacuolization of the Golgi apparatus (44) . When HSV-1 was grown in the presence of monensin, viral titers were decreased and exocytosis of secondarily enveloped particles was limited (45) . Thus, the BAF block falls between the locations of the brefeldin block and the monensin block in alphaherpesvirus infectious cycles. We have not yet studied the effect of nocodazole on VZV assembly because the drug also blocks viral entry; therefore, addition of nocodazole to cultures prevents completion of the multistep growth curve over 72 h that is required to achieve a sufficiently high VZV titer to allow visualization of viral particles by TEM (46) .